Objective: This review examines the evolution of obesity evaluation methods, from traditional anthropometric indices to advanced imaging techniques, focusing on their clinical utility, limitations, and potential for personalized assessment of visceral adiposity and associated metabolic risks.

Methods: A comprehensive analysis of existing literature was conducted, encompassing anthropometric indices (BMI, WC, WHR, WHtR, NC), lipid-related metrics (LAP, VAI, CVAI, mBMI), and imaging technologies (3D scanning, BIA, ultrasound, DXA, CT, MRI). The study highlights the biological roles of white, brown, and beige adipocytes, emphasizing visceral adipose tissue (VAT) as a critical mediator of metabolic diseases.

Conclusion: Although BMI and other anthropometric measurements are still included in the guidelines, indicators that incorporate lipid metabolism information can more accurately reflect the relationship between metabolic diseases and visceral obesity. At the same time, the use of more modern medical equipment, such as ultrasound, X-rays, and CT scans, allows for a more intuitive assessment of the extent of visceral obesity.

White adipose tissue (WAT) delivers lipid-fueled metabolic support to systemic energy expenditure through control of lipolytic and re-esterifying regulatory pathways, facilitated by mitochondrial bioenergetic support. Mitochondria are important sources of reactive oxygen species (ROS) and oxidative damage may potentially derail adipocyte function when mitochondrial homeostasis is challenged by overproduction of ROS. Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α is a transcriptional co-activator that in skeletal muscle plays a central role in mitochondrial biogenesis and function but whether PGC-1α is equally important for mitochondrial function and adaptations in white adipose tissue remains to be fully resolved. The aim of the present study was to characterize the necessity of adipocyte PGC-1α for adaptive regulation of mitochondrial function in distinct white adipose depots. PGC-1α adipose tissue-specific knockout (ATKO) and floxed littermate control mice (CTRL) were subjected to either 24 h of fasting or 48 h of cold exposure. Bioenergetics, ROS handling, basal and adaptive protein responses, markers of protein damage as well as lipid cycling capacity and regulation were characterized in distinct WAT depots. ATKO mice demonstrated impairments in respiration as well as reduced OXPHOS protein content in fed and fasted conditions. Increased ROS emission in tandem with diminished mitochondrial antioxidant defense capacity resulted in increased protein oxidation in ATKO WAT. Adipose tissue PGC-1α knockout also led to changes in regulation of lipolysis and potentially triglyceride reesterification in WAT. In conclusion, PGC-1α regulates adipose tissue mitochondrial respiration and ROS balance as well as lipid cycling during metabolic challenges in a depot specific manner.

Obesity is a worldwide health crisis and poses significant challenges in critical care. Many studies suggest an 'obesity paradox', in which obesity, defined by body mass index (BMI), is associated with better outcomes. However, the inability of BMI to discriminate between fat and muscle or between visceral adipose tissue and subcutaneous adipose tissue, limits its prediction of metabolic ill health. We suggest that the 'obesity paradox' may be more reflective of the limitations of BMI than the protective effect of obesity. We explore the biological processes leading to visceral fat accumulation, and the evidence linking it to outcomes in critical illness. In the 'spillover' hypothesis of adipose tissue expansion, caloric excess and impaired expansion of storage capacity in the subcutaneous adipose tissue lead to accumulation of visceral adipose tissue. This is associated with a chronic inflammatory state, which is integral to the link between visceral adiposity, type 2 diabetes mellitus, and ischaemic heart disease. We review the current evidence on visceral adiposity and critical illness outcomes. In COVID-19, increased visceral adipose tissue, irrespective of BMI, is associated with more severe disease. This is mirrored in acute pancreatitis, suggesting visceral adiposity is linked to poorer outcomes in some hyperinflammatory conditions. We suggest that visceral adiposity's chronic inflammatory state may potentiate acute inflammation in conditions such as COVID-19 and acute pancreatitis. Further work is required to investigate other critical illnesses, especially sepsis and acute respiratory distress syndrome, in which current evidence is scarce. This may give further insights into pathophysiology and inform tailored treatment and nutrition strategies based on body fat distribution.

