Weiling Decoction is a traditional Chinese herbal formula that has the function of removing dampness and transforming turbidity, and it is widely used in the treatment of metabolic diseases. The hypoglycemic and antihyperlipidemic effects of Modified Weiling Decoction (MWLD) have been clinically verified in patients with type 2 diabetes mellitus (T2DM), however, the molecular mechanism remains unclear.

To explore the hypoglycemic mechanism of MWLD based on integrative network pharmacology and experimental validation in vivo and in vitro.

The overlap between T2DM-related genes and target genes of MWLD were deemed to the potential targets of MWLD in alleviating T2DM. Protein-protein interaction analysis was performed to find the core targets from above-mentioned potential targets, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and Gene Ontology (GO) analysis were carried out to gain the key pathways involved in the T2DM improvement by MWLD. T2DM mice and palmitic acid-induced HepG2 cells were employed to validate the mechanism of MWLD predicated by network pharmacology.

A total of 292 target genes from 113 bioactive compounds in MWLD were identified, among of which 42 genes were recognized as core genes of MWLD in ameliorating T2DM. KEGG analysis showed that the therapeutic effect of MWLD on T2DM may be associated with insulin resistance (IR), islet β cell dysfunction, AKT, and MAPK. We found that MWLD significantly reduced fasting blood glucose and improved oral glucose tolerance in T2DM mice. Meanwhile, MWLD activated the AKT/GSK3β pathway to increase liver glycogen production and improve glucose metabolism in T2DM mice. MWLD activated the AKT/mTOR/ULK1 signaling pathway and reversed the increase of autophagy associated proteins (LC3II, Beclin1, Cathepsin B, and LAMP2) in the liver of T2DM mice. Similar results were also confirmed palmitic acid-induced HepG2 cells, an in vitro model for IR. Conversely, AKT inhibitor MK2206 neutralized the effects of MWLD on autophagy and glucose uptake, which was consistent with these results that the main active components of MWLD show strong affinity with AKT1 analyzed by molecular docking.

Both in vivo and in vitro experiments showed that MWLD inhibited excessive autophagy through the AKT/mTOR/ULK1 pathway to improve hepatic IR, and stimulate liver glycogen production through AKT/GSK3β pathway.

Background/Objectives: Diabetes mellitus is characterized by a dysregulated glucose metabolism, necessitating frequent and often invasive monitoring techniques for its effective management. Saliva, a non-invasive and readily accessible biofluid, has been proposed as a potential alternative for glycemic monitoring due to its biochemical correlation with blood glucose levels. This scoping review aims to evaluate the evidence regarding the use of salivary glucose as a biomarker to track glycemic changes in diabetic populations. Methods: This study adhered to the Joanna Briggs Institute guidelines and the PRISMA Extension for Scoping Reviews. A literature search was performed across the PubMed, Scopus, and Web of Science databases, supplemented by manual searches. Results: A total of fifty-seven studies were included, representing populations affected by type 1 diabetes (T1D), type 2 diabetes (T2D), and gestational diabetes (GD). The findings indicated consistent positive correlations between the salivary and blood glucose levels in most studies, although there were significant variations in the sensitivity, specificity, and methodological approaches. Salivary glucose showed promise as a complementary biomarker for glycemic monitoring, particularly due to its non-invasive nature. Conclusions: Challenges such as variability in salivary composition, the absence of standardized collection protocols, and the limited availability of portable devices were noted. This review highlights the potential of saliva as an adjunct sample for diabetes management while stressing the need for further research to bridge existing gaps.

Type 2 diabetes (T2D) is a chronic disease that damages blood vessels and increases the risk of cardiovascular disease (CVD). Heat-shock protein 70 (HSP70), a family of chaperone proteins, has been recently reported as a key player in vascular reactivity that affects large blood vessels like the aorta. Hyperglycemia, a hallmark of diabetes, correlates with the severity of vascular damage and circulating HSP70 levels. In diabetes, blood vessels often show impaired contractility, contributing to vascular dysfunction. However, HSP70's specific role in T2D-related vascular contraction remains unclear. We hypothesized that blocking HSP70 would improve vascular function in a widely used diabetic mouse model (db/db). To test this, we measured both vascular intracellular and serum circulating HSP70 levels in control and diabetic male mice using immunofluorescence and Western blotting. We also examined the aorta's contractile response using a wire myograph system, which measured the force produced in response to phenylephrine (PE), both with and without VER155008, a pharmacological inhibitor that targets the ATPase domain of HSP70, and after removing extracellular calcium. Our findings show that intracellular HSP70 (iHSP70) levels were similar in control and diabetic groups, while circulating HSP70 (eHSP70) levels were higher in the serum of diabetic mice, altering the iHSP70/eHSP70 ratio. Even though VER155008 attenuated both phases of the contractile curve in the diabetic and control groups, enhanced vasoconstriction to PE was only observed in the tonic phase of the curve in the db/db group, which was prevented by iHSP70 inhibition. This effect involved calcium mobilization, as both the maximal and total contraction forces to PE were restored in groups treated with VER155008. Additionally, internal calcium levels in aortic rings treated with VER155008 decreased, as observed in force generation upon calcium reintroduction, which was further corroborated using a biochemical calcium assay. In conclusion, our study demonstrates that blocking HSP70 improves vascular reactivity in the hyperglycemic state of T2D by restoring proper vascular contraction.

This study aims to explore the relationship of serum calcium (Ca) concentration with diabetic kidney disease (DKD) and all-cause mortality among type 2 diabetes mellitus (T2DM) patients using National Health and Nutrition Examination Surveys (NHANES).

Data of T2DM patients aged ≥ 40 years were screened from the NHANES database from 1999 to 2018. The outcomes were the risk of DKD diagnosed by urine albumin-to-creatinine ratio (UACR) ≥ 30 mg/g or estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 and the risk of all-cause mortality ascertained by linkage to National Death Index (NDI) records through 31 December 2019. The weighted univariate and multivariate logistic regression model and cox proportional hazard model were utilized to explore the relationships of serum Ca concentration with DKD and all-cause mortality, respectively, with odds ratios (ORs), hazard ratios (HRs) and 95% confidence interval. The relationships were further explored stratified by age, gender, body mass index (BMI), the duration of T2DM, and the history of cardiovascular disease (CVD), cancer and DKD.

Totally, 6595 T2DM patients were included. Of these patients, 2441 (37.01%) had DKD and 1868 (28.32%) deaths occurred over a mean follow-up of 104.50 (± 1.61) months. In fully adjusted model, we observed high serum Ca concentration was associated with high risk of DKD (OR = 1.45, 95% CI 1.18-1.77) and high all-cause mortality risk (HR = 1.33, 95% CI 1.16-1.52). These relationships remained significant after performing subgroup analyses. The Restricted cubic spline curves shown that linear correlations were observed between serum Ca concentration and DKD as well as all-cause mortality (P < 0.05).

