For over 50 years, health systems the world over have failed people with type 2 diabetes mellitus (T2DM). The WHO documents a quadrupling of people with diabetes in a 34-year period to 422 million in 2014, the overwhelming majority of whom were T2DM. This happened despite extensive scientific literature on the causes of, as well as proven treatments for, this disease. Using a health systems prism to review the extensive medical and nutritional T2DM published research, we identified three main shortcomings of health systems in T2DM: (i) failure in early detection; (ii) failure in understanding the actionable lifestyle drivers; and (iii) subsidizing the causes of the disease. Although small-scale success stories in T2DM control exist, the lack of documented evidence of any country-wide health system's successful attempt to address this epidemic is alarming. The immense and ever-growing health and economic burdens of T2DM should provide all the motivation needed for national and global efforts to counteract the political-economy constraints standing in the way of successful whole-of-system approaches to T2DM.

Adipose tissue represents an organ that is highly dynamic and contributes toward vital survival events such as immune responses, lactation, metabolism fuel, and thermogenesis. Data emerging from recent studies support the notion of adipose tissue being organized into a complex system characterized by a discrete anatomy, elevated physiological plasticity, and specific vascular and nerve supplies. Vasoactive intestinal peptide (VIP), along with its receptors, type 1 (VPAC1) and type 2 (VPAC2), has been implicated in various physiological and pathophysiological processes. However, studies on VIP and its receptors in adipose tissue are limited. To explore VIP's presence and activity, as well as its adipose tissue-based receptors, we conducted a study on isolated adipocytes and adipose tissue from inguinal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT) in normal and cold-stressed rats. Our findings indicate the presence of the gene expression VIP and VPAC1 in both WAT and BAT under normal conditions, while VPAC2 was absent. In both WAT and BAT, cold exposure upregulated VIP gene expression. However, the response of VIP receptors to cold exposure is controversial. VPAC2 gene expression was induced in both WAT and BAT, while VPAC1 gene expression presented no change of significance in BAT and a slight reduction in WAT. Additionally, VIP, VPAC1, and VPAC2 proteins were identified from Western blot studies on white and brown adipocytes. After exposure to cold there was an increase of significance in the VIP, VPAC1, and VPAC2 protein levels. This study provides novel insights into how VIP and its receptors alter gene expression and protein levels in adipose tissue and adipocytes during cold stress, indicating their potential involvement in adipose tissue regulation. The findings propose VIP's potentially crucial role in adipose tissue's adaptation to cold stress by affecting the metabolic and biochemical functions of subcutaneous and interscapular adipocytes, with potentially significant implications in the context of developing therapies targeting metabolic disorders.

This study aimed to investigate the correlation between metabolic dysfunction-associated steatotic liver disease (MASLD) and atherosclerotic cardiovascular disease (ASCVD) in individuals with type 1 diabetes (T1D).

Adults with T1D (n = 659) were consecutively screened for liver steatosis via abdominal ultrasound. The presence of macrovascular disease (including coronary artery disease [CAD], peripheral artery disease [PAD], or ischaemic stroke [CVA, cerebrovascular accident]) was identified via electronic medical records. The 5- and 10-year risks of fatal/nonfatal ASCVD were assessed via the Steno Type 1 Risk Engine. Insulin resistance was assessed via the estimated glucose disposal rate (eGDR).

The MASLD prevalence was 16.8%. The prevalence of composite ASCVD (18.9 vs. 6.8%, p < 0.001), CAD (9.9 vs. 4.7%, p = 0.031), PAD (9.0 vs. 2.2%, p < 0.001) and CVA (6.3 vs. 1.1%, p = 0.002) was greater in people with MASLD. The 5-year (7.8 [2.1-14.4] vs. 4.8 [1.6-12.0]%, p = 0.034) and 10-year (15.0 [4.1-26.8] vs. 9.4 [3.1-22.5]%, p = 0.035) risks of ASCVD were greater in those with MASLD. MASLD was associated with prevalent ASCVD (adjusted OR 4.26, 95% CI 1.79-10.11, p < 0.001), independent of age, sex, diabetes duration, smoking, statin use, LDL-cholesterol, the glomerular filtration rate, albuminuria, and metabolic syndrome.

MASLD is associated with both an increased prevalence of ASCVD and an increased calculated risk of fatal/nonfatal ASCVD in people with T1D.

There is evidence that physical and chemical factors and risky lifestyle behaviours are significantly correlated with elevated susceptibility to coronary heart disease (CHD). Nevertheless, the mediation factors of this relationship are little investigated. This article attempts to assess the mediating factors between CHD and physical activity (PA) in rural residents. We conducted a cross-sectional study of 9,004 permanent residents in rural regions of Xinxiang County, Henan Province. The correlation between CHD and PA was evaluated using a logistic regression model, as well as the association between CHD and its associated risk factors. The robustness of the outcomes was evaluated through sensitivity analysis. The mediating factors of the correlation between CHD and PA in rural residents were explored through mediation analysis. The results showed that CHD was associated with PA (0.72, 95%CI:0.56-0.95), and the levels of fasting insulin (FINS), total cholesterol (TC), and blood glucose (GLU) were associated with PA (-0.92, 95%CI: (-1.48, -0.37), 0.08, 95%CI: (0.01, 0.15), -0.17, 95%CI: (-0.28, -0.06)). The levels of FINS, TC and GLU had significant mediating effects on the association of PA with CHD (1.00, 95%CI: (-0.0028, 0.0000), 1.00, 95%CI: (-0.0016, 0.0000), 1.00, 95%CI: (-0.0014, 0.0000)). In rural populations, PA is associated with CHD, possibly mediated by FINS, TC and GLU, rather than relying solely on the direct effects of PA.

Background: Current research inadequately substantiates the impacts of dietary inflammatory potential based on the dietary inflammatory index (DII) on population health and environmental sustainability in Chinese adults. Objectives: We aimed to investigate the associations between the DII with the risk of all-cause mortality and greenhouse gas (GHG) emissions in Chinese adults. Methods: Data from adults (N = 15,318) in the China Health and Nutrition Survey 1997-2015 wave were included in the analysis. DII and energy-adjusted DII (E-DII) were calculated using dietary intake data collected with a combination of 3-day consecutive 24-h dietary recalls and the food weighing method. The total GHG emissions were calculated by summing the amount of emissions from all the food groups consumed by the participants. Cox proportional hazards regression models and linear regression models were conducted for statistical analysis. Results: A pro-inflammatory diet, as reflected by higher DII and E-DII scores was associated with an increased risk of all-cause mortality (DII: Q5 vs. Q1: HR = 1.82; 95% CI: 1.45-2.30; p-trend < 0.0001; E-DII: Q5 vs. Q1: HR = 1.86; 95% CI: 1.38-2.52; p-trend < 0.0001) and higher amounts of GHG emissions (both p-trend < 0.0001). Conclusions: These findings demonstrated positive associations between pro-inflammatory potentials with an increased risk of all-cause mortality and higher GHG emissions among Chinese adults, suggesting dual adverse impacts of a pro-inflammatory diet on health and environmental sustainability.

