The fat-to-muscle mass ratio (FMR) has served as a marker for various diseases. This study aimed to explore sex-specific associations between FMR in different body regions (whole body, trunk, arm, and leg) and cancer incidence.

We included 435,986 cancer-free participants (203,133 men and 232,853 women) from the UK Biobank at baseline. FMR was calculated as the ratio of fat mass to muscle mass in each body region. Multivariable Cox proportional hazards models, along with Cox models incorporating restricted cubic splines (RCS) function, were employed to examine both linear and non-linear associations between FMR and cancer risk in men and women. Additionally, a combined grouping of body mass index (BMI) and FMR was used to assess the joint impact of body composition on cancer incidence.

During the follow-up period, 62,060 new cancer cases were recorded. Our analysis showed significant associations between both total and regional FMR and the risk of several cancers. In men, higher whole body FMR was associated with an increased risk of esophagus, stomach, colorectal, liver, pancreas, and kidney cancers, while a decreased risk was observed for prostate and non-melanoma skin cancers (FDR < 0.05). In women, higher FMR was associated with a higher incidence of gallbladder, pancreas, kidney, thyroid, breast, and uterus cancers (FDR < 0.05). Non-linear associations were observed for several cancer types, with specific FMR cut-off points presented using RCS curves. The analysis by combining BMI and FMR suggested potential interaction patterns, revealing some masked risks; for example, a significant increase in cancer incidence was also observed in individuals exhibiting high FMRs despite having low BMI.

Our findings suggested that both total and regional FMR may serve as potential biomarkers for assessing the risk of overall and site-specific cancers.

While metabolic dysfunction is linked to schizophrenia, the relationship between metabolic parameters, cognitive function, and psychopathological symptoms across different body mass index (BMI) categories remains inadequately understood. This study aimed to explore the distinct metabolic predictors of cognitive and psychopathological outcomes in schizophrenia patients stratified by BMI. A total of 1034 patients with schizophrenia were recruited and categorized into underweight, normal weight, overweight and obesity groups. Cognitive function was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status, and psychopathological symptoms were evaluated using the Positive and Negative Syndrome Scale. Metabolic profiles and anthropometric measures were obtained via standard tests. Significant metabolic differences were found across BMI groups, except for low-density lipoprotein. Underweight patients performed worse in language compared to obese patients, which had higher positive symptom but lower negative symptom scores. Multivariate linear regression analysis revealed that in obese patients, elevated triglyceride was independently associated with better cognitive performance (p < 0.05). In overweight patients, waist-hip ratio was significantly correlated with cognitive outcomes, which specifically predicting the severity of positive symptoms (all p < 0.05). In underweight patients, fasting blood glucose (β = 0.77, p < 0.05) and triglyceride (β = 1.28, p < 0.01) were associated with immediate memory deficits, while attention was negatively influenced by high-density lipoprotein levels (β = -0.10, p < 0.05). Schizophrenia patients exhibit distinct BMI-specific metabolic patterns that differentially predict cognitive and psychopathological outcomes, highlighting the importance of tailored metabolic interventions based on BMI stratification.

The accumulation of tail fat in sheep is a manifestation of adaptive evolution to the environment. Sheep with different tail types show significant differences in physiological functions and tail fat deposition. Although these differences reflect the developmental mechanism of tail fat under different gene regulation, the situation of sheep tail fat tissue at the single cell level has not been explored, and its molecular mechanism still needs to be further elucidated.

Here, we characterized the genomic features of sheep with different tail types, detected the transcriptomic differences in tail adipose tissue between fat-tailed and thin-tailed sheep, established a single-cell atlas of sheep tail adipose tissue, and screened potential molecular markers (SESN1, RPRD1A and RASGEF1B) that regulate differences in sheep tail fat deposition through multi-omics integrated analysis. We found that the differential mechanism of sheep tail fat deposition not only involves adipocyte differentiation and proliferation, but is also closely related to cell-specific communication networks (When adipocytes act as signal outputters, LAMININ and other signal pathways are strongly expressed in guangling large tailed sheep and hu sheep), including interactions with immune cells and tissue remodeling to drive the typing of tail fat. In addition, we revealed the differentiation trajectory of sheep tail adipocytes through pseudo-time analysis and constructed the cell communication network of sheep tail adipose tissue.

Our results provide insights into the molecular mechanisms of tail fat deposition in sheep with different tail types, and provide a deeper explanation for the development and functional regulation of adipocytes.

Obesity is a complex, chronic, and recurrent disease marked by abnormal or excessive fat accumulation that poses significant health risks. The distribution of body fat, especially ectopic fat deposition, plays a crucial role in the development of chronic metabolic diseases. Under normal conditions, fatty acids are primarily stored in subcutaneous adipose tissue; however, excessive intake can lead to fat accumulation in visceral adipose tissue and ectopic sites, including the pancreas, heart, and muscle. This redistribution is associated with disruptions in energy metabolism, inflammation, and insulin resistance, impairing organ function and raising the risk of cardiovascular disease, diabetes, and fatty liver. This review explores the roles of visceral and ectopic fat in the development of insulin resistance and related diseases such as type 2 diabetes and metabolic dysfunction-associated steatotic liver disease. Specifically, we examine the structure and characteristics of different fat types, their associations with disease, and the underlying pathogenic mechanisms. Future strategies for managing obesity-related diseases may include lifestyle modifications, surgical interventions, and emerging medications that target lipid metabolism and energy regulation, aiming to improve patient outcomes.

Cellular heterogeneity of human adipose tissue is linked to the pathophysiology of obesity and may impact the response to energy restriction and changes in fat mass. Herein, we provide an optimized pipeline to estimate cellular composition in human abdominal subcutaneous adipose tissue (ASAT) bulk RNA sequencing (RNA-seq) datasets using a single-nuclei RNA-seq signature matrix.

A deconvolution pipeline for ASAT was optimized by benchmarking publicly available algorithms using a signature matrix derived from ASAT single-nuclei RNA-seq data from 20 adults and then applied to estimate ASAT cell-type proportions in publicly available obesity and weight loss studies.

Individuals with obesity had greater proportions of macrophages and lower proportions of adipocyte subpopulations and vascular cells compared with lean individuals. Two months of diet-induced weight loss increased the estimated proportions of macrophages; however, 2 years of diet-induced weight loss reduced the estimated proportions of macrophages, thereby suggesting a biphasic nature of cellular remodeling of ASAT during weight loss.