Elevated serum Ca concentration may predict the high risk of DKD and poor prognosis in T2DM patients, and future large-scale and well-designed prospective cohort study is needed to explore the association of serum Ca concentration and DKD and prognosis in T2DM patients.

Early diagnosis and timely treatment of diabetes are critical for effective disease management and the prevention of complications. Undiagnosed diabetes can lead to an increased risk of several health issues. Although numerous machine learning (ML) models have been designed to detect diabetes, many exhibit unsatisfactory performance, are not publicly available, and lack validation on external datasets. To address these limitations, we have developed REMED-T2D, an advanced ensemble ML approach that enhances predictive accuracy and robustness through the integration of diverse ML algorithms. Our approach involves a rigorous data preprocessing process and systematic evaluation of 20 different algorithms, encompassing both conventional ML and deep learning for diabetes prediction. Firstly, we applied an under-sampling approach to an imbalanced Pima Indian Diabetes dataset and generated five balanced datasets. Using these datasets, we investigated various computational strategies to select the optimal model for accurate diabetes classification. Our results demonstrate that REMED-T2D outperformed state-of-the-art methods on the training dataset, with notable improvements in ACC (1.40-4.60%) and MCC (3.50-9.80%). Extensive external validations revealed that the model trained on a five-feature subset achieved ACC of 92.61 % and 92.26 % on the RTML1 and Pabna datasets, respectively. Moreover, a model based on a seven-feature subset improved ACC by 2.80 % and MCC by 13.27 % on the RTML2 dataset. These results suggest the potential of REMED-T2D to predict diabetes in Asian females. Notably, this is the first study to conduct such a comprehensive analysis using the Pima dataset, incorporating a diverse set of ML algorithms. Furthermore, we have developed a publicly accessible web server (https://balalab-skku.org/REMED-T2D/) to facilitate self-monitoring and timely medical interventions. We believe REMED-T2D will assist healthcare professionals in detecting diabetes earlier and implementing preventive measures, ultimately improving health outcomes for those at risk.

Black and red rice have many physiological effects, including antioxidant capacity and decreasing blood glucose, because they are flavonoid-rich. Here, our study found that Hongcaomi (a red rice variety) of five examined rice cultivars contained the highest total polyphenol content and total flavonoid content and the strongest antioxidant activity, with values of 5.83 mg GAE/g, 1.57 mg RE/g, and 72.63 μmol Trolox/g, respectively. The decreased blood glucose effect showed that the strongest effect was shown by the two red rice cultivars, followed by the black rice cultivar Ashamurasaki, the white rice cultivar Yixiang1B, and the black rice cultivar Chongxuehei which had no effect. The study further found that the strongest physiological effect in red rice was derived from catechin. In addition, our study reveals that pigmented rice could decrease blood glucose levels through many pathways, including repairing liver morphology, improving the expression level of genes involved in gluconeogenesis and glycogenesis pathways, and regulating the composition of the gut microbiota.

Type 2 diabetes mellitus (T2DM) is the fastest-growing metabolic disease in the world. The gut microbiota is linked to T2DM. Recent studies have showed that the metabolism of gut microbiota can trigger T2DM. Low dose radiation (LDR) has been proved to activate various protective bioeffects on diabetes. However, the underlying mechanisms remain unclear.

In this study, T2DM model was established using high fat diet combined with streptozocin (STZ) injection in C57BL/6 mice, and then exposed to multiple 75 mGy LDR every other day for one month. The changes of blood glucose levels, body weight, and the damage of pancreas were measured. In addition, 16 S rDNA amplicon sequencing was used to detect gut microbiota alteration. Metabolic profiling was carried out using the liquid mass spectrometry system, followed by the combinative analysis of gut microbiota alteration. Furthermore, the inflammatory factors and related pathways were detected.

We found that LDR attenuate blood glucose levels and the weights of body in T2DM mice, and reduce pancreas impairment. In addition, in the gut, LDR regulated the relative abundance of Bacilli, Desulfobacterota, Verrucomicrobiota, and Proteobacteria. The non-target metabolomics analysis found that LDR significantly improve the metabolic abnormalities in T2DM, which is closely related to the gut microbiota abundance. Furthermore, the inflammatory effects activated by TLR4/MyD88/NF-κB pathways in T2DM were ameliorated by LDR.

These results suggest that LDR may exert a beneficial role in T2DM by modulating gut microbiota and metabolites, especially in TLR4/MyD88/NF-κB pathway.

Studies have shown that the prognosis of dental implant treatment in patients with diabetes is not as good as that in the non-diabetes population. The nerve plays a crucial role in bone metabolism, but the role and the mechanism of peripheral nerves in regulating peri-implant osteogenesis under Type 2 diabetes mellitus (T2DM) situation remains unclear. In this study, it was shown that high glucose-stimulated Schwann cells (SCs) inhibited peri-implant osteogenesis via their exosomes. SCs-derived exosomes were analyzed for their miRNA cargo, identifying miR-15b-5p as significantly downregulated in high glucose conditions. T2DM rats and patients exhibited decreased miR-15b-5p expression, correlating with impaired bone microarchitecture. Luciferase assays and Western blotting confirmed TXNIP as a direct miR-15b-5p target, implicating its involvement in ROS signaling and inflammation-related osteogenesis suppression. Furthermore, normal SCs exosomes improved bone parameters around dental implants in T2DM rats. These findings underscore the therapeutic potential of miR-15b-5p and normal SCs exosomes in mitigating poor peri-implant bone regeneration of T2DM patients, offering insights into the molecular mechanisms of peripheral nerves governing bone regeneration in diabetic conditions.

The aim of this systematic review was to assess the effect of DM (Type 1 and Type 2 Diabetes) and hyperglycaemia on the physical and mechanical properties of dentine which is critical for successful endodontic treatment.

An electronic search of the following databases: PubMed, MEDLINE, Web of Science and the grey literature was performed up until July 2024. In vitro and in vivo studies on the effect of DM or hyperglycaemia on the mechanical and physical properties of dentine were included. Non-English language literature was excluded.

Of the 234 articles identified, 15 met the inclusion criteria. Four studies evaluated how artificially induced glycation or natural glycation of dentine due to aging affects the mechanical properties of dentine. Five studies investigated the influence of Type 2 Diabetes (T2D) on dentine's mechanical properties, while two studies focused on the effects of Type 1 Diabetes (T1D). A further, four studies compared the effects of both T1D and T2D on the dentine. The studies were heterogeneous and a range of mechanical and physical properties were evaluated.