An increasing number of epidemiological studies have explored the relationship between the risk of gastric cancer and specific dietary patterns, but the findings remain inconclusive. We, therefore, performed this comprehensive systematic review and meta-analysis to analyze the available evidence regarding the associations between a priori and a posteriori dietary patterns and the risk of gastric cancer. A systematic search of six electronic databases, including PubMed , Web of Science , EBSCO , Scopus , China National Knowledge Infrastructure ( CNKI ), and Wanfang Data , was carried out to retrieve the relevant articles published up to March 2024. Thirty-six studies (10 cohort and 26 case-control studies) with a total of 2 181 762 participants were included in the final analyses. Combining 15 effect sizes extracted from 12 articles, we observed a reduced risk of gastric cancer in the highest versus the lowest categories of the Mediterranean diet [relative risk (RR), 0.72; 95% confidence interval (CI), 0.61-0.85; P  < 0.001]. Combining 11 effect sizes from 10 articles (involving 694 240 participants), we found that the highest Dietary Inflammatory Index scores were significantly associated with an increased risk of gastric cancer (RR, 1.32; 95% CI, 1.11-1.57; P  < 0.001). A reduced risk of gastric cancer was shown for the highest compared with the lowest categories of healthy dietary pattern (RR, 0.78; 95% CI, 0.67-0.91; P  = 0.002). Conversely, the highest adherence to the Western dietary pattern was associated with an increased risk of gastric cancer (RR, 1.33; 95% CI, 1.19-1.49; P  < 0.001). Our study demonstrated that the Mediterranean diet and a healthy dietary pattern were associated with a decreased risk of gastric cancer. Conversely, the Dietary Inflammatory Index and Western dietary pattern were associated with an increased risk of gastric cancer.

Vascular endothelium is integral to the regulation of vascular homeostasis and maintenance of normal arterial function in healthy individuals. Endothelial dysfunction is a significant contributor to the advancement of atherosclerosis, which can precipitate cardiovascular complications. A notable correlation exists between diabetes and endothelial dysfunction, wherein chronic hyperglycemia and acute fluctuations in glucose levels exacerbate oxidative stress. This results in diminished nitric oxide synthesis and heightened production of endothelin-1, ultimately leading to endothelial impairment. In clinical settings, it is imperative to implement appropriate therapeutic strategies aimed at enhancing endothelial function to prevent and manage diabetes-associated vascular complications. Various antidiabetic agents, including insulin, GLP-1 receptor agonists, sulfonylureas, DPP-4 inhibitors, SGLT2 inhibitors, α-glucosidase inhibitors, thiazolidinediones (TZDs), and metformin, are effective in mitigating blood glucose variability and improving insulin sensitivity by lowering postprandial glucose levels. Additionally, traditional Chinese medicinal compounds, such as turmeric extract, resveratrol, matrine alkaloids, tanshinone, puerarin, tanshinol, paeonol, astragaloside, berberine, and quercetin, exhibit hypoglycemic properties and enhance vascular function through diverse mechanisms. Consequently, larger randomized controlled trials involving both pharmacological and herbal interventions are essential to elucidate their impact on endothelial dysfunction in patients with diabetes. This article aims to explore a comprehensive approach to the treatment of diabetic endothelial dysfunction based on an understanding of its pathophysiology.

There's an increasing role of nailfold capillaroscopy in the evaluation of peripheral vascular disease in chronic inflammatory disorders. Familial Mediterranean fever (FMF) is one such disorder, which raises concerns about increased cardiovascular risk, with scarce data available in children. Therefore, we aimed to evaluate insulin resistance, lipid profile, atherogenic indices, and nailfold capillary (NC) changes in children with FMF.

Fifty-four children diagnosed with FMF were evaluated by measuring complete blood count, ESR, CRP, serum amyloid A (SAA), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), lipid profile, and atherogenic indices, along with a nailfold capillaroscopic examination, both during acute attacks and attack-free periods.

During attack-free periods, patients exhibited higher total leucocytic counts, ESR, CRP, SAA, HOMA-IR, total cholesterol (TC), non-high-density lipoprotein cholesterol (non-HDL-C), Castelli's risk index I (CRI I), and atherogenic coefficient (AC), and a lower hemoglobin level than controls. Additionally, the NC examination identified avascular areas in 14.8% of patients, tortuosities in 18.5%, enlargements in 14.8%, and microhemorrhages in 7.4%. These parameters showed significant increases during acute attacks. HOMA-IR showed positive correlations with TC, non-HDL-C, CRI I, and AC; however, NC changes were strongly connected with disease duration and SAA.

Insulin resistance, alterations in serum lipids and atherogenic indices, and NC changes significantly endure in children with FMF during attack-free periods compared to controls, with more prominence during acute attacks. These parameters are linked to subclinical vascular injury and elevated cardiovascular risk, so their monitoring is crucial in these patients for early detection and intervention.

To examine the association between dietary inflammatory index (DII) and risk of gestational diabetes mellitus (GDM).

A prospective birth cohort study was conducted in Iran. During the first trimester of pregnancy, food intake was measured using a food frequency questionnaire. Each participant's DII score was calculated, and then, the Cox proportional hazard model was used to calculate the hazard ratio (HR) and 95% CI of GDM across the quartiles of DII. We systematically searched the literature to conduct a meta-analysis of observational studies (PROSPERO: CRD42022331703). To estimate the summary relative risk for the highest versus lowest category of DII, a random-effects meta-analysis was performed. The certainty of evidence was assessed using the GRADE approach.

In the prospective cohort study (n = 635 pregnant mothers), the multivariable HRs of GDM for the third and fourth quartiles of DII were 2.98 (95%CI: 1.98, 6.46) and 2.72 (95%CI: 1.11, 6.63), respectively. Based on a meta-analysis of six prospective cohorts and a case-control study (1014 cases of GDM in 7027 pregnant mothers), being in the highest category of the DII was associated with a 27% higher risk of GDM (relative risk: 1.27, 95%CI: 1.01, 1.59; I2 = 50%; low certainty of evidence). A dose-response meta-analysis suggested a positive monotonic association between DII and GDM risk.

Our prospective cohort demonstrated a positive correlation between GDM risk and the inflammatory potential of diet in the first trimester of pregnancy. The results need to be confirmed by larger cohort studies.

Not applicable.

Chronic inflammation is a key factor in type 2 diabetes mellitus (T2DM) development. The cholinergic anti-inflammatory pathway (CAP) reduces inflammation by activating α7 nicotinic acetylcholine receptors (α7nAChRs) on macrophages, suppressing proinflammatory cytokines. Acetylcholinesterase inhibitors (AChEis), primarily used for Alzheimer's disease (AD), may exert anti-inflammatory effects through the CAP. One AChEi, galantamine, also directly agonizes α7nAChRs, potentially enhancing its anti-inflammatory properties.

This study aimed to investigate the association between AChEi use, particularly galantamine, and T2DM risk in AD patients.

We conducted a retrospective analysis of Veterans Health Administration (VA) data, examining early- and late-onset AD patients receiving galantamine or other AD medications. Propensity score matching was used to balance groups and minimize confounding. Cox proportional hazard models assessed T2DM risk for galantamine, other AChEis and memantine.

A total of 40 065 AD patients were included in the study. Among early-onset AD patients, galantamine use significantly reduced T2DM risk (hazard ratio [HR] = 0.80, 95% confidence interval [CI]: 0.66-0.98). Memantine also showed a protective effect (HR = 0.82, 95% CI: 0.69-1) in this group. Neither galantamine nor memantine influenced T2DM risk in late-onset AD. Other AD medications showed no association with T2DM risk.

Galantamine use was associated with a lower risk of T2DM in early-onset AD patients, potentially due to enhanced anti-inflammatory effects through both AChE inhibition and direct α7nAChR agonism. Memantine also demonstrated a protective effect. These findings suggest potential new applications for existing AD medications in T2DM prevention, particularly in early-onset AD patients. Further research, including randomized controlled trials with diverse populations, is needed to confirm these results and the underlying mechanisms.