Our optimized high-throughput pipeline facilitates the assessment of composition changes of highly characterized cell types in large numbers of ASAT samples using low-cost bulk RNA-seq. Our data reveal novel changes in cellular heterogeneity and its association with cardiometabolic health in humans with obesity and following weight loss.

Obesity is increasingly recognized among people with type 1 diabetes mellitus (T1DM). Little is known about the body composition of adolescents with T1DM and its metabolic outcomes. Hence, this study assessed the body composition of adolescents with T1DM and its relationship with glycaemic control, insulin resistance and vascular complications.

One hundred twenty adolescents with T1DM were assessed for anthropometric measures, insulin therapy, bioelectrical impedance analysis (BIA), fasting lipids, glycated haemoglobin, with estimated glucose disposal rate (eGDR) calculation. Regional body fat quantification was performed via Magnetic resonance imaging (MRI) 3-T.

Thirty-three adolescents with T1DM were overweight (27.5%), and 8 were obese (6.6%). Adolescents with T1DM having insulin resistance were found to have significantly higher BMI z score, total body fat %, and visceral/subcutaneous fat % than those without insulin resistance (p < 0.05). Moreover, adolescents with T1DM having microvascular complications showed significantly higher total fat % and visceral/subcutaneous fat % than those without microvascular complications (p < 0.05). Visceral fat % and visceral/subcutaneous fat ratio were positively correlated with waist/hip ratio, eGDR and LDL level (p < 0.05). Waist/hip ratio and eGDR were the most significant independent variables associated with visceral fat % and visceral/subcutaneous fat ratio among adolescents with T1DM using multivariate regression analysis.

Overweight and visceral adiposity are frequently encountered among the studied adolescents with T1DM. Visceral adiposity is associated with insulin resistance, hyperlipidaemia and microvascular complications among adolescents with T1DM independent of glycaemic control and insulin dosage.

Obesity is a devastating worldwide metabolic disease, with the highest prevalence in children and adolescents. Obesity impacts neuronal function but the fate of functional hyperemia, a vital mechanism making possible cerebral blood supply to active brain areas, is unknown in organisms fed a high-caloric Western Diet (WD) since adolescence.

We mapped changes in cerebral blood volume (CBV) in the somatosensory cortex in response to whisker stimulation in adolescent, adult, and middle-aged mice fed a WD since adolescence. To this aim, we used non-invasive and high-resolution functional ultrasound imaging (fUS).

We efficiently mimicked the metabolic syndrome of adolescents in young mice with early weight gain, dysfunctional glucose homeostasis, and insulinemia. Functional hyperemia is compromised as early as 3 weeks of WD and remains impaired after that in adolescent mice. These findings highlight the cerebrovascular vulnerability to WD during adolescence. In WD, ω-6:ω-3 polyunsaturated fatty acids (PUFAs) ratio is unbalanced towards proinflammatory ω-6. A balanced ω-6:ω-3 PUFAs ratio in WD achieved by docosahexaenoic acid supplementation efficiently restores glucose homeostasis and functional hyperemia in adults.

WD triggers a rapid impairment in cerebrovascular activity in adolescence, which is maintained at older ages, and can be rescued by a PUFA-based nutraceutical approach.

Oral treatment extended-release naltrexone/bupropion (NB) leads to significant weight loss, but its effect on body composition remains unclear. We investigated changes in body composition with dual-energy x-ray absorptiometry after treatment with NB or placebo in a subgroup of participants from a randomized control phase 3 study (COR-I).

Observed changes from baseline to week 52 were estimated for total, lean, and fat mass. Changes in body composition were evaluated using linear regression and adjusted for baseline covariates.

The analysis included 82 participants (placebo, n = 26; NB, n = 56) with comparable baseline characteristics (age, BMI, sex). The NB group experienced a significant -7.8% change of total mass (-12.9% change in fat mass and -4.1% in lean mass), compared with a -2.8% change of total mass (-4.8% change in fat mass and -1.4% in lean mass) in the placebo group. The adjusted changes in lean-to-fat mass ratio of 0.069 in the NB group and -0.056 in the placebo group were significantly different (p < 0.05).

NB-induced weight loss is associated with significant reductions in total percent fat mass, increase in total percent lean mass, and change in lean-to-fat mass ratio, in comparison to placebo. Larger studies are needed to further elucidate the clinical significance of these changes and impact of a potentially healthier metabolism.

The consumption of grape seed procyanidin extract (GSPE) may improve metabolic alterations and molecular clock desynchrony in white adipose tissue (WAT), depending on administration timing and metabolic status. To test this hypothesis, inguinal WAT explants from lean and obese PERIOD2::LUCIFERASE (PER2::LUC) circadian reporter mice were treated at the peak or trough of the PER2 luminescence rhythm with metabolites present in the serum of GSPE-administered rats (GSPM). PER2::LUC rhythms of explants from obese animals presented a lower amplitude, longer period and a phase delay. GSPM treatment increased luminescence amplitude and period compared to untreated explants, but only when it was given at the trough of PER2::LUC luminescence. GSPM upregulated lipogenesis and lipolysis genes in explants from lean mice, mostly when given at the luminescence peak. This study provides a valuable platform for testing the effects of natural products ex vivo and warrants further investigation into the chrono-utilisation of plant bioactive compounds.

Among premenopausal women, higher body mass index (BMI) is associated with lower breast cancer risk, although the underlying mechanisms are unclear. Investigating adiposity distribution may help clarify impacts on breast cancer risk. This study was initiated to investigate associations of central and peripheral adiposity with premenopausal breast cancer risk overall and by other risk factors and breast cancer characteristics.

We used individual-level data from 14 prospective cohort studies to estimate hazard ratios (HRs) for premenopausal breast cancer using Cox proportional hazards regression. Analyses included 440,179 women followed for a median of 7.5 years (interquartile range: 4.0-11.3) between 1976 and 2017, with 6,779 incident premenopausal breast cancers.