Adiposity is a major risk factor for the development of cancers, such as breast cancer(BC) in adults. However, the role of central adiposity or general obesity as primary predictors of BC occurrence and progression is not well-established. Therefore, the current study aimed to assess the association between various adiposity indices, including a body shape index(ABSI), abdominal volume index(AVI), body roundness index(BRI), conicity index(CI), body adiposity index(BAI), reciprocal ponderal index(RPI), and waist to height0.5 ratio(WHt0.5R) as surrogates for predicting the odds of BC in adult women. This case-control study was conducted at Shohada and Imam Hossain hospitals in Tehran and included 134 newly diagnosed BC cases and 267 controls. Anthropometric variables, including weight, height, and waist circumference were measured using standard methods, and various adiposity indices were calculated accordingly. The odds ratios(ORs) with 95% confidence intervals(CIs) for BC were reported across tertiles of adiposity indices using multivariable logistic regression. Participants in the highest tertile of BRI(OR:2.07;95% CI:1.04-4.12), BAI(OR:2.06;95% CI:1.05-4.03), and WHt0.5R(OR:1.81;95% CI:1.01-3.55) had significantly higher odds of BC compared to those in the lowest tertile(P < 0.05). Additionally, each SD increase in RPI was associated with lower odds of BC(OR:0.77;95% CI:0.61-0.98,P = 0.034). However, no significant associations were observed for CI, AVI, and ABSI with the odds of BC. Our results suggest that WHtR, BRI, BAI, and WHt0.5R may be more effective predictors of BC odds among the evaluated adiposity indices.

Laparoscopic sleeve gastrectomy (LSG) is an effective treatment for obesity, but early weight loss outcomes vary owing to individual nutritional and metabolic differences. We developed a nomogram model to predict early weight loss after LSG, incorporating computed tomography (CT)-based body composition metrics and preoperative inflammatory-nutritional markers.

We retrospectively analyzed 305 patients with obesity who underwent LSG at the Affiliated Hospital of Qingdao University between January 2016 and June 2023. An external validation cohort of 105 patients from a separate institution was also included. Patients were categorized into optimal remission (%total weight loss [%TWL] ≥ 25%) and suboptimal remission (%TWL < 25%) weight loss groups one year postoperatively. Predictive variables were identified using Least Absolute Shrinkage and Selection Operator (LASSO) regression and multivariate logistic regression. A nomogram was constructed based on the significant predictors. Model performance was assessed using the area under the receiver operating characteristic curve (AUC), calibration curves, decision curve analysis (DCA), and clinical impact curve (CIC).

Independent predictors of suboptimal remission included BMI > 40 kg/m2, elevated total cholesterol, high neutrophil-to-lymphocyte ratio, high cortisol, low skeletal muscle index, and elevated visceral-to-subcutaneous adipose tissue area ratio. The constructed nomogram demonstrated strong predictive performance, with AUCs of 0.864 and 0.842 in the training and external validation cohorts, respectively. Calibration curves indicated excellent agreement between predicted and observed outcomes. DCA and CIC confirmed the model's clinical utility in both cohorts.

The developed nomogram effectively predicts early weight loss outcomes after LSG, supporting targeted perioperative management and personalized nutritional interventions.

The menopausal transition is accompanied by metabolic changes in women. This study explores the Chinese visceral adiposity index (CVAI) as a potential indicator of menopausal status to aid in disease prevention.

A cohort of 404 premenopausal Chinese women aged 45 years and above, from the China Health and Retirement Longitudinal Study (CHARLS), was included. CVAI was calculated from the 2011 survey data, menopausal status was collected in the 2018 survey, representing a 7-year longitudinal follow-up. The cross-sectional study cohort from the National Health and Nutrition Examination Survey (NHANES) included 3577 women aged 40-60 with CVAI and self-reported menopausal status from 2003 to 2020. Logistic regression models were estimated the odds ratio (OR) of the menopause data and 95% confidence intervals (CIs).