Chronic coronary artery disease (CAD) remains a significant global healthcare burden. Current risk assessment methods have notable limitations in early detection and risk stratification. Hence, there is an urgent need for innovative biomarkers that facilitate the premature CAD diagnosis, ultimately leading to reduction in associated morbidity and mortality rates. This review comprehensively examines recent advances in emerging biomarkers for CAD detection. Our analysis delves into various aspects of these biomarkers such as their mechanisms of action, roles in the pathophysiology of the disease, and different measurement techniques employed in clinical practice. Comparative assessment of biomarker performance between CAD patients and control groups was also presented relying on their sensitivity, specificity, and area under the curve at specific cutoff points. In this regard, prominent biomarkers including Tenascin-C, IL-37, PTX3, transthyretin, soluble interleukin-6 receptor α, and miR-15a are identified as having high diagnostic potential for chronic CAD that indeed showcase promising performance metrics. These findings underscore the role of novel biomarkers in enhancing CAD risk stratification and improving patient outcomes through early intervention. However, the pursuit of an ideal and inclusive biomarker continues due to the multifaceted nature of CAD. Future randomized controlled trials are essential to bridge the gap between research findings and clinical practice in order to augment the practical application of these biomarkers in routine healthcare settings.

Many previous studies explored the relationship between diabetes and insulin resistance (IR); however, addressing the research gap where no bibliometric analysis had been conducted to summarize and analyze these publications, we will undertake a comprehensive bibliometric analysis to investigate the current status and emerging trends in publications examining the association between diabetes and IR.

We retrieved publications related to the interaction between diabetes and IR from the Web of Science Core Collection (WoSCC). By utilizing software such as CiteSpace, VOSviewer, and Excel 2019, we analyzed and extracted relevant information from the literature to identify and delineate the research hotspots and directions in the study of diabetes and IR.

From 1900 to 2024, a total of 2,698 publications were included in the bibliometric analysis, showing a steady annual increase in the number of publications. The USA led in this research field, with the Harvard University being a key research institution. The author Olefsky JM, published the most papers;Defronzo RA was the most cited author. DIABETES was the journal with the highest number of published papers and was also the most cited journal. The main discipline in the field of diabetes and IR research was Endocrinology and Metabolism. The most cited article was "Mechanisms linking obesity to insulin resistance and type 2 diabetes (2006)";"The IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045(2018)" was the most cited reference. "insulin resistance" was the most frequently occurring keyword. The main research hotspots and frontier areas in diabetes and IR research were as follows: (1) The association between IR, diabetes, and obesity was a popular research topic; (2) Cardiovascular diseases secondary to diabetes and IR were another hot topic among researchers; (3) As a core pathological change in diabetes, IR was a major therapeutic target for improving diabetes.

This study summarized the research trends and hotspots in the field of diabetes and IR, provided valuable information and insights for scholars who focused on diabetes and IR scientific research, and offered a reference for future research directions.

The link between serum total bilirubin and metabolic syndrome and its components has been previously proposed. However, it is unknown whether total bilirubin is a risk factor of metabolic syndrome and its components in obese Egyptians. Therefore, this study was conducted to clarify the association of total bilirubin levels with metabolic syndrome and its components in obese Egyptians.

A total of 200 adults with obesity were enrolled in this study. Obese participants were evaluated for metabolic syndrome; there were 92 obese participants with metabolic syndrome and 108 obese participants without metabolic syndrome. Anthropometric measurements, fasting blood glucose (FBG), fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), HOMA-β (%), lipid profile, uric acid, alanine aminotransferase, aspartate aminotransferase, and serum total bilirubin were assessed.

Total bilirubin was significantly lower in obese participants with metabolic syndrome than in those without metabolic syndrome. Compared with middle bilirubin tertile, high and low bilirubin tertiles were independently associated with metabolic syndrome. Regarding metabolic syndrome components, a significant positive association between low bilirubin tertile and hypertension was found independent of the all studied confounding factors, whereas the association of total bilirubin level with waist circumference (WC), FBG, high-density lipoprotein cholesterol, and triglycerides was dependent on body mass index (BMI), HOMA-IR, and high sensitive C-reactive protein (hs-CRP).

Total bilirubin is an independent risk factor of metabolic syndrome in obese Egyptians. We have found an independent association between high bilirubin level and reduced risk of metabolic syndrome, whereas low bilirubin level was associated with increased risk of metabolic syndrome. Bilirubin is also independently associated with hypertension, but its association with other components of metabolic syndrome is mainly dependent on BMI, HOMA-IR, and hs-CRP.

One of the major inflammatory markers, C-reactive protein (CRP), is often elevated in people who have had a heart attack, vascular problems, stroke, or sudden cardiac death. Obesity is associated with higher CRP levels because adipose tissue activates cytokines. Obesity and overweight increase the risk of heart disease, as does an elevated CRP level.

The purpose of this study was to evaluate the association of high-sensitivity CRP (hs-CRP) level with obese normal individuals in North Indian population.

This cross-sectional study included 50 individuals between the ages of 18 and 50 years who were overweight or obese. The degree of obesity was determined by anthropometric measurements. The patients' height, weight, waist circumference (WC), hip circumference, and blood pressure were measured. Enzyme-linked immunosorbent assay-based CRP level was determined from the blood.

The mean WC (cm) was significantly higher in the obese (103.42 ± 9.79) than in the overweight (89.00 ± 8.72). The mean hip circumference (cm) was also significantly smaller in the obese group (99.95 ± 8.07) than in the overweight group (131.29 ± 15.82). The waist-to-hip ratio (WHR) was significantly more in the obese group (88.37%) than in the overweight group (0.00%). WC (cm), hip circumference (cm), WHR, systolic blood pressure (mmHg), and diastolic blood pressure (mmHg) were not significantly correlated with hs-CRP in overweight and obese participants.

Compared with obesity, hs-CRP was not related to obesity. A relationship between hs-CRP and WC, hip circumference, and WHR was not found.

Type 2 diabetes (T2D) is a disease characterized by heterogeneously progressive loss of islet β cell insulin secretion usually occurring after the presence of insulin resistance (IR) and it is one component of metabolic syndrome (MS), and we named it metabolic dysfunction syndrome (MDS). The pathogenesis of T2D is not fully understood, with IR and β cell dysfunction playing central roles in its pathophysiology. Dyslipidemia, hyperglycemia, along with other metabolic disorders, results in IR and/or islet β cell dysfunction via some shared pathways, such as inflammation, endoplasmic reticulum stress (ERS), oxidative stress, and ectopic lipid deposition. There is currently no cure for T2D, but it can be prevented or in remission by lifestyle intervention and/or some medication. If prevention fails, holistic and personalized management should be taken as soon as possible through timely detection and diagnosis, considering target organ protection, comorbidities, treatment goals, and other factors in reality. T2D is often accompanied by other components of MDS, such as preobesity/obesity, metabolic dysfunction associated steatotic liver disease, dyslipidemia, which usually occurs before it, and they are considered as the upstream diseases of T2D. It is more appropriate to call "diabetic complications" as "MDS-related target organ damage (TOD)", since their development involves not only hyperglycemia but also other metabolic disorders of MDS, promoting an up-to-date management philosophy. In this review, we aim to summarize the underlying mechanism, screening, diagnosis, prevention, and treatment of T2D, especially regarding the personalized selection of hypoglycemic agents and holistic management based on the concept of "MDS-related TOD".

The association between inflammatory score, insulin resistance (IR), and metabolic-associated fatty liver disease (MAFLD) is inconclusive.

The objective of this study was to examine the relationship between the inflammatory score and MAFLD and investigate the potential mediating effect of IR (evaluated by triglyceride-glucose index) in this association.