All central adiposity measures were inversely associated with breast cancer risk overall when not controlling for BMI (e.g. for waist circumference, HR per 10 cm increase: 0.92, 95% confidence interval (CI): 0.90-0.94) whereas in models adjusting for BMI, these measures were no longer associated with risk (e.g. for waist circumference: HR 0.99, 95% CI: 0.95-1.03). This finding was consistent across age categories, with some evidence that BMI-adjusted associations differed by breast cancer subtype. Inverse associations for in situ breast cancer were observed with waist-to-height and waist-to-hip ratios and a positive association was observed for oestrogen-receptor-positive breast cancer with hip circumference (HR per 10 cm increase: 1.08, 95% CI: 1.10-1.14). For luminal B, HER2-positive breast cancer, we observed an inverse association with hip circumference (HR per 10 cm: 0.84, 95% CI: 0.71-0.98), but positive associations with waist circumference (HR per 10 cm: 1.18, 95% CI: 1.03-1.36), waist-to-hip ratio (HR per 0.1 units: 1.29, 95% CI: 1.15-1.45) and waist-to height ratio (HR per 0.1 units: 1.46, 95% CI: 1.17-1.84).

Our analyses did not support an association between central adiposity and overall premenopausal breast cancer risk after adjustment for BMI. However, our findings suggest associations might differ by breast cancer hormone receptor and intrinsic subtypes.

The relationship between obesity and some respiratory diseases has been well documented. However there have been few studies on the association between visceral adipose tissue (VAT) and chronic respiratory diseases (CRDs), it remains unclear whether VAT is causally associated with CRDs.

We used two-sample Mendelian randomization (MR) to illuminate the effects of VAT on four CRDs: chronic obstructive pulmonary disease (COPD), allergic asthma, interstitial lung disease (ILD), and sarcoidosis. Inverse variance weighted (IVW) served as the primary assessment method. MR Egger, weighted median, Simple mode and Weighted mode were the supplementary methods for MR analysis. We used multivariate MR analysis to adjust for the effect of body mass index (BMI) on outcomes, Egger intercept, MR-pleiotropy residual sum and outlier, and leave-one-out analysis to confirm the MR results' consistency.

Genetically-predicted VAT was associated with an increased risk of COPD (OR = 1.56; 95% CI: 1.34-1.82; P = 1.16×10-8), allergic asthma (OR = 1.44; 95% CI: 1.20-1.73; P = 8.63×10-5), and ILD (OR = 1.15; 95% CI: 1.04-1.26; P = 4.62×10-3). However, there was limited evidence to support an association between VAT and sarcoidosis. In multivariate MR analysis, VAT's associations with COPD, allergic asthma, and ILD persisted after adjusting for BMI.

This study provides evidence for a potential causal relationship between VAT and COPD, allergic asthma, and ILD; these relationships were independent of the effect of BMI.

Obesity is a highly prevalent chronic multisystem disease associated with shortened life expectancy due to a number of adverse health outcomes. Epidemiological data link body weight and parameters of central fat distribution to an increasing risk for type 2 diabetes, hypertension, fatty liver diseases, cardiovascular diseases including myocardial infarction, heart failure, atrial fibrillation, stroke, obstructive sleep apnoea, osteoarthritis, mental disorders and some types of cancer. However, the individual risk to develop cardiometabolic and other obesity-related diseases cannot entirely be explained by increased fat mass. Rather than excess fat accumulation, dysfunction of adipose tissue may represent the mechanistic link between obesity and adverse health outcomes. There are people living with obesity who seem to be protected against the premature development of cardiometabolic diseases. On the other hand, people with normal weight may develop typical obesity diseases upon dysfunction of adipose tissue and predominantly visceral fat distribution. The mechanisms linking impaired function of adipose tissue in people with obesity include adipocyte hypertrophy, altered cellular composition, limited expandability of safe subcutaneous fat stores, ectopic fat deposition in visceral depots, the liver and other organs, hypoxia, a variety of stresses, inflammatory processes, and the release of pro-inflammatory, diabetogenic and atherogenic signals. Genetic and environmental factors might contribute either alone or via interaction with intrinsic biological factors to variation in adipose tissue function. There are still many open questions regarding the mechanisms of how increased body weight causes obesity-related disorders and whether these pathologies could be reversed. Evidence-based weight loss interventions using behaviour change, pharmacological or surgical approaches have clarified the beneficial effects of realistic and sustained weight loss on obesity-related complications as hard outcomes. This review focusses on recent advances in understanding epidemiological trends and mechanisms of obesity-related diseases. PLAIN LANGUAGE SUMMARY: Obesity is a chronic complex and progressive disease characterized by excessive fat deposition that may impair health and quality of life. Worldwide, the number of adults living with obesity has more than doubled since 1990. Obesity may lead to reduced life expectancy, because it increases the risk for type 2 diabetes, cardiovascular diseases (e.g., myocardial infarction, high blood pressure, stroke), fatty liver diseases, musculoskeletal diseases, chronic respiratory diseases, depression and certain types of cancer. However, not every person with obesity develops these diseases. For better prevention and treatment, it is important to understand the mechanisms linking high fat mass to obesity related diseases. It has become clear that fat mass alone cannot explain the higher risk of obesity complications. People with obesity can have either high or low risk of developing complications. Compared to people with a low risk for obesity complications those with a high risk to develop obesity related diseases are characterized by higher central fat deposition in the abdominal region, on average bigger fat cells, higher number of immune cells in adipose tissue and altered signals released from adipose tissue that may directly affect the brain, liver, vasculature and other organs. Both inherited and environment factors may cause these abnormalities of adipose tissue function. However, weight loss through behaviour changes (e.g., lower calorie intake, higher physical activity), medications or obesity surgery can improve health, quality of life and reduce the risk for obesity related diseases.