DM and AGEs negatively influence the physical and mechanical properties of dentine however, there remains a paucity of evidence and further studies are needed.

Diabetes Mellitus (DM) is a chronic metabolic disease characterised by hyperglycaemia, an altered immune response and complications associated with collagen connective tissues. DM can influence bone metabolism and alter its physical and mechanical properties via glycation processes within collagen and changes to osteoblast activities. While bone and dentine share similarities, dentine is unique as it is intimately associated with the dental pulp. Inflammation within the pulp can induce calcification and tertiary dentine deposition and so exploring the influence of DM on the mechanical properties of dentine is warranted to understand the clinical significance.

Cardiovascular complications are a primary focus in the clinical management of type 2 diabetes, as they are the leading causes of disability and mortality in individuals with diabetes. Insulin resistance and endothelial dysfunction commonly coexist in diabetic patients. An increasing body of research indicates a reciprocal and interconnected association between endothelial function and insulin resistance. Insulin resistance can manifest in two distinct forms: endothelial and metabolic, with the former predominantly affecting vascular endothelial cells and the latter primarily impacting peripheral cells. The understanding of endothelial insulin resistance is crucial in comprehending the pathophysiology of cardiovascular complications in type 2 diabetes. Hence, the objective of this study is to examine the correlations, interplays, and molecular pathways linking endothelial insulin resistance and metabolic insulin resistance, with the aim of offering novel insights and scholarly resources for the prevention and management of diabetic vascular complications.

Background/Objectives: Barley dietary fiber (BDF), particularly β-glucan, has shown potential in modulating postprandial glycemic responses and improving metabolic health. This study aimed to assess the effects of Saechalssalbori (Hordeum vulgare L.), a glutinous barley variety rich in β-glucan, on postprandial blood glucose, insulin, glucagon, triglycerides, and appetite-related hormones in healthy adults. Methods: In this randomized, double-blind, placebo-controlled, crossover trial, healthy adults (n = 67) with fasting blood glucose levels below 126 mg/dL were assigned to consume either BDF or placebo (rice flour). Fasting and postprandial blood samples were collected at 30, 60, 120, and 180 min after consumption. Blood glucose, insulin, glucagon, triglycerides, and appetite-related hormones (ghrelin, PYY) were measured, and appetite was assessed using the visual analog scale (VAS). The study was approved by the Institutional Review Board (CHAMC 2022-08-040-007) and registered (KCT0009166). Results: BDF consumption significantly delayed the postprandial increase in blood glucose compared with placebo, reduced insulin secretion, and slightly increased glucagon and triglycerides. BDF also lowered hunger and increased satiety, with associated increases in ghrelin and PYY levels. Conclusions: BDF consumption, particularly from β-glucan-rich barley, may improve postprandial glycemic control and suppress appetite, making it a promising dietary intervention for managing metabolic conditions such as diabetes. Further studies are needed to explore its long-term impact on glycemic variability.

The risk of cardiovascular complications is significantly elevated in patients with diabetic kidney disease (DKD). Recognizing the link between the progression of DKD and an increased risk of cardiovascular disease (CVD), it is crucial to focus on the early prediction and management of CVD risk factors among these patients to potentially enhance their health outcomes.

This study sought to bridge the existing gap by developing and validating machine learning (ML) models that utilize clinical data and shear wave elastography (SWE) radiomics features to identify patients at risk of CVD, ultimately aiming to improve the management of DKD.

This study conducted a retrospective analysis of 586 patients with DKD, dividing them into training and external validation cohorts. We categorized patients based on the presence or absence of CVD. Utilizing SWE imaging, we extracted and standardized radiomics features to develop multiple ML models. These models underwent internal validation using radiomics features alone, clinical data, or a combination thereof. The optimal model was then identified, and its feature importance was assessed through the Shapley Additive Explanations (SHAP) method, before proceeding to external validation.

Among the 586 patients analyzed, 30.7% (180/586) were identified as at risk for CVD. The study pinpointed six significant radiomics features related to CVD, alongside six critical pieces of clinical data. The Support Vector Machine (SVM) model outperformed others in both internal and external validations. Further, SHAP analysis highlighted five principal determinants of CVD risk, comprising three clinical indicators and two SWE radiomics features.

This study highlights the effectiveness of an SVM model that combines clinical and radiomics features in predicting CVD risk among DKD patients. It enables early prediction of CVD in this patient group, thereby supporting the implementation of timely and suitable interventions.

This study aims to assess the therapeutic potential of combining Shen-Ling-Bai-Zhu-San (SLBZS) or prebiotics with intermittent fasting (IF) in type 2 diabetes mellitus (T2DM) mice and to investigate the synergistic effects and underlying mechanisms.

Type 2 diabetic mouse models were induced using high-fat diet (HFD) and streptozotocin (STZ), followed by IF treatment. Mice were then grouped for combined therapy with different doses of SLBZS and prebiotics. Fasting blood glucose (FBG) levels, body weight variations, and oral glucose tolerance tests were assessed to elucidate metabolic alterations. The hepatic and renal parameters were evaluated to determine systemic changes in T2DM mice, while the insulin levels were quantified by ELISA to assess glucose homeostasis. Gut microbiota alterations were examined via 16S rRNA sequencing. Alterations of the genes in relevant signaling pathways were analyzed using RT-qPCR.

IF improved FBG, body weight, insulin levels, and other diabetes indicators. Combined IF with SLBZS or prebiotics yielded similar effects. Furthermore, it ameliorated dyslipidemia and mitigated hepatic and renal parameters in T2DM mice. Pancreatic tissue histopathology showed islet cell restoration post-intervention. IF therapy reduced the abnormally elevated GSK-3β gene expression and increased the abnormally reduced GLUT2 genes. Further analysis indicated that the combination of IF with prebiotics and high doses of SLBZS upregulated the expression of the INSR and IRS1 genes. Gut microbiota analysis revealed restored diversity and structure, with notable changes in specific bacterial families. At the family level, the contents of Akkermansiaceae and Bifidobacteriaceae were restored. Phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) analysis suggested metabolic pathway alterations.

IF improved type 2 diabetic symptoms, with combined SLBZS and prebiotics showing similar effects. IF with high concentration of SLBZS and prebiotics doses upregulated the INSR and IRS1 genes and had superior effects on gut microbiota compared to IF alone.

The aim of this study was to determine the association between insulin glargine usage and the potential increase in cancer risk among the Lithuanian population diagnosed with type 2 diabetes mellitus (T2DM).