Calculating inflammatory score was performed based on white blood cells and high-sensitivity C-reactive protein. The association between the inflammatory score and MAFLD was evaluated based on the weighted multifactor logistic regression model. Restricted cubic splines (RCS) were used to visualize the dose-response relationship between the inflammatory score and MAFLD. We also conducted a mediation analysis to assess the extent to which IR mediates this association.

Among the 1090 participants, 563 were ultimately diagnosed with MAFLD. Multivariate logistic regression results indicated a close positive association between inflammatory score and MAFLD (odds ratio = 1.235, 95% confidence interval 1.069-1.427, p = .007). The RCS results indicated a linear dose-response relationship between the inflammatory score and the risk of MAFLD after adjusting for potential confounding factors. Furthermore, the mediation analysis results showed that IR partially mediated the association between the inflammatory score and MAFLD (percent mediation = 33%).

Our research results indicate that the inflammatory score is positively associated with the risk of MAFLD, and IR plays a partial mediating effect in this association.

The high prevalence of diabetes mellitus (DM) poses a significant public health challenge, with diabetic kidney disease (DKD) as one of its most serious consequences. It has become increasingly clear that type 2 DM (T2D) and the complications of DKD are not purely metabolic disorders. This review outlines emerging evidence related to the step-by-step contribution of macrophages to the development and progression of DKD in individuals who specifically develop T2D as a result of obesity. The macrophage is a prominent inflammatory cell that contributes to obesity, where adipocyte hypertrophy leads to macrophage recruitment and eventually to the expansion of adipose tissue. The recruited macrophages secrete proinflammatory cytokines, which cause systemic inflammation, glucose dysregulation, and insulin sensitivity, ultimately contributing to the development of T2D. Under such pathological changes, the kidney is susceptible to elevated glucose and thereby activates signaling pathways that ultimately drive monocyte recruitment. In particular, the early recruitment of proinflammatory macrophages in the diabetic kidney produces inflammatory cytokines/chemokines that contribute to inflammation and tissue damage associated with DKD pathology. Macrophage activation and recruitment are crucial inciting factors that also persist as DKD progresses. Thus, targeting macrophage activation and function could be a promising therapeutic approach, potentially offering significant benefits for managing DKD at all stages of progression.

Background: Obesity is a growing global health concern, often accompanied by dyslipidemia, contributing to cardiovascular risk. Understanding the patterns of dyslipidemia in different glycemic states is crucial for targeted interventions. This study compares dyslipidemia patterns in normoglycemic and prediabetic obesity to improve clinical management strategies. Methods: The study analyzed the complete lipid profiles of 138 subjects, comparing the medians, prevalence, diagnostic performance, and risk assessment of each lipid parameter across 54 non-obese (NO), 44 normoglycemic obese (NG-OB), and 40 pre-diabetic obese (PreDM-OB) groups. Results: Elevated total cholesterol (TC) and low-density lipoprotein (LDL) were the most prevalent forms of dyslipidemia observed in obesity (45.35% and 43.53%, respectively). Stratification by glycemic status revealed that triglyceride (TG) levels were elevated in both the NG-OB and PreDM-OB groups, with a more marked increase in the latter group (73.07 mg/dL vs. 97.87 mg/dL vs. 121.8 mg/dL, respectively). Elevated LDL showed better diagnostic performance and higher odds ratios (OR) in the NG-OB group (AUC = 0.660, p = 0.006; OR = 2.78, p = 0.022). Conversely, low high-density lipoprotein (HDL) was more common and exhibited significant diagnostic performance, with higher OR values in the PreDM-OB group (AUC = 0.687, p = 0.002; OR = 3.69, p = 0.018). Importantly, all lipid ratios were elevated in obesity, with TC/HDL showing the highest predictive ability for prediabetes (AUC = 0.7491, p < 0.001). Conclusions: These findings revealed unique and common lipid abnormalities in normoglycemic and prediabetic obesity. Future research should explore the effects of targeted lipid management on obesity-associated complications.

To examine the associations of abnormal maternal glucose regulation in pregnancy with offspring adiposity, insulin resistance, adipokine, and inflammatory markers during childhood and adolescence.

Project Viva is a prospective prebirth cohort (n = 2128 live births) initiated from 1999 through 2002 in Eastern Massachusetts, US. During the second trimester of pregnancy, clinicians used 2-step oral glucose challenge testing to screen for gestational diabetes mellitus. In the offspring, we measured anthropometry, insulin resistance, adipokines, lipids, and inflammatory markers in mid-childhood (n = 1107), early adolescence (n = 1027), and mid-adolescence (n = 693). We used multivariable linear regression models and generalized estimating equations adjusted for child age and sex, and for maternal age, race/ethnicity, education, parity, and smoking during pregnancy; we further adjusted for prepregnancy body mass index (BMI).

In mid-adolescence (17.1 [0.8] years of age), offspring of mothers with gestational diabetes mellitus (n = 27) had a higher BMI z-score (β; 95% Cl; 0.41 SD; 0.00, 0.82), sum of skinfolds (8.15 mm; 2.48, 13.82), homeostatic model assessment for insulin resistance (0.81 units; 0.13, 1.50), leptin z-score (0.40 SD; 0.01, 0.78), and leptin/adiponectin ratio z-score (0.51 SD; CI 0.09, 0.93) compared with offspring of mothers with normoglycemia (multivariable-adjusted models). The associations with BMI, homeostatic model assessment for insulin resistance, and adiponectin seemed stronger in mid-adolescence compared with earlier time points. The associations were attenuated toward the null after adjustment for maternal prepregnancy BMI.

Exposure to gestational diabetes mellitus is associated with higher adiposity, insulin resistance, and altered adipokines in mid-adolescence. Our findings suggest that the peripubertal period could be a key time for the emergence of prenatally programmed metabolic abnormalities.

Vitamin D's role extends beyond classical calcium and phosphate homeostasis to encompass a pivotal influence on immune modulation and metabolic health. The mechanisms by which vitamin D exerts these effects involve its conversion to hormonally active calcitriol, which binds intracellular vitamin D receptors, initiating various downstream cascades. In this review, we tease out the evidence showing the relationship between vitamin D deficiency and prediabetes within the context of subclinical inflammation, with a special focus on the novel monocyte-to-HDL ratio (MHR), a novel inflammatory marker reflecting subclinical inflammation. This was based on a thorough literature review using reputable databases covering the period from 1980 to 2024. In light of this, we discuss calcitriol's anti-inflammatory effects and consequently link vitamin D deficiency to both overt and subclinical inflammation. Additionally, the utility of several biomarkers, notably MHR, in investigating this association is also discussed. We further reviewed the role of vitamin D deficiency in precipitating prediabetes and type 2 diabetes mellitus (T2DM) via insulin resistance, decreased insulin synthesis and secretion, and subclinical inflammation. Taken together, this mini review highlights that vitamin D deficiency is significantly associated with subclinical inflammation, playing a critical role in the development of prediabetes and the progression to T2DM. Addressing vitamin D deficiency through appropriate interventions may serve as a preventative measure against the development of prediabetes and T2DM.

This single case study describes the audiological and vestibular findings of a female patient, aged 62, with diabetes mellitus and rheumatoid arthritis. Based on this case study, we hypothesize that individuals with diabetes mellitus and rheumatoid arthritis are more vulnerable to vestibular impairment. The current findings indicate that central vestibular lesions and bilateral sensorineural hearing loss are related to rheumatoid arthritis and diabetes. Therefore concluding early detection and follow-up is required to understand pathophysiology in detail.