In the CHARLS cohort, the adjusted OR for menopause in the fourth quartile of CVAI compared to the first quartile was 5.23 (95% CI: 1.59, 17.17; P for trend: 0.005). Additionally, a significant difference in the association between menopausal status and CVAI was found between rural and urban populations (P for interaction = 0.029). Moreover, in the NHANES cohort, the CVAI and the menopausal status were associated after adjustment (OR: 1.02, 95% CI: 1.002, 1.037, P: 0.029). In the stratified analysis, the association of CVAI with the status of menopause was observed among other ethnicities which including Asians (OR: 1.092, 95% CI: 1.012, 1.178, P: 0.025). Finally, a nomogram was developed to facilitate the clinical assessment of menopause based on the CVAI.

The CVAI demonstrated a significant association with the odds of menopausal status in both Chinese and the US populations, suggesting its potential as a correlative marker for menopausal status, but the associational strength may vary by population.

Hypothyroidism increases the risk of cardiovascular disease. In recent years, it has been suggested that the Visceral Adiposity Index (VAI) and the Plasma Atherogenicity Index (PAI) may serve as markers of cardiovascular risk. This study aimed to investigate the potential utility of VAI and PAI as predictors of increased cardiovascular risk in patients with hypothyroidism.

A retrospective analysis was conducted on 134 participants, including 85 hypothyroid patients and 49 individuals with normal thyroid function who visited the Family Medicine Clinic of Konya Training and Research Hospital between March 2016 and June 2017. Sociodemographic characteristics, anthropometric measurements, blood lipid profiles, and thyroid hormone levels were analyzed for all participants. VAI and PAI levels were calculated.

Among the participants, 111 (82.8%) were female, and 23 (17.2%) were male. In the hypothyroid group, triglycerides (TG) (p=0.001), Visceral Adiposity Index (VAI) (p<0.001), and Plasma Atherogenic Index (PAI) (p<0.001) were significantly higher, in contrast high-density lipoprotein (HDL) (p<0.001) was substantially lower than in the control group. Patients were divided into three categories based on PAI levels: low, moderate, and high risk. Compared to the moderate-risk group, the high-risk group had higher weight (p=0.007), BMI (p=0.012), WC (p=0.001), TG (p<0.001), VAI (p<0.001), and PAI (p<0.001), but lower HDL (p<0.001). PAI showed a positive correlation with age, weight, BMI, WC, systolic and diastolic blood pressure, thyroid-stimulating hormone (TSH), TG, total cholesterol, and VAI, and a negative correlation with HDL.

This study demonstrates that cardiovascular risk is increased in hypothyroid patients, VAI and PAI are reliable markers for assessing cardiovascular disease risk in this population. These findings may aid primary care physicians in early identification and management of cardiovascular risk in hypothyroid patients. Limitations include the retrospective design and limited male representation in the sample.

We previously identified tetraspanin 7 (Tspan7) as a candidate gene influencing body weight in an obesity-related gene screening study. However, the mechanisms underlying its involvement in body weight regulation remained unclear. This study aims to investigate the role of TSPAN7 from a metabolic perspective.

We utilized genetically modified mice, including adipose tissue-specific Tspan7-knockout and Tspan7-overexpressing models, as well as human adipose-derived stem cells with TSPAN7 knockdown and overexpression. Morphological, molecular, and omics analyses, including proteomics and transcriptomics, were performed to investigate TSPAN7 function. Physiological effects were assessed by measuring blood markers associated with lipid regulation under metabolic challenges, such as high-fat feeding and aging.

We show that TSPAN7 is involved in regulating lipid droplet formation and stabilization. Tspan7-knockout mice exhibited an increased proportion of small-sized adipocytes and a reduced visceral-to-subcutaneous fat ratio. This shift in fat distribution was associated with improved insulin sensitivity and altered branched-chain amino acid metabolism, as evidenced by increased expression of the branched-chain α-keto acid dehydrogenase complex subunit B in Tspan7-modified mice. Mechanistically, TSPAN7 deficiency promoted subcutaneous fat expansion, alleviating metabolic stress on visceral fat, a major contributor to insulin resistance.

TSPAN7 influences lipid metabolism by modulating adipose tissue remodeling, particularly under metabolic challenges, such as high-fat diet exposure and aging. Its modulation enhances subcutaneous fat storage capacity while mitigating visceral fat accumulation, leading to improved insulin sensitivity. These findings position TSPAN7 as a potential target for therapeutic interventions aimed at improving metabolic health and preventing obesity-related diseases.