A retrospective cohort study was conducted. The cohort of insulin users was established by identifying all male and female patients diagnosed with T2DM, as recorded in the National Health Insurance Fund database between 1 January 2000 and 31 December 2012. The risk of cancer among insulin glargine users was compared with the risk in non-glargine insulin users. Cox proportional hazard models were used to estimate hazard ratios (HR) and their 95% confidence intervals (CI).

The overall cancer risk for all sites combined showed no significant difference (HR 0.84, 95% CI 0.67-1.05). Although a general decrease in the risk of cancers was observed at most sites for glargine users, the use of insulin glargine was associated with a non-significant increase in the risk of mouth and pharynx, stomach, non-melanoma skin, breast, cervical, ovarian, and central nervous system cancers. There was a tendency for a lower risk of colon, rectum, rectosigmoid, and anus cancer among glargine users (HR 0.45, 95% CI 0.18-1.12, p = 0.09).

Our research contributes to the growing body of evidence showing that insulin glargine is not associated with an increased risk of all cancers or specific types of cancer.

Boiled silkworm cocoons have been used to treat 'Xiaoke disease' (diabetes mellitus) recorded in Chinese medicine for over 800 years. In recent years, it has been found that the active substance silk sericin (SS) has therapeutic benefits in treating type 2 diabetes mellitus (T2DM). SS promotes pancreatic islet signalling, the proliferation of pancreatic islet cells, and insulin secretion. It is inferred that SS enters the bloodstream after oral administration and plays a role in the body's circulation. As a natural protein, SS needs to resist digestion by proteases in the gastrointestinal tract and cross the gastrointestinal barrier after oral administration. It is currently unclear how SS crosses the gastrointestinal barrier and whether it exerts therapeutic effects on T2DM by entering the circulation.

To study how SS crosses the gastrointestinal barrier and whether it enters the body circulation to exert a therapeutic effect on T2DM.

SS was extracted from silkworm cocoons using an alkaline method with sodium carbonate. The antidigestive capacity of SS was detected using SDS-PAGE gel electrophoresis experiments. The mode of uptake and translocation of orally consumed SS in vivo was analysed using the AP-side to BL-side and BL-side-AP-side translocations, apparent Permeability coefficient (Papp), and Exocytosis rates (ER). The study compared the differences between the adSS group and the adSS + EDTA group by using Ethylenediaminetetraacetic acid (EDTA) to separate the tight junctions between Caco-2 cells. The aim was to analyze whether the transport mode of oral filaggrin proteins in vivo could be absorbed by bypass transport. By administering SS through oral and intraperitoneal injection to type 2 diabetic mice, we measured its concentration in the blood, as well as blood glucose and insulin levels, to determine its effectiveness in treating diabetes and its ability to enter the body's circulation for treatment.

The molecular weight of SS decreased from 10k∼25 kDa to 10k∼15 kDa after in vitro simulated gastrointestinal fluid digestion, indicating its good antidigestive properties. The apparent Papp was greater than 1 × 10-6 cm·s-1, and the ER was between 0.5 and 1.5, indicating that adSS was well-absorbed and mainly passively transported. The Caco-2 cell model showed that the addition of EDTA promoted the transport of adSS, resulting in significantly larger Papp and ER values, indicating that adSS was absorbed by bypass transport. After oral administration of SS, the concentration of SS in the blood was lower than after intraperitoneal injection, which is 60% of intraperitoneal administration. Mice with a T2DM model who were administered SS for 5 weeks showed significant improvement in insulin resistance and glucose tolerance. Additionally, the pancreatic tissue appeared more regular. In the treatment of T2DM, injections of SS have been shown to be more effective than oral administration. Both oral and intraperitoneal injections have been partially involved in the circulation.

SS is enzymatically cleaved by proteolytic enzymes in the gastrointestinal tract. The smaller molecules are partially absorbed into the body's circulation through passive and paracrine transport, exerting a therapeutic effect on T2DM.

Diabetes mellitus (DM) poses a significant health burden globally, impacting millions due to its metabolic disruptions. Among its complications, diabetic peripheral neuropathy (DPN) is a prevalent concern, affecting sensory and motor nerves. While various diagnostic methods exist, discrepancies persist in prevalence estimates of DPN among diabetic populations.

This meta-analysis aimed to assess the prevalence of DPN in individuals with DM, focusing on sural nerve conduction velocity (NCV) measurements. Additionally, the study explored how different evaluation techniques influenced prevalence estimates.

A systematic literature search was conducted following PRISMA guidelines across multiple databases. Studies reporting sural nerve NCV measurements in diabetic patients were included. Data extraction, quality assessment, and statistical analyses were performed to synthesize findings.

Twenty-six studies met the inclusion criteria, providing insights into sural nerve NCV among diabetic individuals. Pooled analysis revealed a mean sural nerve NCV of 42.12 m/s (95% CI: 39.87-44.36), indicative of reduced conduction velocity in diabetic populations. Furthermore, sural nerve amplitude was significantly lower in diabetic individuals, with a pooled mean of 4.68 μV (95% CI: 3.11-6.25).

Individuals with type 2 DM exhibit impaired sural nerve function, as evidenced by reduced NCV and amplitude measurements. Timely NCV assessment, alongside glycemic monitoring, is crucial for identifying and managing DPN to prevent further complications. Interventions addressing glycemic control, dietary regulation, and lifestyle modifications are recommended to mitigate the progression of neuropathy in diabetic populations.

Various strategies aim to better assess risks and refine prevention for patients with type 2 diabetes mellitus (T2DM), who vary in cardiovascular disease (CVD) risk. However, the prognostic value of personality and its association with lifestyle factors remain elusive.

We identified 8794 patients with T2DM from the UK Biobank database between 2006 and 2010 and followed them up until the end of 2021. We assessed personality traits using the Big Five proxies derived from UK Biobank data: sociability, warmth, diligence, curiosity, and nervousness. Healthy lifestyle behaviors were determined from information about obesity, smoking status, and physical activity. The primary outcome was a composite of incident CVD, including myocardial infarction (MI), ischemic stroke (IS), atrial fibrillation (AF), and heart failure (HF).

During a median follow-up of 13.6 years, a total of 2110 patients experienced CVDs. Among personality traits, diligence was significantly associated with a reduced risk of primary and secondary outcomes. The adjusted HRs with 95% CIs were: composite CVD, 0.93 (0.89-0.97); MI 0.90 (0.82-1.00); IS 0.83 (0.74-0.94); AF 0.92 (0.85-0.98); HF 0.84 (0.76-0.91). Healthy lifestyle behaviors significantly reduced the risk of composite CVDs in groups with high and low diligence. The findings of a structural equation model showed that diligence directly affected the risk of the primary outcome or indirectly by modifying lifestyle behaviors.