Affective disorders (AD) have been linked to inflammatory processes, although the underlying mechanisms of this relationship are still not fully elucidated. It is hypothesized that demographic, somatic, lifestyle, and personality variables predict inflammatory parameters in AD.

To identify biopsychosocial factors contributing to inflammation in AD measured with two parameters, C-reactive protein (CRP) and leukocytes.

This observational study investigated 186 hospital inpatients diagnosed with AD using demographic parameters, serum inflammatory markers, somatic variables, psychological questionnaires, and lifestyle parameters. Hierarchical regression analyses were used to predict inflammatory markers from demographic, somatic, lifestyle, and personality variables.

Analyses showed that 33.8% of the variance of CRP was explained by body mass index and other somatic medication (e.g. anti-diabetics), age and education, and age of affective disorder diagnosis. For leukocytes, 20.1% of the variance was explained by smoking, diet, metabolic syndrome (MetS), and anti-inflammatory medication (e.g. non-steroidal anti-inflammatory drugs). Other psychiatric or behavioural variables did not reach significance.

Metabolic components seem important, with mounting evidence for a metabolic affective disorder subtype. Lifestyle modifications and psychoeducation should be employed to prevent or treat MetS in AD.

Metabolic syndrome (MetS), marked by enduring metabolic inflammation, has detrimental effects on cognitive performance and brain structure, influencing behavior. This study aimed to investigate whether maternal MetS could negatively impact the neurodevelopment and metabolism of offspring. To test this hypothesis, 2 months old female Wistar rats were subjected to a 10-week regimen of tap water alone or supplemented with 20% fructose to induce MetS. Dams were mated with healthy males to generate litters: OC (offspring from control dams) and OMetS (offspring from dams with MetS). To isolate prenatal effects, all pups were breastfed by control nurse dams, maintaining a standard diet and water ad libitum until weaning. Behavioral assessments were conducted between postnatal days (PN) 22 and 95, and metabolic parameters were analyzed post-sacrifice on PN100. Results from the elevated plus maze, the open field, and the marble burying tests revealed a heightened anxiety-like phenotype in OMetS females. The novel object recognition test showed that exclusively OMetS males had long-term memory impairment. In the reciprocal social interaction test, OMetS displayed a lower number of social interactions, with a notable increase in "socially inactive" behavior observed exclusively in females. Additionally, in the three-chamber test, social preference and social novelty indexes were found to be lower solely among OMetS females. An increase in visceral fat concomitantly with hypertriglyceridemia was the relevant postmortem metabolic finding in OMetS females. In summary, maternal MetS leads to enduring damage and adverse effects on offspring neurobehavior and metabolism, with notable sexual dimorphism.

We conducted this single-center, retrospective, cohort study to examine whether insulin resistance (IR) and high-sensitivity C-reactive protein (hsCRP) have a relationship with metabolic abnormalities in patients with type 2 diabetes mellitus (T2DM). In a total of 3758 patients (n = 3758) with T2DM, we analyzed medical records and thereby evaluated their baseline characteristics such as age, sex, duration of T2DM, systolic blood pressure (SBP), diastolic blood pressure (DBP), waist circumference, body mass index (BMI), visceral fat thickness (VFT), fasting plasma insulin levels, C-peptide levels, glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), homeostatic model assessment of insulin resistance (HOMA-IR), homeostatic model assessment of β-cell function (HOMA-β), aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), albuminuria, intima-media thickness (IMT) and hsCRP. The patients were stratified according to the tertile of the K index of the insulin tolerance test (KITT) or hsCRP. Thus, they were divided into the lowest (≥2.37), middle (1.54-2.36) and highest tertile (0-1.53) of KITT and the lowest (0.00-0.49), middle (0.50-1.21) and highest tertile (≥1.22) of hsCRP. Moreover, associations of KITT and hsCRP with metabolic abnormalities, such as steatotic liver disease (SLD), metabolic syndrome (MetS), albuminuria, diabetic retinopathy and carotid atherosclerosis, were also analyzed. There was a significant positive correlation between the prevalence of SLD, MetS, albuminuria and diabetic retinopathy and KITT (p < 0.001). Moreover, there was a significant positive association between the prevalence of SLD, MetS and albuminuria and hsCRP (p < 0.001). In conclusion, our results indicate that clinicians should consider the relationships of IR and hsCRP with metabolic abnormalities in the management of patients with T2DM. However, further large-scale, prospective, multi-center studies are warranted to confirm our results.

Body Mass Index (BMI) has a significant impact on Coronavirus disease (COVID-19) patient outcomes; however, major adverse cardiac and cerebrovascular outcomes in patients with severe sepsis have been poorly understood. Our study aims to explore and provide insight into its association.

This is an observational study looking at the impact of BMI on COVID-19-severe sepsis hospitalizations. The primary outcomes are adjusted odds of all-cause in-hospital mortality, respiratory failure, and major adverse cardiac and cerebrovascular events (MACCE), which include acute myocardial infarction, cardiac arrest, and acute ischemic stroke. The secondary outcome was healthcare resource utilization. Coexisting comorbidities and patient features were adjusted with multivariable regression analyses.

Of 51,740 patients with severe COVID-19-sepsis admissions, 11.4% were overweight, 24.8% had Class I obesity (BMI 30-34.9), 19.8% had Class II obesity (BMI 35-39.9), and 43.9% had the categorization of Class III obesity (BMI >40) cohorts with age>18 years. The odds of MACCE in patients with class II obesity and class III obesity (OR 1.09 and 1.54; 95CI 0.93-1.29 and 1.33-1.79) were significantly higher than in overweight (p < 0.001). Class I, Class II, and Class III patients with obesity revealed lower odds of respiratory failure compared to overweight (OR 0.89, 0.82, and 0.82; 95CI 0.75-1.05, 0.69-0.97, and 0.70-0.97), but failed to achieve statistical significance (p = 0.079). On multivariable regression analysis, all-cause in-hospital mortality revealed significantly higher odds in patients with Class III obesity, Class II, and Class I (OR 1.56, 1.17, and 1.06; 95CI 1.34-1.81, 0.99-1.38, and 0.91-1.24) vs. overweight patients (p < 0.001).

Patients with Class II and Class III obesity had significantly higher odds of MACCE and in-hospital mortality in COVID-19-severe sepsis admissions.

Amputation confers disabilities upon patients and is linked to substantial morbidity and death attributed to heart disease. While some studies have focused on traumatic amputees in veterans, few studies have focused on traumatic amputees within the general population. Therefore, the present study aimed to assess the risk of heart disease in patients with traumatic amputation with disability within the general population using a large-scale nationwide population-based cohort.

We used data from the Korean National Health Insurance System. A total of 22 950 participants with amputation were selected with 1:3 age, sex-matched controls between 2010 and 2018. We used Cox proportional hazard models to calculate the risk of myocardial infarction, heart failure, and atrial fibrillation among amputees. Participants with amputation had a higher risk of myocardial infarction (adjusted hazard ratio [aHR], 1.30 [95% CI, 1.14-1.47]), heart failure (aHR, 1.27 [95% CI, 1.17-1.38]), and atrial fibrillation (aHR, 1.17 [95% CI, 1.03-1.33]). The risks of myocardial infarction and heart failure were further increased by the presence of disability (aHR, 1.43 [95% CI, 1.04-1.95]; and aHR, 1.38 [95% CI, 1.13-1.67], respectively).

We demonstrate an increased risk of myocardial infarction, heart failure, and atrial fibrillation among individuals with amputation, and the risk further increased in those with disabilities. Clinicians should pay attention to the increased risk for heart disease in patients with amputation.