Omentin-1, a novel adipocytokine predominantly secreted by visceral adipose tissue, has emerged as a significant factor in cardiovascular health, particularly regarding hypertension (HTN) and heart failure (HF). This manuscript investigates the multifaceted roles of omentin-1 in these conditions, emphasizing its protective effects on vascular function and its potential as both a biomarker and therapeutic target. Clinical studies indicate that reduced circulating levels of omentin-1 are associated with metabolic syndrome (MetS) and increased cardiovascular risk, while animal studies demonstrate its ability to ameliorate endothelial dysfunction and lower blood pressure. Omentin-1 exerts its beneficial effects through various signaling pathways, including AMP-activated protein kinase (AMPK) and protein kinase B (Akt), thereby promoting vasodilation, enhancing insulin sensitivity, and mitigating inflammation. In the context of HF, particularly heart failure with preserved ejection fraction (HFpEF), omentin-1 levels exhibit a negative correlation with diastolic dysfunction and inflammatory markers, suggesting its role in cardiac protection. Additionally, the manuscript discusses the implications of omentin-1 in managing obesity-related cardiovascular diseases and its potential utility as a prognostic marker for adverse outcomes in HF patients. Collectively, omentin-1 represents a promising avenue for research in cardiovascular health, with the potential to inform novel therapeutic strategies aimed at improving outcomes in patients with HTN and HF. Further research is necessary to elucidate the details of omentin-1 function and evaluate its potential in the treatment of cardiovascular disease.

This study aims to explore the correlation between visceral adiposity index (VAI) and diabetes kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM), so as to provide a clinical basis for the prevention and treatment of DKD.

This study retrospectively analyzed 1817 patients with T2DM hospitalized in the department of Endocrinology, Peking University International Hospital from January 2017 to August 2021, including 1053 males and 764 females. According the level of VAI, subjects were divided into three groups.

(1) The results showed that with the increase of VAI level, the proportion of DKD gradually increased, and there was a statistical difference (p < 0.05). With the increase of VAI levels, there is an increasing trend in males, age, WC, BMI, WHtR, WHR, VAI, LAP, ABSI, C-Index, CUN-BAE, SBP, DBP, HbA1c, FBG, PBG, UACR, TG, while HDL-C levels show a decreasing trend (p all <0.05). (2)Logistic regression showed that after adjusting age, sex, diabetic duration, smoking, drinking, BP, blood glucose and blood lipids, high level of VAI was an independent risk factor for DKD (HR=1.38, 95% CI 1.18, 1.63). (3)The model to predict the risk of DKD using anthropometric indicators, showed that the AUC of the models ranked VAI>ABSI>C-index>WHR>AVI=BRI>BMI>CUN-BAE>LAP>WHtR.(4)The predictive ability for DKD of Model 1 with VAI was higher than that of Model 2 with BMI.

The increase of VAI is an independent predictor of DKD occurrence in patients with T2DM, which provides a certain clinical basis for preventing the development of DKD in patients with T2DM.

Caloric restriction (CR) is a dietary intervention that delays the onset of age-related diseases and enhances survival in diverse organisms, and although changes in adipose tissues have been implicated in the beneficial effects of CR the molecular details are unknown. Here we show shared and depot-specific adaptations to life-long CR in subcutaneous and visceral adipose depots taken from advanced age male rhesus monkeys. Differential gene expression and pathway analysis identified key differences between the depots in metabolic, immune, and inflammatory pathways. In response to CR, RNA processing and proteostasis-related pathways were enriched in both depots but changes in metabolic, growth, and inflammatory pathways were depot-specific. Commonalities and differences that distinguish adipose depots are shared among monkeys and humans and the response to CR is highly conserved. These data reveal depot-specificity in adipose tissue adaptation that likely reflects differences in function and contribution to age-related disease vulnerability.

Mitochondria play a central role in nutrient metabolism, besides being responsible for the production of adenosine triphosphate (ATP), the main source of cellular energy. However, the ATP production process is associated with the generation of reactive oxygen species (ROS), which excessive accumulation can cause mitochondrial dysfunction. This dysfunction, in turn, causes the accumulation of fatty acids in the adipose tissue, triggering a local inflammatory process that can evolve into systemic inflammation. In women with obesity, an increase in lipid levels in the placental environment is observed. The high presence of fatty acids compromises the structural integrity and mitochondrial membrane, culminating in the release of ROS. This process damages the DNA of placental cells and causes an inflammatory state, affecting metabolic efficiency. This vicious cycle is characterized by defects in mitochondrial ATP production, which can lead to lipid accumulation and inflammation. In pregnant women with obesity, these mitochondrial changes play a determining role in pregnancy outcomes. Hence, the objective of this study was to search the literature to review the impact of mitochondrial dysfunction in the maternal obesity.

Inconsistent results have been reported regarding the effects of different types of algae, such as Spirulina and Chlorella, on anthropometric indices.

To conduct a meta-analysis to assess the efficacy of algae supplementation on anthropometric indices.

A comprehensive systematic search was conducted to find relevant articles published from January 1990 to January 2024.

Randomized controlled trials (RCTs) comparing algae supplementation with a placebo or control group were included. The risk of bias and certainty of the evidence were evaluated using the Cochrane risk-of-bias tool and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology, respectively. The random-effects model was used to find the Weighted mean differences (WMDs) for each outcome.

Of 9079 distinct articles in the initial screening, 61 clinical trials were included in this meta-analysis. Algae supplementation resulted in lower body mass index (WMD, -0.27 kg/m2 (95% CI, -0.42 to -0.13); GRADE rating, low), body weight (WMD: -0.78 kg [-1.18 to -0.38]; GRADE rating, low), waist circumference (WMD, -0.68 cm [-1.27 to -0.10]; GRADE rating, very low), kilograms of body fat (WMD, -0.65 kg [-1.13 to -0.17]; GRADE rating, low), and body fat percentage (WMD, -0.9% [-1.62 to -0.17]; GRADE rating, very low) compared with placebo or controls. Nevertheless, the statistically significant effects of algae supplementation on hip circumference (WMD, -0.20 cm [-0.73 to 0.32]; GRADE rating, moderate), waist to hip ratio (WMD, -0.01 [-0.01 to 0.00]; GRADE rating, moderate), and lean body mass (WMD, -0.30 kg [-0.62 to 0.02]; GRADE rating, moderate) were not observed.

Overall, the findings of this meta-analysis indicate supplementation with algae may exert beneficial effects on anthropometric indices. However, due to between-studies heterogeneity and very low to low levels of GRADE for significant outcomes, the results should be interpreted with caution.

PROSPERO registration no. CRD42024522923.

This article highlights the prevalence, epidemiology, and pathophysiology of obesity in the United States, including its increasing link to cardiovascular disease (CVD). We discuss food policies-ranging from societal to regional, state, and federal levels-and their healthcare impact. While multiple examples show some success in reducing the global obesity pandemic via the food chain, much research is still needed to demonstrate the robust impact of these multi-prong interventions and their ability to decrease the CVD burden.8.