This study revealed which personality traits can influence CVD risk during T2DM and how patients might benefit from adopting healthy lifestyle behaviors in relation to personality.

Litchi chinensis Sonn (Litchi) has been listed in the Chinese Pharmacopeia, and is an economically and medicinally valuable species within the family Sapindaceae. However, the material basis of its pharmacological action and the pharmacodynamic substances associated with its hypoglycemic effect are still unclear. The predominant objective of this study was to establish the fingerprint profile of litchi leaves and to evaluate the relationship between the components of the high-performance liquid chromatography (HPLC) fingerprint of litchi leaves, assess its hypoglycemic effect by measuring α-glucosidase and α-amylase inhibition, and find the spectrum-effect relationship of litchi leaves by bivariate correlation analysis, Grey relational analysis and partial least squares regression analysis. In this study, the fingerprint of litchi leaves was established by HPLC, and a total of 15 common peaks were identified that clearly calibrated eight components, with P1 being gallic acid, P2 being protocatechuic acid, P3 being catechin, P6 being epicatechin, P12 being rutin, P13 being astragalin, P14 being quercetin and P15 being kaempferol. The similarities between the fingerprints of 11 batches of litchi leaves were 0.766-0.979. Simultaneously, the results of the spectrum-effect relationship showed that the chemical constituents represented by peaks P8, P3, P12, P14, P2, P13, and P11 were relevant to the hypoglycemic effect.

In an increasingly aging and overweight population, osteoporosis and type 2 diabetes (T2DM) are major public health concerns. T2DM patients experience prejudicial effects on their bone health, affecting their physical capacity. Exercise in hypoxia (EH) and a low-carbohydrate diet (LCD) have been suggested for therapeutic benefits in T2DM, improving bone mineral content (BMC) and glycemic control. This study investigated the effects of EH combined with an LCD on body composition and functional and physiologic capacity in T2DM patients. Older T2DM patients (n = 42) were randomly assigned to the following groups: (1) control group: control diet + exercise in normoxia; (2) EH group: control diet + EH; (3) intervention group: LCD + EH. Cardiopulmonary tests (BRUCE protocol), body composition (DEXA), and functional capacity (6MWT, handgrip strength) were evaluated. Body mass index (kg/m2) and body fat (%) decreased in all groups (p < 0.001). BMC (kg) increased in all groups (p < 0.001) and was significantly higher in the EH and EH + LCD groups (p < 0.001). VO2peak improved in all groups (p < 0.001), but more so in the hypoxia groups (p = 0.019). Functional capacity was increased in all groups (p < 0.001), but more so in the EH group in 6MWT (p = 0.030). EH with and without an LCD is a therapeutic strategy for improving bone mass in T2DM, which is associated with cardiorespiratory and functional improvements.

Albuminuria is a well-known predictor of chronic kidney disease in patients with type 2 diabetes mellitus (DM). However, proteinuria is associated with chronic complications in patients without albuminuria. In this retrospective cohort study, we explored whether non-albumin proteinuria is associated with all-cause mortality and compared the effects of non-albumin proteinuria on all-cause mortality between patients with and without albuminuria. We retrospectively collected data from patients with type 2 DM for whom we had obtained measurements of both urinary albumin-to-creatinine ratio (UACR) and urinary protein-to-creatinine ratio (UPCR) from the same spot urine specimen. Urinary non-albumin protein-creatinine ratio (UNAPCR) was defined as UPCR-UACR. Of the 1809 enrolled subjects, 695 (38.4%) patients died over a median follow-up of 6.4 years. The cohort was separated into four subgroups according to UACR (30 mg/g) and UNAPCR (120 mg/g) to examine whether these indices are associated with all-cause mortality. Compared with the low UACR and low UNAPCR subgroup as the reference group, multivariable Cox regression analyses indicated no significant difference in mortality in the high UACR and low UNAPCR subgroup (hazard ratio [HR] 1.189, 95% confidence interval [CI] 0.889-1.589, P = 0.243), but mortality risks were significantly higher in the low UACR and high UNAPCR subgroup (HR 2.204, 95% CI 1.448-3.356, P < 0.001) and in the high UACR with high UNAPCR subgroup (HR 1.796, 95% CI 1.451-2.221, P < 0.001). In the multivariable Cox regression model with inclusion of both UACR and UNAPCR, UNAPCR ≥ 120 mg/g was significantly associated with an increased mortality risk (HR 1.655, 95% CI 1.324-2.070, P < 0.001), but UACR ≥ 30 mg/g was not significantly associated with mortality risk (HR 1.046, 95% CI 0.820-1.334, P = 0.717). In conclusion, UNAPCR is an independent predictor of all-cause mortality in patients with type 2 DM.

Type 2 diabetes mellitus (T2DM) and depression are often linked. Several studies have reported the role of molecular markers either in diabetes or depression. The present study aimed at molecular level profiling of Indoleamine-2,3-dioxygenase (IDO), brain-derived neurotrophic factor (BDNF) and cellular senescence in patients with type 2 diabetes with and without depression compared to individuals with healthy controls.

A total of 120 individuals diagnosed with T2DM were enlisted for the study, with a subset of participants with and without exhibiting depression. The gene expression analysis was done using quantitative real-time PCR.

Indoleamine 2,3 dioxygenase (p < 0.001) and senescence genes (p < 0.001) were significantly upregulated, while brain derived neurotrophic factor (p < 0.01) was significantly downregulated in T2DM patients comorbid with and without depression when compared to healthy controls.

Indoleamine 2,3 dioxygenase, Brain derived neurotrophic factor and cellular senescence may play a role in the progression of the disease. The aforementioned discoveries offer significant contributions to our understanding of the molecular mechanisms that underlie T2DM with depression, potentially aiding in the advancement of prediction and diagnostic methods for this particular ailment.

Isoquinoline alkaloids are an important class of natural products that are abundant in the plant kingdom and exhibit a wide range of structural diversity and biological activities. With the deepening of research in recent years, more and more isoquinoline alkaloids have been isolated and identified and proved to contain a variety of biological activities and pharmacological effects. In this review, we introduce the research progress of isoquinoline alkaloids from 2019 to 2022, mainly in the part of biological activities, including antitumor, antimicrobial, antidiabetic, antiviral, anti-inflammatory, antioxidant, neuroprotective, hepatoprotective, analgesic, and other activities. This study provides a clear direction for the rational development and utilization of isoquinoline alkaloids, suggesting that these alkaloids have great potential in the field of drug research.

Diabetes places a significant burden on personal and public health. However, a comprehensive assessment of the burden of diabetes in older adults is lacking. We aimed to estimate the global burden of diabetes and explore trends for the population aged ≥70 from 1990 to 2019.