Biomaterials are pivotal in the realms of tissue engineering, regenerative medicine, and drug delivery and serve as fundamental building blocks. Within this dynamic landscape, polymeric biomaterials emerge as the frontrunners, offering unparalleled versatility across physical, chemical, and biological domains. Natural polymers, in particular, captivate attention for their inherent bioactivity. Among these, carrageenan (CRG), extracted from red seaweeds, stands out as a naturally occurring polysaccharide with immense potential in various biomedical applications. CRG boasts a unique array of properties, encompassing antiviral, antibacterial, immunomodulatory, antihyperlipidemic, antioxidant, and antitumor attributes, positioning it as an attractive choice for cutting-edge research in drug delivery, wound healing, and tissue regeneration. This comprehensive review encapsulates the multifaceted properties of CRG, shedding light on the chemical modifications that it undergoes. Additionally, it spotlights pioneering research that harnesses the potential of CRG to craft scaffolds and drug delivery systems, offering high efficacy in the realms of tissue repair and disease intervention. In essence, this review celebrates the remarkable versatility of CRG and its transformative role in advancing biomedical solutions.

Obesity and postprandial hypertriglyceridemia, characterized by an increase in triglyceride-rich lipoproteins (TRLs), cause chronic low-grade inflammation. It is unclear how postprandial TRLs affect inflammation in white adipocytes.

The objectives of the study were to explore the inflammatory response of postprandial TRLs in white adipocytes and investigate the possible mechanism.

We measured postprandial triglyceride (TG) and high-sensitivity C-reactive protein (hsCRP) concentrations in 204 recruited subjects and treated white adipocytes from mice with postprandial TRLs from above patients with hypertriglyceridemia.

Serum hsCRP concentrations and BMI were positively related to TG concentrations in the postprandial state. Postprandial TRLs increased mRNA and protein expression of inflammatory factors, including interleukin-1β, via the NOD-like receptor protein 3 (NLRP3)/Caspase-1 pathway, and impaired autophagy flux in white adipocytes of mice. TRLs also induced lysosomal damage as evidenced by the reduced protein expression of lysosome-associated membrane proteins-1 and Cathepsin L. Inhibition of Cathepsin B, NLRP3, and mTOR signaling improved autophagy/lysosome dysfunction and inhibited the activation of the NLRP3/Caspase-1 pathway and inflammatory factors induced by TRLs in white adipocytes.

Our results suggest that postprandial hypertriglyceridemia causes chronic inflammation in adipocytes through TRL-induced lysosomal dysfunction and impaired autophagic flux in an mTOR-dependent manner.

Inflammation is a condition that is closely linked to diabetes mellitus type 2 (T2DM), short for T2DM several different antidiabetic medications have been produced to regulate hyperglycemia, with indications that these therapies may have anti-inflammatory effects along with their glucose-lowering efficacy. Thus, this research was planned to explore the impact of antidiabetic agents on the cytokine expression levels -interleukin (IL)-1β, IL-6, IL-17, and IL-37 when patients have T2DM. In this study, 168 eligible subject matter was split into two groups: 50 healthy individuals and 118 cases with T2DM, who were classified into two subgroups: 30 untreated patients and 88 patients treated with metformin-based therapy. The outcome exhibited a significant increase within HbA1c% and proinflammatory cytokines (i.e., IL-1β, IL- 6, and IL-17), whereas IL-37 decreased considerably in untreated cases with T2DM compared to those in subjects who are healthy. Furthermore, the results showed increased levels Regarding waist size, body mass index and assessment using that homeostasis model, cholesterol, triglycerides, low-density lipoprotein levels, and heart danger elements in untreated cases with T2DM in comparison with hygienic subjects. Notably, treated patients with T2DM revealed an ameliorative impact on HbA1c, IL-6, IL-17, IL-37, IL-1β levels and lipid profile compared with untreated patients with T2DM. Antidiabetic agents may have a beneficial activity on the inflammatory status by reducing blood glucose levels, hyperlipidemia, and proinflammatory cytokines. The anti-inflammatory activity of IL-37 can apply a potentially effective therapeutic goal in treating T2DM and its complications.

Cardiometabolic risk prediction models that incorporate metabolic syndrome traits to predict cardiovascular outcomes may help identify high-risk populations early in the progression of cardiometabolic disease.

The purpose of this study was to examine whether a modified cardiometabolic disease staging (CMDS) system, a validated diabetes prediction model, predicts major adverse cardiovascular events (MACE).

We developed a predictive model using data accessible in clinical practice [fasting glucose, blood pressure, body mass index, cholesterol, triglycerides, smoking status, diabetes status, hypertension medication use] from the REGARDS (REasons for Geographic And Racial Differences in Stroke) study to predict MACE [cardiovascular death, nonfatal myocardial infarction, and/or nonfatal stroke]. Predictive performance was assessed using receiver operating characteristic curves, mean squared errors, misclassification, and area under the curve (AUC) statistics.

Among 20,234 REGARDS participants with no history of stroke or myocardial infarction (mean age 64 ± 9.3 years, 58% female, 41% non-Hispanic Black, and 18% diabetes), 2,695 developed incident MACE (13.3%) during a median 10-year follow-up. The CMDS development model in REGARDS for MACE had an AUC of 0.721. Our CMDS model performed similarly to both the ACC/AHA 10-year risk estimate (AUC 0.721 vs 0.716) and the Framingham risk score (AUC 0.673).

The CMDS predicted the onset of MACE with good predictive ability and performed similarly or better than 2 commonly known cardiovascular disease prediction risk tools. These data underscore the importance of insulin resistance as a cardiovascular disease risk factor and that CMDS can be used to identify individuals at high risk for progression to cardiovascular disease.

The cardiovascular and renovascular complications of metabolic deterioration are associated with localized adipose tissue dysfunction. We have previously demonstrated that metabolic impairment delineated the heightened vulnerability of both the perivascular (PVAT) and perirenal adipose tissue (PRAT) depots to hypoxia and inflammation, predisposing to cardioautonomic, vascular and renal deterioration. Interventions either addressing underlying metabolic disturbances or halting adipose tissue dysfunction rescued the observed pathological and functional manifestations. Several lines of evidence implicate adipose tissue thromboinflammation, which entails the activation of the proinflammatory properties of the blood clotting cascade, in the pathogenesis of metabolic and cardiovascular diseases. Despite offering valuable tools to interrupt the thromboinflammatory cycle, there exists a significant knowledge gap regarding the potential pleiotropic effects of anticoagulant drugs on adipose inflammation and cardiovascular function. As such, a systemic investigation of the consequences of PVAT and PRAT thromboinflammation and its interruption in the context of metabolic disease has not been attempted. Here, using an established prediabetic rat model, we demonstrate that metabolic disturbances are associated with PVAT and PRAT thromboinflammation in addition to cardioautonomic, vascular and renal functional decline. Administration of rivaroxaban, a FXa inhibitor, reduced PVAT and PRAT thromboinflammation and ameliorated the cardioautonomic, vascular and renal deterioration associated with prediabetes. Our present work outlines the involvement of PVAT and PRAT thromboinflammation during early metabolic derangement and offers novel perspectives into targeting adipose tissue thrombo-inflammatory pathways for the management its complications in future translational efforts.

We investigated whether genetic predisposition, the Lifestyle Inflammation Score (LIS), or the Food-based Dietary Inflammatory Index (FDII) were associated with diabetes incidence and whether these factors interact.