This study aimed to explore the association between remnant cholesterol and metabolic dysfunction-associated fatty liver disease (MAFLD) in an adult population in the United States.

Data were collected from the National Health and Nutrition Examination Survey database during 2017-2020. Weighted multivariable logistic regression analyses and receiver operating characteristic (ROC) curves were used to investigate the association between remnant cholesterol and the risk of MAFLD. Subgroup and interaction analyses were performed. To further investigate the possible non-linear relationship between remnant cholesterol and MAFLD, a restricted cubic spline was used.

Among the included 3633 participants, the prevalence rate of MAFLD was 34.56%. After full adjustment, higher remnant cholesterol was associated with the risk of MAFLD (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.01-1.06; P = 0.02), and compared with the lowest quartile of remnant cholesterol, the highest quartile of remnant cholesterol was more likely to be associated with MAFLD (OR, 3.70; 95%CI, 2.37,5.76; P < 0.0001). A non-linear relationship between remnant cholesterol and MAFLD was found in the restricted cubic spline regression model, suggesting that the risk of MAFLD initially increased rapidly and then gradually slowed down.

Remnant cholesterol was identified as a potential risk factor for MAFLD, and a non-linear relationship between remnant cholesterol and the prevalence of MAFLD was detected. Large-scale, high-quality prospective studies are required to validate these findings.

Obesity is closely associated with lipid metabolism, and the accumulation of lipids leads to low-level inflammation in the body, which can trigger cardiovascular disease. This study aimed to explore the association between a novel marker of lipid accumulation, the abdominal volume index (AVI), inflammatory parameters, and mortality.

This study enrolled 2,109 older adult senior citizens (aged over 60 years) with hypertension from the National Health and Nutrition Examination Survey. The primary endpoints included all-cause mortality and cardiovascular mortality, which were assessed by linking the data to the National Death Index records. Cox regression model and subgroup analysis were constructed to investigate the associations between AVI and both all-cause and cardiovascular mortality. Restricted cubic splines were employed to further explore the relationships among AVI, inflammatory parameters, and mortality. By considering inflammatory factors as mediators, we investigate the mediating effects of AVI on mortality.

After a median follow-up of 69 months, there were 1,260 deaths, with 337 attributed to cardiovascular causes within the older adult population studied. In the multivariable-adjusted model, AVI was positively associated with both all-cause and cardiovascular mortality [Hazard Ratio (HR) = 1.09, 95% CI = 1.06-1.11 for all-cause mortality; HR = 1.07, 95% CI = 1.03-1.12 for cardiovascular mortality]. Kaplan-Meier survival plots indicated an overall median survival time of 144 months. Mediation analysis revealed that Systemic Inflammatory Response Index (SIRI), Monocyte-to-HDL ratio (MHR), and Neutrophil-to-Lymphocyte ratio (NLR) mediated 27.15%, 35.15%, and 16.55%, respectively, of the association between AVI and all-cause mortality.

AVI is positively associated with all-cause mortality in older adults with hypertension, and this association appears to be partially mediated by inflammatory parameters.

Growing evidence has suggested that the consumption of chia seed can decrease blood pressure and obesity in adults. However, even studies have reported uncertain findings. The current meta-analysis aimed to assess the findings of randomized controlled trials (RCTs) on the efficacy of chia seed supplementation on blood pressure (systolic blood pressure [SBP], diastolic blood pressure [DBP]) and body composition (waist circumference [WC], weight, body mass index [BMI]) in adults.

A systematic search of the literature was carried out in the PubMed, Web of Knowledge, Scopus, Cochrane Central Library, and EMBASE from inception up to October 2024. Data were extracted and analyzed using a random-effects model, and reported as weighted mean differences (WMD) with 95% confidence intervals (CI).

A total of eight RCTs involving 372 participants were included in the meta-analysis. The results showed that chia consumption significantly reduced DBP (WMD: -7.49 mmHg; 95% CI: -9.64, -5.34; P < 0.001) and SBP (WMD: -5.61 mmHg; 95% CI: -8.77, -2.44; P = 0.001). Moreover, consuming chia seeds was linked to a notable decrease in WC (WMD: -1.46 cm; 95% CI: -2.68, -0.25; P = 0.01), but it had no significant effect on, BMI (WMD: -0.31 kg/m2; 95% CI: - 0.96, 0.34; P = 0.34) and weight (WMD: 0.09 kg; 95% CI: -0.76, 0.93; P = 0.84).

Chia consumption can significantly reduce SBP, DBP, and WC in adults, but no significant impact was showed on BMI and weight. To verify these results, more studies involving a greater number of participants are required.

The impact of overweight and obesity on pathological outcomes, complications, and oncologic outcomes following surgery for gastric adenocarcinoma has been poorly reported in Western populations. This study aimed to better understand the impact of overweight and obesity on both surgical and oncological outcomes in patients who underwent surgery for gastric cancer.

Data were retrospectively collected from a multi-institutional European database. 1589 patients underwent surgery for gastric adenocarcinoma between 2007 and 2017. Patients were divided into three groups according to their body mass index (BMI): 722 normoponderal patients (45.4 %), 585 overweight patients (36.8 %), and 282 obese patients (17.7 %).

The tumor stage, administration of perioperative chemotherapy, number of harvested lymph nodes, and reoperation rates were similar. Tumor location differed between the groups, with more distal locations in normoponderal patients than in overweight patients (51.4 % vs. 44.1 %, p = 0.04). Surgical complications were more frequent in obese patients than in normoponderal patients (34.8 % vs. 24.2 %, p = 0.005), and severe postoperative complications too. The medical complication rate was higher in overweight and obese patients (31.5 % and 32.6 % vs. 24.1 %, p = 0.003). There was no difference in the overall survival.

Obesity was not related to tumor stage, pre- or intraoperative strategies, or survival in patients undergoing surgery for gastric adenocarcinoma. However, postoperative morbidity increases in patients with obesity. Surgery for gastric adenocarcinoma should be proposed for all patients and should be performed as usual, regardless of their BMI. However, obese patients should be counseled regarding the higher risk of postoperative complications.