Using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, the prevalence, mortality, and disability-adjusted life-years (DALYs) of diabetes among people aged ≥70 were estimated by sex and age group in 2019. We also assessed the epidemiological trend of diabetes from 1990 to 2019.

In 2019, 110.1 million (95% uncertainty interval [UI]: 101.2-119.4) people aged ≥70 years were living with diabetes (types 1 and 2 combined) with a global prevalence of 23.7% (21.8%-25.8%). Worldwide, 181.9 deaths (163.0-194.7) per 100,000 population and 4512.3 DALYs (3861.3-5264.2) per 100,000 population occurred due to diabetes. In 2019, minor sex-related disparities in the burden of diabetes were identified among specific age and sex groups. From 1990 to 2019, the prevalence of diabetes increased by 39.7% (37.7%-41.7%), and the related mortality and DALY rates also increased (16.4% [9.43%-22.9%] and 22.3% [17.2%-27.0%], respectively).

The global burden of diabetes in adults aged ≥70 has increased markedly from 1990 to 2019. As the population continues to age, there is an urgent need to combat the increasing disease burden.

Diabetes mellitus is a metabolic disorder characterized by high blood sugar levels. In recent years, T2DM has become a worldwide health issue due to an increase in incidence and prevalence. Diabetic kidney disease (DKD) is one of the devastating consequences of diabetes, especially owing to T2DM and the key clinical manifestation of DKD is weakened renal function and progressive proteinuria. DKD affects approximately 1/3rd of patients with diabetes mellitus, and T2DM is the predominant cause of end-stage kidney disease (ESKD). Several lines of studies have observed the association between vitamin D deficiency and the progression and etiology of type II diabetes mellitus. Emerging experimental evidence has shown that T2DM is associated with various kinds of kidney diseases. Recent evidence has also shown that an alteration in VDR (vitamin D receptor) signaling in podocytes leads to DKD. The present review aims to examine vitamin D metabolism and its correlation with T2DM. Furthermore, we discuss the potential role of vitamin D and VDR in diabetic kidney disease.

Diabetes is a group of diseases marked by poor control of blood glucose levels. Diabetes mellitus (DM) occurs when pancreatic cells fail to make insulin, which is required to keep blood glucose levels stable, disorders, and so on. High glucose levels in the blood induce diabetic effects, which can cause catastrophic damage to bodily organs such as the eyes and lower extremities. Diabetes is classified into many forms, one of which is controlled by hyperglycemia or Diabetic Kidney Disease (DKD), and another that is not controlled by hyperglycemia (nondiabetic kidney disease or NDKD) and is caused by other factors such as hypertension, hereditary. DKD is associated with diabetic nephropathy (DN), a leading cause of chronic kidney disease (CKD) and end-stage renal failure. The disease is characterized by glomerular basement membrane thickening, glomerular sclerosis, and mesangial expansion, resulting in a progressive decrease in glomerular filtration rate, glomerular hypertension, and renal failure or nephrotic syndrome. It is also represented by some microvascular complications such as nerve ischemia produced by intracellular metabolic changes, microvascular illness, and the direct impact of excessive blood glucose on neuronal activity. Therefore, DKD-induced nephrotic failure is worse than NDKD. MicroRNAs (miRNAs) are important in the development and progression of several diseases, including diabetic kidney disease (DKD). These dysregulated miRNAs can impact various cellular processes, including inflammation, fibrosis, oxidative stress, and apoptosis, all of which are implicated during DKD. MiRNAs can alter the course of DKD by targeting several essential mechanisms. Understanding the miRNAs implicated in DKD and their involvement in disease development might lead to identifying possible therapeutic targets for DKD prevention and therapy. Therefore, this review focuses specifically on DKD-associated DN, as well as how in-silico approaches may aid in improving the management of the disease.

Although most studies have shown that neighborhood social cohesion (NSC) is associated with life satisfaction among patients with type 2 diabetes mellitus (T2DM), it remains unclear how NSC is linked to life satisfaction. The present study aims to examine the potential mediation effect of depressive symptoms and sleep quality on the relationship between NSC and life satisfaction among Chinese individuals with T2DM.

A cross-sectional survey was conducted from August 2019 to November 2020 involving 1747 T2DM patients. The main information was obtained using the Center for Epidemiological Survey Depression Scale (CES-D), self-report sleep quality and life satisfaction questionnaire and NSC scales. Mediation analyses were performed using the PROCESS macro in SPSS.

The results manifested that the NSC was positively associated with sleep quality (r = 0.219) and life satisfaction (r = 0.214), while negatively correlated with depressive symptoms (r = -0.232). Depressive symptoms were found to be negatively associated with life satisfaction (r = -0.263). NSC influenced life satisfaction through three mediating pathways: (a) depressive symptoms (effect = 0.0081); (b) depressive symptoms and sleep quality (effect = 0.0019); and (c) sleep quality (effect = 0.0015). The total mediating effect accounted for 28.1% of the overall effect.

Our findings support the hypothesis that depressive symptoms and sleep quality mediated the relationship between NSC and life satisfaction in patients with T2DM. It is important to encourage T2DM patients to participate in social interactions and enhance their level of NSC. Additionally, efforts should be made to actively reduce depressive symptoms and improve sleep quality, so as to improve their life satisfaction.

Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are aging related diseases with high incidence. Because of the correlation of incidence rate and some possible mechanisms of comorbidity, the two diseases have been studied in combination by many researchers, and even some scholars call AD type 3 diabetes. But the relationship between the two is still controversial.

This study used seed-based d mapping software to conduct a meta-analysis of the whole brain resting state functional magnetic resonance imaging (rs-fMRI) study, exploring the differences in amplitude low-frequency fluctuation (ALFF) and cerebral blood flow (CBF) between patients (AD or T2DM) and healthy controls (HCs), and searching for neuroimaging evidence that can explain the relationship between the two diseases.

The final study included 22 datasets of ALFF and 22 datasets of CBF. The results of T2DM group showed that ALFF increased in both cerebellum and left inferior temporal gyrus regions, but decreased in left middle occipital gyrus, right inferior occipital gyrus, and left anterior central gyrus regions. In the T2DM group, CBF increased in the right supplementary motor area, while decreased in the middle occipital gyrus and inferior parietal gyrus. The results of the AD group showed that the ALFF increased in the right cerebellum, right hippocampus, and right striatum, while decreased in the precuneus gyrus and right superior temporal gyrus. In the AD group, CBF in the anterior precuneus gyrus and inferior parietal gyrus decreased. Multimodal analysis within a disease showed that ALFF and CBF both decreased in the occipital lobe of the T2DM group and in the precuneus and parietal lobe of the AD group. In addition, there was a common decrease of CBF in the right middle occipital gyrus in both groups.