The study was conducted using population-based cohort data derived from the Korean Genome and Epidemiology Study, which included 6568 people aged 40-69 years. Based on 25 genetic variants related to diabetes, genetic risk scores (GRSs) were determined and LISs and FDIIs were calculated and stratified into quartiles. We investigated the effects of gene-lifestyle interactions on the incident diabetes. The multivariate Cox proportional hazard model was used to generate hazard ratios with 95 % CIs. During the 16-year follow-up period, diabetes incidence was 13.6 per 1000 person-years. A dose-response association with diabetes was observed for both GRS and LIS quartiles but not for FDII quartiles. The GRS and LIS were also independently associated with diabetes incidence in a multivariate model. Compared to the bottom quartile, the top LIS quartile and the top GRS quartile had a 2.4-fold (95 % CI, 2.0-2.8) and a 1.4-fold (95 % CI, 1.2-1.7) higher diabetes risk, respectively. However, the FDII exhibited null association. When each genetic variant was evaluated, the top versus bottom LIS quartiles exhibited heterogeneous diabetes risks for rs560887 within G6PC2, rs7072268 within HK1, and rs837763 within CDT1; however, these differences were not statistically significant in multiple comparison.

Both GRS and LIS factors independently affect the incident diabetes, but their interaction effect showed insignificant association. Therefore, regardless of genetic susceptibility, more effort is needed to lower the risk for diabetes by improving lifestyle behaviors.

The aim of this study was to systematically review and analyze differences in the levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) comparing metabolically healthy but obese (MHO) with metabolically healthy non-obese (MHNO), metabolically unhealthy non-obese (MUNO), and metabolically unhealthy obese (MUO) subjects.

We searched PubMed, Embase, Web of Science, and Scopus for studies that matched the relevant search terms. Differences in inflammatory marker levels between MHO and the other three phenotypes were pooled as standardized mean differences (SMD) or differences of medians (DM) using a random-effects model. We included 91 studies reporting data on 435,007 individuals. The CRP levels were higher in MHO than in MHNO subjects (SMD = 0.63, 95% CI: 0.49, 0.76; DM = 0.83 mg/L, 95% CI: 0.56, 1.11). The CRP levels were higher in MHO than in MUNO subjects (SMD = 0.16, 95% CI: 0.05, 0.28; DM = 0.39 mg/L, 95% CI: 0.09, 0.69). The CRP levels were lower in MHO than in MUO individuals (SMD = -0.43, 95% CI: -0.54, -0.31; DM = -0.82 mg/L, 95% CI: -1.16, -0.48). The IL-6 levels in MHO were higher than in MHNO while lower than in MUO subjects. The TNF-α levels in MHO were higher than in MHNO individuals.

This review provides evidence that CRP levels in MHO are higher than in MHNO and MUNO subjects but lower than in MUO individuals. Additionally, IL-6 levels in MHO are higher than in MHNO but lower than in MUO subjects, and TNF-α levels in MHO are higher than in MHNO individuals.

PROSPERO number: CRD42021234948.

The C-reactive protein (CRP)-triglyceride-glucose (TyG) index (CTI), which is a measure representing the level of inflammation and insulin resistance (IR), is related to poor cancer prognosis; however, the CTI has not been validated in patients with cancer cachexia. Thus, this study aimed to explore the potential clinical value of the CTI in patients with cancer cachexia.

In this study, our prospective multicenter cohort included 1411 patients with cancer cachexia (mean age 59.45 ± 11.38, 63.3% male), which was a combined analysis of multiple cancer types. We randomly selected 30% of the patients for the internal test cohort (mean age 58.90 ± 11.22% 61.4% male). Additionally, we included 307 patients with cancer cachexia in the external validation cohort (mean age 61.16 ± 11, 58.5% male). Receiver operating characteristic (ROC) and calibration curves were performed to investigate the prognostic value of CTI. The prognostic value of the CTI was also investigated performing univariate and multivariate survival analyses.

The survival curve indicated that the CTI showed a significant prognostic value in the total, internal, and external validation cohorts. Prognostic ROC curves and calibration curves revealed that the CTI showed good consistency in predicting the survival of patients with cancer cachexia. Multivariate survival analysis showed that an elevated CTI increased the risk of death by 22% (total cohort, 95% confidence interval [CI] = 1.13-1.33), 34% (internal test cohort, 95%CI = 1.11-1.62), and 35% (external validation cohort, 95%CI = 1.14-1.59) for each increase in the standard deviation of CTI. High CTI reliably predicted shorter survival (total cohort, hazard ratio [HR] = 1.45, 95%CI = 1.22-1.71; internal test cohort, HR = 1.62, 95%CI = 1.12-2.36; external validation cohort, HR = 1.61, 95%CI = 1.15-2.26). High CTI significantly predicted shorter survival in different tumor subgroups, such as esophageal [HR = 2.11, 95%CI = 1.05-4.21] and colorectal cancer [HR = 2.29, 95%CI = 1.42-3.71]. The mediating effects analysis found that the mediating proportions of PGSGA, ECOG PS, and EORTC QLQ-C30 on the direct effects of CTI were 21.72%, 19.63%, and 11.61%, respectively We found that there was a significant positive correlation between the CTI and 90-day [HR = 2.48, 95%CI = 1.52-4.14] and 180-day mortality [HR = 1.77,95%CI = 1.24-2.55] in patients with cancer cachexia.

The CTI can predict the short- and long-term survival of patients with cancer cachexia and provide a useful prognostic tool for clinical practice.

Metabolic diseases are the major causes of macrovascular and microvascular complications which lead to morbidity and mortality. Traditionally, garlic has been used as food and medicine for more than 5000 years. However, efficacy studies have shown conflicting results regarding the garlic effect.

This study aims to evaluate the efficacy of garlic on the components of metabolic syndrome (MetS) in metabolic disease patients.

This study was a systematic review and meta-analysis of randomized controlled trials (RCTs). Pubmed, Cochrane Central Register of Controlled Trials (CENTRAL), and Google scholar were searched till December 25, 2021 for identifying the relevant studies that have shown the effects of garlic on components of metabolic syndrome in metabolic disease patients. The mean difference with 95% CI was calculated using fixed-effect or random-effect models.

The effect of garlic has shown significant changes on waist circumference (p-value= <0.0001), total cholesterol (p < 0.0001), low density lipoprotein (p = 0.01), high density lipoprotein (p < 0.00001), triglycerides (p < 0.00001), systolic blood pressure (p < 0.00001), diastolic blood pressure (p < 0.00001), glucose (p < 0.00001), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) (p = 0.04), C-reactive protein (p < 0.00001), tumor necrosis factor (TNF)-α (p = 0.002), interleukin (IL)-6 (p = 0.0001). Subgroup analysis has shown the favorable effects of garlic in metabolic disease patients.

Our meta-analysis results confirm the findings that garlic could be useful as an anti-hyperlipidemic, anti-hyperglycemic, anti-hypertensive and anti-inflammatory drug.

This study aimed to investigate the effects of aerobic interval training and resistance training on anti-inflammatory adipokines, high sensitivity C-reactive protein, and clinical outcomes in sedentary men with metabolic syndrome.

A total of 33 sedentary men with metabolic syndrome (age: 46.2 ± 4.6 years; body mass index: 35.4 ± 1.9 kg.m2) were randomly assigned to one of 3 groups: aerobic interval training (n = 12), resistance training (n = 10), or control (n = 11). Participants in the exercise groups completed a 12-week training program, 3 sessions per week, while those in the control group maintained their sedentary lifestyle. The levels of high sensitivity C-reactive protein (hs-CRP), omentin-1, adiponectin, lipid profiles, blood pressure, glucose metabolism, body composition, and peak oxygen uptake (VO2peak) were measured at baseline and after the intervention.