Although the cardiometabolic index (CMI) has gained recognition as a new tool for evaluating metabolic health, the relationship between CMI and cardiovascular disease (CVD) remains unclear. This research sought to explore the potential association between CMI and CVD.

Participants from the 2007-2018 National Health and Nutrition Examination Survey (NHANES) were selected. Multivariable logistic regression analyses and smooth curve fitting were utilized to investigate this relationship, along with subgroup evaluations and interaction analyses.

This study included 12,837 subjects and the prevalence of CVD was 11.83%. After full adjustment, participants presenting with an increase of one unit in Ln-transformed CMI associated a 15% higher odds of CVD prevalence (OR = 1.15, 95% CI: 1.05-1.26). In the fully adjusted model, individuals falling into the highest CMI quartile (Quartile 4) demonstrated substantially 35% higher odds than those in the lowest CMI quartile (Quartile 1) (OR = 1.35, 95% CI: 1.11-1.66). In addition, there was no nonlinear relationship between CMI and CVD in our selected sample. This positive association was not greatly influenced by any of the stratifications.

Among US adults, having higher CMI levels is substantially associated with higher odds of CVD prevalence. This finding suggests that regular monitoring of CMI levels could enable physicians to initiate early interventions, potentially slowing the progression of CVD. However, in order to corroborate our findings, further prospective investigations are still required.

The aim of this study was to evaluate long-term inflammatory, biochemical and behavioral parameters in adult male and female Wistar rats submitted to a model of high-fat and high fructose diet and sepsis. In the study we used 8-month-old male and female rats. High-fat and high fructose diet was provided for 4 months, and sepsis was induced shortly afterwards. Behavioral tests were performed at 10, 30 and 60 days after sepsis induction, at 30- and 60-days metabolic parameters, leptin and cytokines (prefrontal cortex and hippocampus) were determined. High-fat and high-fructose diet was able to induce glucose intolerance. Sepsis favored anxious behavior at 10 days after sepsis, remaining at 30 days and with apparent improvement at 60 days in females and maintenance of behavior in males. Cognitive damage was observed both at 30 and 60 days in animals from both groups. Plasma metabolic parameters were elevated only males exposed to a high-fat high-fructose diet and submitted to CLP only at 30 days. Long-term brain inflammation was not consistently affected both by sex and high-fat and high fructose diet.The relationship between high-fat and high fructose diet, gender and sepsis is still contradictory, as are the mechanisms involved in this paradox. Models and analyses need to be standardized in order to better understand how this event occurs.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), encompasses a spectrum of liver diseases characterized by hepatic steatosis, the presence of at least one cardiometabolic risk factor, and no other apparent cause. Metabolic syndrome (MetS) is a cluster of clinical conditions associated with increased risk of cardiovascular disease, type 2 diabetes, and overall morbidity and mortality. This narrative review summarizes the changes in the management of people with MetS and NAFLD/MASLD from screening to therapeutic strategies that have occurred in the last decades. Specifically, we underline the clinical importance of considering the different impacts of simple steatosis and advanced fibrosis and provide an up-to-date overview on non-invasive diagnostic tests (i.e., imaging and serum biomarkers), which now offer acceptable accuracy and are globally more accessible. Early detection of MetS and MASLD is a top priority as it allows for timely interventions, primarily through lifestyle modification. The liver and cardiovascular benefits of a global and multidimensional approach are not negligible. Therefore, a holistic approach to both conditions, MetS and related chronic liver disease, should be applied to improve overall health and longevity.

Cardiovascular-kidney-metabolic (CKM) syndrome is a condition characterized by the interplay between cardiovascular disease, kidney disease, diabetes, and obesity, resulting in adverse health outcomes. This study aimed to investigate the differential associations between various adipose tissue types and the progression of CKM syndrome, as well as their relationship with the individual components of the syndrome.