Based on neuroimaging evidence, we believe that T2DM and AD are two diseases with their respective characteristics of central nervous activity and cerebral perfusion. The changes in CBF between the two diseases partially overlap, which is consistent with their respective clinical characteristics and also indicates a close relationship between them.

PROSPERO [CRD42022370014].

Prebiotics exert favorable effects on the host through interactions with probiotics, and their beneficial impacts have been extensively validated across various chronic ailments, including diabetes. This study presents findings from a case-control investigation involving 10 individuals with type 2 diabetes mellitus (T2DM) and 10 healthy counterparts. Fresh stool specimens were collected from all participants. Following a 24-h fermentation period in mediums containing xylitol and mannitol, the observed increase in Lactobacillus abundance within the case group exceeded that of the control group. Similarly, in mediums containing soluble starch, choline, and L-carnitine, the augmentation of Bifidobacterium within the case group surpassed that of the controls. Notably, a statistically significant divergence in sugar degradation rate emerged between the case and control groups, specifically in the medium harboring lactulose and isomalto-oligosaccharides. Remarkably, the degradation rate of lactulose exhibited a positive correlation with the expansion of Bifidobacterium (R 2 = .147, p = .037). Likewise, the degradation rate of isomalto-oligosaccharides demonstrated a positive correlation with Bifidobacterium proliferation (R 2 = .165, p = .041). In conclusion, prebiotics like xylitol and mannitol exhibit the capacity to enhance intestinal probiotic populations in individuals newly diagnosed with diabetes. The modifications in the intestinal flora homeostasis of diabetic patients may be evidenced by alterations in the degradation rate of specific prebiotic substrates.

A substantial amount of evidence suggests a close relationship between osteoporosis (OP) and Type 2 Diabetes Mellitus (T2DM), but the mechanisms involved remain unknown. Therefore, we conducted this study with the aim of screening for hub genes common to both diseases and conducting a preliminary exploration of common regulatory mechanisms. In the present study, we first screened genes significantly associated with OP and T2DM by the univariate logistic regression algorithm. And then, based on cross-analysis and random forest algorithm, we obtained three hub genes (ACAA2, GATAD2A, and VPS35) and validated the critical roles and predictive performance of the three genes in both diseases by differential expression analysis, receiver operating characteristic (ROC) curves, and genome wide association study (GWAS) analysis. Finally, based on gene set enrichment analysis (GSEA) and the construction of the miRNA-mRNA regulatory network, we conducted a preliminary exploration of the co-regulatory mechanisms of three hub genes in two diseases. In conclusion, this study provides promising biomarkers for predicting and treating both diseases and offers novel directions for exploring the common regulatory mechanisms of both diseases.

Nuts are energy-dense, high-fat foods, and whether nut consumption influences mortality risk among individuals with type 2 diabetes (T2D) remains unclear.

This study aimed to investigate the associations of nut consumption with all-cause mortality among adults with T2D and to further explore the potential mediation effects of cardiometabolic biomarkers.

The current analysis included 5090 US participants with T2D from the National Health and Nutrition Examination Survey (1999-2014). Cox proportional hazards models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).

After 35,632 person-y of follow-up, 1174 deaths were documented. Higher nut consumption was significantly associated with a lower risk of all-cause mortality among individuals with T2D. After multivariable adjustment including lifestyles and dietary factors, diabetes duration, and glycated hemoglobin, compared with participants who did not consume nuts, the HR (95% CI) for those who consumed nuts over 3.5 ounce equivalent (oz.eq)/wk was 0.64 (0.50, 0.82; P-trend < 0.001) for all-cause mortality. A linear dose-response relationship was observed between nut consumption and all-cause mortality among individuals with T2D (Poverall=0.004, Pnonlinearity=0.35). In substitution analyses, replacing one serving of red and processed meat, refined grains, eggs, and dairy foods with one serving of nuts was associated with a 18% to 22% lower risk of all-cause mortality. In addition, mediation analysis suggested that C-reactive protein and γ-glutamine transaminase explained 6.7% and 9.1% of the relationship between nut consumption with all-cause mortality, respectively.

Higher nut consumption was significantly associated with lower all-cause mortality among individuals with T2D. These findings indicate a potential benefit of nut consumption in the prevention of premature death among individuals with T2D.

There is a lack of research regarding the relationship between creatinine to cystatin C to waist circumference ratio (CCR/WC ratios) and the development of type 2 diabetes mellitus (T2DM). We aimed to evaluate the association between CCR/WC ratios and incident T2DM in Chinese adults.

This prospective study was from the China Health and Retirement Longitudinal Study (2011, 2013, 2015, and 2018). The participants were divided into three groups by tertiaries of the CCR/WC ratios. Cox proportional-hazards models were used to identify the relationship between CCR/WC and T2DM.

Overall, 5938 participants were included for analysis, 766 of whom developed T2DM between 2011 and 2018. Risk of incident T2DM was decreased with tertiaries 2, 3 versus tertiary 1 of the CCR/WC index (adjusted hazard ratio [HR] 0.772 [95% confidence interval 0.647-0.921] and 0.724 [0.596-0.880], p for trend = .001 across tertiaries of the CCR/WC index). The results were consistent excluding participants with T2DM in the first 2 years.

This study demonstrated that CCR/WC was negatively correlated with the risk of T2DM in Chinese adults. Early detection is necessary to control the development of T2DM in Chinese with low CCR/WC levels.

Grains contain bioactive components that potentially have protective effects on chronic diseases such as diabetes. The anti-diabetic effects of blended grain ethanol extract (BGE) were evaluated in streptozotocin-nicotinamide (STZ-NA)-induced diabetic rats. BGE was prepared by mixing oat, sorghum, adzuki bean, finger millet, and proso millet (30:30:15:15:10). The rats were assigned into four groups, normal control, diabetic model control (DM), STZ-NA rats administered 200 mg/kg body weight (bw) of metformin, and STZ-NA rats administered 500 mg/kg bw of BGE (BGE). After 6 weeks of administration, the homeostatic model assessment of insulin resistance (12%) in BGE decreased compared to DM. Strikingly, the fasting blood glucose (23%) and oral glucose tolerance test (15%) were improved in BGE compared to DM. BGE also increased insulin immunoreactivities in pancreatic β-cells. In sum, BGE exhibits anti-hyperglycemic effects by improving fasting glucose levels and insulin secretion from pancreatic β-cells in the STZ-NA-induced diabetic rats.

Diabetes is one of the most common diseases and major public health burdens worldwide. Type 2 diabetes mellitus (T2DM) is associated with chronic hepatitis C virus (HCV) infection, and lncRNAs play an important role in HCV-induced T2DM. We aimed to explore the effect of lncRNA AC040162.3 on HCV-induced T2DM.