Both aerobic interval training and resistance training significantly improved the levels of omentin-1 and adiponectin, as well as reduced inflammation, as indicated by a decrease in hs-CRP levels. Exercise training also led to significant improvements in lipid profiles, blood pressure, glucose metabolism, and body composition. Specifically, the aerobic interval training group had significantly greater increases in high-density lipoprotein cholesterol and VO2peak, as well as greater reductions in low-density lipoprotein cholesterol, triglycerides, and total cholesterol compared to the resistance training group.

Exercise training, particularly aerobic interval training and resistance training, can be an effective non-pharmacological intervention for managing inflammation and improving cardiovascular health in metabolic syndrome patients.

Insulin resistance has been regarded as a hallmark of diabetes heart disease (DHD). Numerous studies have shown that insulin resistance can affect blood circulation and myocardium, which indirectly cause cardiac hypertrophy and ventricular remodeling, participating in the pathogenesis of DHD. Meanwhile, hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with insulin resistance can directly impair the metabolism and function of the heart. Targeting insulin resistance is a potential therapeutic strategy for the prevention of DHD. Currently, the role of insulin resistance in the pathogenic development of DHD is still under active research, as the pathological roles involved are complex and not yet fully understood, and the related therapeutic approaches are not well developed. In this review, we describe insulin resistance and add recent advances in the major pathological and physiological changes and underlying mechanisms by which insulin resistance leads to myocardial remodeling and dysfunction in the diabetic heart, including exosomal dysfunction, ferroptosis, and epigenetic factors. In addition, we discuss potential therapeutic approaches to improve insulin resistance and accelerate the development of cardiovascular protection drugs.

The objective of this study was to explore the effects of three weekly frequency doses of high-intensity functional training (HIFT) on an array of cardiometabolic markers in adults with metabolic syndrome (MetS). Twenty-one men and women, randomized into one (HIFT1), two (HIFT2), or three (HIFT3) days per week of HIFT, completed 3-weeks of familiarization plus a 12-week progressive training program. Pre- and post-intervention, several cardiometabolic, body composition, oxygen consumption, metabolic syndrome severity, and perceptions of fitness measurements were assessed. Additionally, an exercise enjoyment survey was administered post-intervention. A Cohen's d was used to demonstrate within-group change effect size. Although this study was not fully powered, a one-way and two-way ANOVA were used to compare the dose groups to provide provisional insights. No differences were found when frequency dose groups were compared. Many cardiometabolic, body composition, and fitness improvements were seen within each group, with clinically meaningful improvements in the metabolic syndrome severity score (MSSS) (HIFT1: -0.105, d = 0.28; HIFT2: -0.382, d = 1.20; HIFT3: -0.467, d = 1.07), waist circumference (HIFT1: -4.1cm, d = 3.33; HIFT2: -5.4cm, d = 0.89; HIFT3: -0.7cm, d = 0.20), and blood glucose (HIFT1: -9.5mg/dL, d = 0.98; HIFT2: -4.9mg/dL, d = 1.00; HIFT3: -1.7mg/dL, d = 0.23). All three groups similarly reported high exercise enjoyment and likeliness to continue after the intervention. In conclusion, HIFT performed once, twice, or thrice a week elicits improvements in MetS and is considered enjoyable. HIFT, even at a low weekly dose, therefore represents a potential strategy to reduce the global MetS burden.

The relationship between Helicobacter pylori (H. pylori) and fast plasma glucose (FPG) on nondiabetes populations is still inconclusive. Nowadays, not only the high infection rate of H. pylori but also the high FPG level is threatening the Chinese people.

A retrospective cohort study has been established to analyze the relationship between H. pylori infection and FPG level, 18 164 individuals performed healthy examination in Taizhou Hospital Health Examination Center from 2017 to 2022 were included, and hematological indicators, body parameters, and H. pylori detection by 13 C-urea breath test were collected from patients. The follow-up intervals were greater than 12 months.

H. pylori infection was regarded as an independent risk factor for elevated FPG after multivariate logistic regression. Additionally, the average interval time were 33.6 ± 13.3 months. Mean changed FPG values in the persistent infection group were higher than in the subgroup of persistent negative (P = 0.029) as well as eradication infection (P = 0.007). The aforementioned changes began to appear after 2 years of follow-up. Similarly, when compared with the subgroup of persistent infection, mean changed triglyceride/high density lipoprotein (TG/HDL) values were much lower in the subgroup of persistent negative (P = 0.008) and eradication infection (P = 0.018), but the differences appeared after 3 years of follow-up.

H. pylori infection is an independent risk factor for elevated FPG in non-diabetes mellitus (DM) individuals. Persistent H. pylori infection causes an increase in FPG level and TG/HDL, which may be a risk factor for diabetes mellitus.

Polycystic ovary syndrome (PCOS) affects approximately 4% to 12% of females of reproductive age. Previous studies have shown an association between systemic and periodontal diseases. This study aimed to compare the prevalence of periodontal disease in women with PCOS and healthy women.

A total of 196 women aged 17 to 45 years were included in this study. Oral hygiene index-simplified (OHI-S), gingival index (GI), community periodontal index (CPI), and loss of attachment (LA) were assessed. Individuals who smoked, were pregnant, had any systemic disease (such as type 1 or type 2 diabetes mellitus, cardiovascular disease, malignancy, osteoporosis, and thyroid dysfunction), had a history of systemic antibiotic use in the past three months, or received any periodontal intervention in the past 6 months of screening were excluded. Student t-test was used to analyze the data. A p-value of <0.05 was considered statistically significant.

Despite similar OHI-S scores (p=0.972) in the two groups, women with PCOS had significantly higher GI, CPI, and LA scores than healthy women (p<0.001).

Periodontal disease was more prevalent in women with PCOS than in healthy women. This finding may be due to the synergistic effects of PCOS and periodontitis on proinflammatory cytokines. PCOS may have an effect on periodontal disease, and vice versa. Hence, education on periodontal health and early detection and intervention for periodontal diseases is of paramount importance in patients with PCOS.

Metabolic syndrome and elevated high-sensitivity C-reactive protein (hsCRP) levels are associated with risk of cardiovascular diseases. A reduced myocardial mechano-energetic efficiency (MEE) has been found to be an independent predictor of cardiovascular disease.

To evaluate the association between metabolic syndrome and hsCRP levels with impaired MEE.

Myocardial MEE was assessed by a validated echocardiography-derived measure in 1975 nondiabetic and prediabetic individuals subdivided into 2 groups according to the presence of metabolic syndrome.

Individuals with metabolic syndrome exhibited increased stroke work and myocardial oxygen consumption estimated by rate pressure product, and a reduced MEE per gram of left ventricular mass (MEEi) compared with subjects without metabolic syndrome, after adjusting for age and sex. Myocardial MEEi progressively decreased in parallel with the increase in the number of metabolic syndrome components. In a multivariable regression analysis, both metabolic syndrome and hsCRP contributed to reduced myocardial MEEi independently of sex, total cholesterol, high-density lipoprotein, triglycerides, fasting, and 2-hour postload glucose levels. When the study population was divided into 4 groups by the presence or absence of metabolic syndrome and by hsCRP levels above and below 3 mg/L, hsCRP levels ≥3 mg/L were associated with reduced myocardial MEEi both in subjects with metabolic syndrome and in those without the syndrome.

Nondiabetic and prediabetic individuals with metabolic syndrome exhibit increased stroke work and myocardial oxygen consumption, and an impaired MEEi, an established predictor of adverse cardiovascular events, and elevated hsCRP levels in combination with metabolic syndrome aggravate the myocardial MEEi impairment.