Obesity is a complex, multifactorial, chronic disease that acts as a gateway to a range of other diseases. Evidence from recent studies suggests that changes in oxygen availability in the microenvironment of metabolic organs may exert an important role in the development of obesity-related cardiometabolic complications. In this review, we will first discuss results from observational and controlled laboratory studies that examined the relationship between reduced oxygen availability and obesity-related metabolic derangements. Next, the effects of alterations in oxygen partial pressure (pO2) in the adipose tissue, skeletal muscle and the liver microenvironment on physiological processes in these key metabolic organs will be addressed, and how this might relate to cardiometabolic complications. Since many obesity-related chronic diseases, including type 2 diabetes mellitus, cardiovascular diseases, chronic kidney disease, chronic obstructive pulmonary disease and obstructive sleep apnea, are characterized by changes in pO2 in the tissue microenvironment, a better understanding of the metabolic impact of altered tissue oxygenation can provide valuable insights into the complex interplay between environmental and biological factors involved in the pathophysiology of metabolic impairments. This may ultimately contribute to the development of novel strategies to prevent and treat obesity-related cardiometabolic diseases.

This study investigated the mechanisms related to lipid metabolism regulation after combined supplementation with deer antler polysaccharides and postbiotics.

Thirty-two male mice were divided into high-fat diet, HD + deer antler polysaccharides, HD + Bacillus coagulans postbiotics, and HD + deer antler polysaccharides + B. coagulans postbiotics groups. The diets contained 60% fat. After 9 weeks, the effects of deer antler polysaccharides and postbiotics on lipid metabolism were assessed through blood biochemical, histological tissue staining, and polymerase chain reaction analyses.

Supplementation with deer antler polysaccharides and postbiotics significantly inhibited weight gain in obese mice, reduced serum total cholesterol, triglyceride, and low-density lipoprotein levels and markedly increased the serum high-density lipoprotein level. Additionally, hepatic lipid droplet accumulation and adipocyte hypertrophy improved. The expressions of the lipid synthesis genes, sterol regulatory element-binding protein 1 (i.e. SREBP-1c), and fatty acid synthase (i.e. FAS), significantly decreased, while peroxisome proliferator-activated receptor alpha (i.e. PPAR-α) and acyl-CoA oxidase 1 (i.e. ACOX1) expression significantly increased. The expressions of the inflammation-related genes, tumor necrosis factor-alpha (i.e. TNF-α), interleukin (IL)-6, and IL-1 also significantly decreased.

Thus, combined deer antler polysaccharides and postbiotic supplementation regulated obesity in mice, potentially by modulating lipid synthesis and inflammation-related gene expression.

To investigate the association of metabolic status newly defined or obesity with asymptomatic intracranial arterial stenosis (aICAS) among populations in rural China.

The cross-sectional study is based on the Rose asymptomatic IntraCranial Artery Stenosis (RICAS) cohort, which enrolled 2005 participants aged 40 years or older without a history of clinical stroke or transient ischemic attack. Metabolically healthy status (MH) was defined by a newly proposed criterion: (1) systolic blood pressure (SBP) < 130 mmHg and without antihypertensive medication; (2) a waist-to-hip ratio (WHR) below 1.03 for men and below 0.95 for women; (3) no diabetes. All participants were categorized based on their metabolic status and obesity. Multivariate logistic regression models were used to investigate the association between metabolic status or obesity and aICAS.

Among 2005 participants, 1597 (79.65%) were defined as metabolically unhealthy status (MU) according to the new criterion. MU was significantly associated with aICAS (OR 2.02, 95% CI 1.11-3.68, P = 0.021), especially moderate-to-severe aICAS (OR 2.43, 95% CI 1.04-5.72, P = 0.042). The prevalence of aICAS increased with the numbers of metabolic disorders (P for linear trend <0.001). Both metabolically unhealthy normal-weight (MUN) (OR 2.11, 95% CI 1.10-4.03, P = 0.025) and metabolically unhealthy obesity (MUO) (OR 3.30, 95% CI 1.64-6.64, P = 0.001) were significantly correlated with aICAS, but not metabolically healthy obesity (MHO). Subgroup analysis further confirmed the association between MU and aICAS risk only in men (P for interaction = 0.042).

MU defined by the new criterion was significantly associated with aICAS, especially with moderate-to-severe aICAS. This novel criterion effectively identifies individuals with a high prevalence of aICAS among populations with obesity, which could be crucial for stroke prevention.

Understanding the risks and effects of gestational weight gain (GWG) is a prominent area of perinatal research but approaches for quantifying GWG are evolving and remain underdeveloped, especially in clinical settings for underserved demographic subgroups. To fill this gap, we demonstrated and compared six GWG metrics across pre-pregnancy BMI classifications: total GWG, trimester-specific linear rate of GWG, adherence to total and trimester-specific recommendations, area under the curve, and GWG for gestational age z-scores.

We used clinical data on 44,801 pregnant people from community-based health care organizations with extensive longitudinal measures and substantial representation of understudied subgroups.

Total GWG was lower in individuals with higher pre-pregnancy BMI; yet more temporally resolved analyses revealed differences in trimester-specific weight change. Differences included common first trimester weight loss in people with pre-pregnancy class II or III obesity and substantial first trimester weight gain in people with pre-pregnancy underweight, with the greatest pre-pregnancy BMI-related variation in GWG occurring in the second trimester. These differences are reflected to varying degrees in the AUC and GWG z-score metrics.

Our findings inform development of GWG guidelines within BMI categories, especially in obesity subclasses and underweight, and selection, refinement, and application of GWG metrics in future research. GWG metrics differ to varying degrees across BMI categories in a population consisting of several underserved subgroups: pregnant people of color, with larger body sizes, or with lower incomes. Stronger evidence on safe levels of first trimester weight loss and obesity class-specific recommendations is needed.

The mechanisms distinguishing metabolically healthy from unhealthy phenotypes within the same BMI categories remain unclear. This study aimed to investigate the associations between regional fat distribution and metabolically unhealthy phenotypes in Chinese adults across different BMI categories.

This cross-sectional study involving 11833 Chinese adults aged 20 years and older. Covariance analysis, adjusted for age, compared the percentage of regional fat (trunk, leg, or arm fat divided by whole-body fat) between metabolically healthy and unhealthy participants. Trends in regional fat percentage with the number of metabolic abnormalities were assessed by the Jonckheere-Terpstra test. Odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated by logistic regression models. All analyses were performed separately by sex.