HCV was used to infect MIN6 cells to establish an in vitro model. HCV copy number and miRNA expression were detected by Real Time Quantitative PCR (RT-qPCR). Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect the secretion of insulin, and methyl thiazolyl tetrazolium (MTT) was applied to analyze cell viability. Apoptosis was analyzed by Western blotting and flow cytometry. In addition, Western blotting and TdT-mediated dUTP Nick End Labeling (TUNEL) were used to analyze pyroptosis. Luciferase reporter assays were used to investigate the targeting relationship.

The expression of LncRNA AC040162.3 and NLRP3 was markedly increased in HCV-T2DM, while the expression of miR-223-3p was remarkably inhibited. In vitro experiments demonstrated that lncRNA AC040162.3 silencing or miR-223-3p overexpression remarkably alleviated HCV-induced T2DM deterioration by inhibiting cell apoptosis and pyroptosis and enhancing cell viability. We then demonstrated that silencing lncRNA AC040162.3 promoted the expression of miR-223-3p and that miR-223-3p bound to lncRNA AC040162.3 and the NLRP3 binding site. In addition, the protective effects of LncRNA AC040162.3 silencing in HCV-infected MIN6 cells were reversed by overexpression of NLRP3 or silencing of miR-223-3p.

Silencing of lncRNA AC040162.3 alleviates the process of HCV-induced T2DM by governing the miR-223-3p/NLRP3 axis.

Fenugreek is an ancient herb that has been used for centuries to treat diabetes. However, how the fenugreek-derived chemical compounds work in treating diabetes remains unclarified. Herein, we integrate molecular docking and network pharmacology to elucidate the active constituents and potential mechanisms of fenugreek against diabetes. First, 19 active compounds from fenugreek and 71 key diabetes-related targets were identified through network pharmacology analysis. Then, molecular docking and simulations results suggest diosgenin, luteolin and quercetin against diabetes via regulation of the genes ESR1, CAV1, VEGFA, TP53, CAT, AKT1, IL6 and IL1. These compounds and genes may be key factors of fenugreek in treating diabetes. Cells results demonstrate that fenugreek has good biological safety and can effectively improve the glucose consumption of IR-HepG2 cells. Pathway enrichment analysis revealed that the anti-diabetic effect of fenugreek was regulated by the AGE-RAGE and NF-κB signalling pathways. It is mainly associated with anti-oxidative stress, anti-inflammatory response and β-cell protection. Our study identified the active constituents and potential signalling pathways involved in the anti-diabetic effect of fenugreek. These findings provide a theoretical basis for understanding the mechanism of the anti-diabetic effect of fenugreek. Finally, this study may help for developing anti-diabetic dietary supplements or drugs based on fenugreek.

To investigate the effectiveness of non-pharmacological interventions (NPIs) on glycemic control in patients with type 2 diabetes (T2D) and to provide guidance for clinical healthcare-giver.

Network meta-analysis (NMA).

Randomized controlled trials comparing the effect of NPIs with usual care, waitlist, or other NPIs on glycemic control in patients with T2D.

This NMA was guided by frequentist framework. PubMed, Embase, the Cochrane Library Central Register of Controlled Trials, Cumulated Index to Nursing and Allied Health Literature, and Web of Science were searched from their inception until January 2023. The primary outcome was HbA1c and secondary outcomes were cardiovascular risk scores and related psychosocial scores. Mean differences and standardized mean differences were pooled using NMA. Study quality was assessed with the Confidence in Network Meta-analysis.

A total of 107 studies (10,496 participants) were included. The median sample size of the included studies was 64 (range, 10-563) and the median duration was 3 months (range, 1-24). Compared to usual care, all NPIs except acupuncture (MD: -0.28; 95 % CI: -1.02, 0.26) and psychological therapy (MD: -0.29; 95 % CI: -0.66, 0.08) showed significantly differences in improving glycemic control in patients with T2D. And according to the results of surface under the cumulative ranking analysis and Cluster ranking, meditation therapy was considered to the best choice when balancing the efficacy of glycemic control with self-efficacy and diabetes related problems, while nutrition therapy was considered to the best choice when balancing quality of life with risk of cardiovascular complications.

These findings validate the efficacy of NPIs for glycemic control in patients with T2D and suggest that healthcare-giver should consider both the efficacy of interventions and the psychosocial needs of patients when developing NPIs programs.

Vascular complications of diabetes pose a severe threat to human health. Prevention and treatment protocols based on a single vascular complication are no longer suitable for the long-term management of patients with diabetes. Diabetic panvascular disease (DPD) is a clinical syndrome in which vessels of various sizes, including macrovessels and microvessels in the cardiac, cerebral, renal, ophthalmic, and peripheral systems of patients with diabetes, develop atherosclerosis as a common pathology. Pathological manifestations of DPDs usually manifest macrovascular atherosclerosis, as well as microvascular endothelial function impairment, basement membrane thickening, and microthrombosis. Cardiac, cerebral, and peripheral microangiopathy coexist with microangiopathy, while renal and retinal are predominantly microangiopathic. The following associations exist between DPDs: numerous similar molecular mechanisms, and risk-predictive relationships between diseases. Aggressive glycemic control combined with early comprehensive vascular intervention is the key to prevention and treatment. In addition to the widely recommended metformin, glucagon-like peptide-1 agonist, and sodium-glucose cotransporter-2 inhibitors, for the latest molecular mechanisms, aldose reductase inhibitors, peroxisome proliferator-activated receptor-γ agonizts, glucokinases agonizts, mitochondrial energy modulators, etc. are under active development. DPDs are proposed for patients to obtain more systematic clinical care requires a comprehensive diabetes care center focusing on panvascular diseases. This would leverage the advantages of a cross-disciplinary approach to achieve better integration of the pathogenesis and therapeutic evidence. Such a strategy would confer more clinical benefits to patients and promote the comprehensive development of DPD as a discipline.

About 1 in 10 adults worldwide are estimated to have diabetes mellitus. They are at risk of developing life-threatening complications resulting in reduced quality of life, increased mortality and higher healthcare costs. The ability to prevent or delay type 2 diabetes mellitus (T2DM) by modifying some of its risk factors has been hypothesized for decades. The long and often gradual time-course of increasing dysglycemia prior to diabetes diagnosis suggests that interventions during that period could be effective in preventing T2DM. In addition to lifestyle modifications, certain drugs prevent or slow development of hyperglycemia. Recently, drugs used for obesity management were shown to prevent T2DM. In this review, we discuss various pharmacotherapeutic options for preventing T2DM.