We conducted a retrospective review of 441 individuals with preserved left ventricular (LV) systolic function who underwent both transthoracic echocardiography and abdominal computed tomography. LV structural and functional parameters, along with the thickness of epicardial adipose tissue (EAT), perirenal adipose tissue (PAT), and subcutaneous adipose tissue (SAT), were assessed through these imaging modalities. Additionally, the triglyceride and glucose (TyG) index was evaluated as a marker of insulin resistance, while glomerular filtration rate (GFR) was estimated to assess kidney function.

EAT and PAT demonstrated a progressive increase in thickness with advancing stages of CKM syndrome, whereas body mass index and SAT did not show similar trends. EAT was predominantly associated with markers of LV diastolic dysfunction, while PAT was uniquely associated with GFR, independent of other adipose tissue. Furthermore, the TyG index was independently correlated with the thickness of both EAT and PAT, but not with SAT thickness.

Heart, kidney, and metabolic disorders associated with CKM syndrome demonstrated varying correlations depending on the specific regional adipose tissue depot. EAT and PAT were identified as key regional adipose tissue linked to the progression of CKM syndrome.

Gestational diabetes mellitus (GDM) is regarded by many as maternal maladaptation to physiological insulin resistance during the second half of pregnancy. However, recent evidence indicates that alterations in carbohydrate metabolism can already be detected in early pregnancy. This observation, the increasing prevalence of GDM, and the significant short and long-term implications for the mother and offspring call for reevaluation of the conceptual paradigm of GDM as a syndrome. This review will present evidence for the syndromic nature of GDM and the controversies regarding screening, diagnosis, management, and treatment.

Dysregulation of adipose tissue (AT) homeostasis in obesity contributes to metabolic stress and disorders. Here, we identified that Coiled-coil-helix-coiled-coil-helix domain containing 10 (Chchd10) is a novel regulator of AT remodeling upon excess energy intake. Chchd10 is significantly reduced in the white adipose tissue (WAT) of mice in response to high-fat diet (HFD) feeding. AT-Chchd10 deficiency accelerates adipogenesis predominantly in subcutaneous AT of mice to store excess energy in response to short-term HFD feeding while upregulates glutathione S-transferase A4 (GSTA4) to facilitate 4-HNE clearance mainly in visceral AT to prevent protein carbonylation-induced cell dysfunction after long-term HFD feeding. Hence, Chchd10 deficiency attenuates diet-induced obesity and related metabolic disorders in mice. Mechanistically, Chchd10 deficiency enhances adipogenesis and GSTA4 expression by activating TDP43/Raptor/p62/Keap1/NRF2 axis. Notably, the beneficial effect of Chchd10 deficiency is eliminated in hypertrophic adipocytes, where p62 is strikingly reduced. Collectively, Chchd10 is a metabolic sensor maintaining AT homeostasis, and the loss of p62 in adipose tissue under obese conditions impairs Chchd10-mediated AT remodeling.

Obesity is a global health crisis, with increasing evidence linking environmental factors such as exposure to endocrine-disrupting chemicals (EDCs) to its development. This study examines the transgenerational effects of exposure to the model obesogen, tributyltin (TBT), on obesity and metabolic health, specifically focusing on how these effects interact with a diet modeling the 50th percentile of US dietary consumption [the Total Western Diet (TWD)]. Pregnant F0 dams were exposed to TBT, and their offspring were subjected at adulthood to different diets, including a high-fat diet and TWD, across multiple subsequent generations (F1-F3). We found that TBT exposure predisposed male offspring to increased fat accumulation, insulin resistance, and metabolic dysfunction, effects that were exacerbated by the TWD. Notably, male offspring displayed elevated leptin levels, hepatic fibrosis, and inflammatory responses under TWD exposure, suggesting an additive or synergistic relationship between obesogen exposure and dietary fat intake. These transgenerational effects were largely absent in female offspring, underscoring sex-specific vulnerabilities to environmental and dietary factors. Our results demonstrated that the combination of prenatal TBT exposure and TWD amplifies metabolic disturbances across generations, highlighting the need to consider both environmental chemicals and dietary patterns in addressing the obesity pandemic. This study underscores the critical role of early-life EDC exposures and dietary factors in shaping long-term metabolic health and the potential for transgenerational programming of susceptibility to obesity and metabolic disorders.