In non-obese individuals, metabolically unhealthy participants exhibited higher percent trunk fat and lower percent leg fat compared to healthy participants. Additionally, percent trunk fat increased and percent leg fat decreased with the number of metabolic abnormalities. After adjustment for demographic and lifestyle factors, as well as BMI, higher percent trunk fat was associated with increased odds of being metabolically unhealthy [highest vs. lowest quartile: ORs (95%CI) of 1.64 (1.35, 2.00) for men and 2.00 (1.63, 2.46) for women]. Conversely, compared with the lowest quartile, the ORs (95%CI) of metabolically unhealthy phenotype in the highest quartile for percent arm and leg fat were 0.64 (0.53, 0.78) and 0.60 (0.49, 0.74) for men, and 0.72 (0.56, 0.93) and 0.46 (0.36, 0.59) for women, respectively. Significant interactions between BMI and percentage of trunk and leg fat were observed in both sexes, with stronger associations found in individuals with normal weight and overweight.

Trunk fat is associated with a higher risk of metabolically unhealthy phenotype, while leg and arm fat are protective factors. Regional fat distribution assessments are crucial for identifying metabolically unhealthy phenotypes, particularly in non-obese individuals.

There are limited population-based studies examining the correlation between body roundness index (BRI) and mortality in diabetes and prediabetes patients.

Our final analysis encompassed 15,848 patients with diabetes and prediabetes sourced from the National Health and Nutrition Examination Survey(NHANES) spanning from 2003 to 2018. Cox proportional hazards model and restricted cubic splines (RCS) were utilized to assess the correlation between BRI and both all-cause mortality and cardiovascular mortality.

During an average follow-up period of 92.9 months, 2655 participants (12.73 %) died, including 730 (3.44 %) from cardiovascular diseases. RCS demonstrated a U-shaped nonlinear association between BRI with all-cause mortality and cardiovascular mortality, with threshold values of 5.54 and 5.21, respectively. When BRI was below the threshold, a negative correlation was observed between BRI and all-cause mortality (HR 0.87, 95 % CI 0.81-0.93).The correlation with cardiovascular mortality is not significant. Conversely, when BRI was above the threshold, a positive correlation was observed between BRI with all-cause mortality (HR 1.10, 95 % CI 1.06-1.14) and cardiovascular mortality (HR 1.13, 95 % CI 1.07-1.20).

Our research indicates that among US adults with diabetes or prediabetes, BRI exhibits a U-shaped relationship with all-cause and cardiovascular mortality, with threshold values of 5.54 and 5.21, respectively.

The prevailing guidelines for obesity in Asian Indians, published in 2009, relied solely on body mass index (BMI) criteria. Recognizing the limitations of BMI in accurately diagnosing obesity and the emergence of new research revealing the association between generalized and abdominal adiposity in Asian Indians and early-onset co-morbid diseases, a comprehensive redefinition was needed.

In a Delphi process focused on obesity in India, experts were invited via email to participate in five rounds. The survey questions were administered through Google Form to gather insights from the selected experts.

In Stage 1 Obesity, individuals exhibit increased adiposity (BMI>23 kg/m2) without discernible effects on organ functions or daily activities. Stage 2 Obesity denotes a more advanced state characterized by heightened adiposity (generalized and abdominal), impacting both physical and organ functions, resulting in functional limitations during day-to-day activities, and contributing to co-morbid diseases. The criteria for Stage 2 Obesity include a mandatory BMI exceeding 23 kg/m2 and at least one of the following: excess waist circumference or waist-to-height ratio. Additionally, the presence of one or more symptoms indicative of limitations in daily activities or one or more obesity-related comorbid conditions/diseases are needed to support the stage 2 obesity.

This refined framework seeks to enhance precision in identifying obesity and its associated health risks among Asian Indians living in India, and facilitation of rational management, and aligns with worldwide initiative of new definition of obesity.

Our aim was risk estimation for cardiovascular disease (CVD) across obesity phenotypes over 18 years of follow-up using both time-invariant and time-varying approaches.

This prospective cohort study included 9752 participants aged ≥30 years examined in the first and second phases of the Tehran Lipid and Glucose Study (1999-2001 and 2002-2005). Six phenotypes [i.e., metabolically healthy normal weight (MHNW), overweight (MHOW), and obese (MHO), as well as metabolically unhealthy normal weight (MUNW), overweight (MUOW), and obese (MUO)] were defined based on the body mass index (BMI) and metabolic status. Incident CVD was documented until March 2018. Time-invariant and time-varying Cox regression models were used to estimate CVD hazard ratio (HRs) for obesity phenotypes. Mean age of the participants was 46.6 ± 12.0 years, and 53.9 % of them were women. During 18 years of follow-up, 1083 new CVD events occurred. In metabolically unhealthy individuals, but not metabolically healthy people, multivariable-adjusted HRs for CVD events increased by BMI according to time-varying (HR = 1.6, 95 % CI = 1.13-2.26 for MUNW; HR = 1.92, 95 % CI = 1.43-2.58 for MUOW; HR = 1.94, 95 % CI = 1.4-2.68 for MUO) and time-invariant (HR = 1.85, 95 % CI = 1.01-3.39 for MUNW; HR = 2.75, 95 % CI = 1.63-4.63 for MUOW, and HR = 3.26, 95 % CI = 1.95-5.47 for MUO) models.

Metabolically unhealthy overweight and obese individuals are at increased risk of CVD and should be regularly screened to prevent possible cardiovascular events.

To observe the effects of liraglutide on abdominal fat distribution in Chinese subjects with obesity in 12 weeks, and further to explore the correlation between abdominal fat content and glucose metabolism after monotherapy.

This study recruited 71 obese subjects. All the subjects have received liraglutide monotherapy (0.6 mg-1.8 mg/d) for 12 weeks. Clinical assessment, laboratory assays and magnetic resonance imaging (MRI) examination were accessed at baseline and after 12 weeks treatment. MRI was applied to measure abdominal fat distribution, calculated by proton-density fat fraction (PDFF).

After 12 weeks of liraglutide monotherapy, body weight in the obese participants decreased significantly (P < 0.001). Fasting blood glucose (FBG) levels, 2 h post-load blood glucose (2hPBG) levels, and glycosylated hemoglobin (HbA1c) were remarkably improved after liraglutide monotherapy (all P < 0.001). Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were significantly reduced after liraglutide monotheraphy (both P < 0.001). There was a notable reduction in liver fat content (LFC) after liraglutide monotherapy (P < 0.001). In the further analysis, LFC was greater in obese subjects with impaired glucose regulation (IGR) at baseline compared to those with normal glucose tolerance (NGT) (P = 0.002). The LFC reduction in IGR group was significantly greater than those in NGT group after liraglutide treatment (P < 0.001). Pearson correlation analysis showed that reduction of LFC was significantly correlated with improvement of FBG (r = 0.587, P < 0.001) and HbA1c (r = 0.607, P < 0.001) in obese patients.

LFC was significantly reduced after liraglutide monotherapy for 12 weeks in subjects with obesity. The LFC reduction is likely to be associated with IGR remission in obese subjects.

Excess adipose tissue may promote chronic systemic inflammation and oxidative stress, causing endothelial damage. Early evidence indicates that obesity may be associated with poorer cerebral perfusion. The purpose of this study was to examine the relationship between body composition and cerebral hemodynamics. A total of 248 middle-aged adults (50-58 years old; 55% women) underwent a ramp test on a cycle-ergometer until volitional exhaustion. Gas exchange was assessed on a breath-by-breath basis. Mean middle cerebral artery velocity (MCAv) was measured using transcranial Doppler, and pulsatility index (PI) was calculated. Body composition was assessed by dual X-ray absorptiometry. Statistical analyses were performed using a compositional data approach including a 3-compartment model for body composition (trunk fat mass, extremities fat mass, and fat-free mass). The unadjusted models for the whole sample showed that trunk fat mass relative to other compartments was negatively associated with MCAvrest, MCAvmax, and gain, and positively associated with PImax; extremities fat mass relative to other compartments was positively associated with MCAvrest and MCAvmax, and negatively associated with PImax; and fat-free mass relative to other compartments was positively associated with PImax. These associations were sex-dependent, remaining in the women's subgroup. However, after adjusting for confounders, these associations became nonsignificant, except for PImax in the whole sample and women's subgroup. These findings suggest a possible association between cerebral hemodynamics and body composition in middle-aged adults, highlighting sex-specific differences. Moreover, our results indicate that higher trunk fat mass relative to other compartments may negatively affect cerebral hemodynamics, reducing MCAv and increasing PImax.

Obesity is a metabolic disorder that occurs when excess energy taken into the body is stored as fat. It is known that this metabolic imbalance affects the development of other diseases such as cancer, cardiovascular diseases, insulin resistance, and diabetes. The main cellular component of adipose tissue is adipocytes, and the environmental interactions of adipocytes are important to study the mechanism of disorder formation. Breast tissue is rich in adipose tissue and obesity is known to be an important risk factor in the development of breast cancer. Altered adipogenesis and lipogenesis processes in adipocytes in breast tissue support tumor development through the transfer of fatty acids released from adipocytes. We believe that blending adipocyte biology with breast cancer development is important for investigating the mechanisms that regulate breast tumor malignant behavior and providing new targets for treatment. Fatty acids, which are an energy source for breast cancer cells, are discussed from molecular perspectives in this review.

The patient with obesity is at risk of developing cardiovascular disease and risk factors. Obesity negatively impacts prognosis and increases cardiovascular morbidity and mortality. Therefore, a comprehensive risk assessment is needed to define the cardiovascular risk of the patient and, thus, a tailored management and treatment. Chronic and successful management of these patients involves the evaluation of the various therapeutic strategies available (comprehensive lifestyle intervention, weight-loss medications, and bariatric surgery) and the diagnosis and treatment of cardiovascular complications (coronary artery disease, heart failure, and atrial fibrillation). Cardiac rehabilitation in patients with obesity is showing beneficial effect and a positive impact on weight loss, cardiovascular risk factors, mental health, functional capacity, and adherence to lifestyle interventions and pharmacological treatment. Long-term weight loss and maintenance represent a key objective during the management of the patient with obesity to reduce the risk of future adverse events. Multidisciplinary management and interventions are necessary to prevent and reduce overall cardiovascular risk and mortality. The aim of our review is to propose a comprehensive, critical and updated overview regarding risk assessment, physical activity, and the management of cardiovascular complications in patient with obesity.

Shared decision-making is recommended as a person-centred approach to decision-making in antenatal care. Little is known about the implementation of shared decision-making in antenatal care.

An exploratory study to understand how shared decision-making is implemented in antenatal clinics and whether body mass index influences maternity clinicians' use of shared decision-making when providing antenatal care for women.

Twenty-six antenatal clinic consultations were audio-recorded with maternity clinicians and women with body mass index ≥ 35 kg/m2, and a comparison group of women with body mass index 18.5-24.9 kg/m2. Data were analysed quantitatively using the OPTION12 scale. Narrative case studies are presented to compare shared decision-making behaviour related to induction of labour.

Twelve clinicians and 26 pregnant women were recruited to the study. The total scores ranged from 0 to 24, with a mean score of 9 and a median of 9.5 indicating low implementation of shared decision-making by clinicians and limited involvement of women in decision-making. No difference was observed in OPTION12 scores in decision-making for women by body mass index.

This study suggests that shared decision-making is limited in the antenatal clinic setting for all women, regardless of body mass index. Further research is required to confirm the findings of this exploratory study.

The perspectives of women with body mass index ≥ 35 kg/m2 informed many aspects of this study including the language/terminology adopted by researchers. A consumer group reviewed the language used in the study materials, to ensure readability and avoidance of stigmatising terminology.

The obesity pandemic, with its associated comorbidities of hypertension and diabetes, constitutes a global public health issue. Importantly, there is an increasing prevalence of aldosterone excess related to obesity and resultant poor health outcomes. Nevertheless, the association between aldosterone and obesity still needs to be clarified. In this review, the authors discuss the role of white adipose tissue in linking obesity, aldosterone excess, and hypertension. The consequences of aldosterone excess in obesity are presented as genomic, non-genomic, and non-epithelial effects. Moreover, the authors emphasize the value of interference with aldosterone pathophysiology (as with mineralocorticoid antagonists) in obesity, thus reducing the adverse clinical impact of aldosterone in myocardial infarction, heart failure, kidney dysfunction, and associated mortality.