Background/Objectives: This study examines the relationship between visceral fat (VF), metabolic health, and dietary patterns in patients with obstructive bronchial diseases (OBDs) using bioelectrical impedance analysis (BIA). Methods: A total of 75 patients diagnosed with OBD, including chronic obstructive pulmonary disease (COPD) and/or asthma, were assessed for VF levels via BIA. Dietary habits were evaluated using a structured questionnaire to explore their correlation with VF accumulation. Results: The study cohort comprised predominantly male participants (66.7%), with the majority aged between 61 and 70 years (46.7%). Significant gender differences in VF distribution were observed, with 60% of females maintaining normal VF levels (1-9) compared to only 28% of males, while 38% of males exhibited very high VF levels (15-30; p = 0.003). Body mass index (BMI) showed a strong correlation with VF (p < 0.0001), as overweight and obese individuals predominantly displayed elevated VF levels (≥10). Moreover, metabolic syndrome (MS) was present in 66.7% of participants, with these individuals exhibiting significantly higher VF levels compared to those without MS (p = 0.001). Dietary analysis revealed that frequent consumption of fast food (r = 0.717, p < 0.001), carbonated drinks (r = 0.366, p = 0.001), and refined carbohydrates (r = 0.438, p < 0.001) was significantly associated with increased VF accumulation. Conversely, higher intake of water (r = -0.551, p < 0.001), fruits (r = -0.581, p < 0.001), and vegetables (r = -0.482, p < 0.001) correlated with lower VF levels. Lack of physical activity was also strongly linked to VF accumulation (r = 0.481, p < 0.001), further reinforcing the role of lifestyle factors in metabolic health. Conclusions: The findings underscore the significant impact of dietary habits and physical activity on VF accumulation in OBD patients. BMI and MS emerged as critical predictors of VF, while unhealthy dietary patterns and sedentary lifestyles further exacerbated VF deposition. Elevated VF levels were linked to adverse lipid profiles, reinforcing the need for dietary and lifestyle modifications in managing metabolic health among OBD patients. Although no direct association was identified between VF and forced expiratory volume in one second (FEV1), the results highlight the necessity of integrated nutritional and metabolic interventions in the management of chronic respiratory diseases.

Polygenic severe obesity (body mass index [BMI] ≥40 kg/m2) has increased, especially in Hispanic/Latino populations, yet we know little about the underlying mechanistic pathways. We analyzed whole-blood multiomics data to identify genes differentially regulated in severe obesity in Mexican Americans from the Cameron County Hispanic Cohort. Our RNA sequencing analysis identified 124 genes significantly differentially expressed between severe obesity cases (BMI ≥40 kg/m2) and controls (BMI <25 kg/m2); 33% replicated in an independent sample from the same population. Our integrative approach identified inflammatory genes, including IL4R, ZNF438, and LILRA5. Several genes displayed transcriptomic effects on severe obesity in subcutaneous adipose tissue. We further showed that the genetic regulation of these genes is associated with several traits in a large biobank, including bone fractures, obstructive sleep apnea, and hyperaldosteronism, illuminating potential risk mechanisms. Our findings furnish a molecular architecture of the severe obesity phenotype across multiple molecular domains.

The objective of this study was to elucidate associations between adiposity reduction and changes in HbA1c and insulin use among adults with type 2 diabetes and overweight or obesity.

Changes in BMI, waist circumference, and total percent fat mass were obtained over 8 years among 1316 individuals (aged 45-76 years) enrolled in the Look AHEAD (Action for Health in Diabetes) clinical trial of weight loss. Generalized linear models were used to assess relationships between 5% decreases in adiposity measures with glycated hemoglobin (HbA1c) and insulin use over time.

A 5% reduction in total percent fat was associated with 0.15% (95% CI: 0.12%-0.18%) lower mean HbA1c. Similarly, 5% reductions in waist circumference and BMI were also associated with slightly lower mean HbA1c: 0.16% (95% CI: 0.13%-0.19%) and 0.13% (95% CI: 0.11%-0.16%), respectively. These reductions were associated with lower odds of insulin use over time, ranging from 21% lower odds for a 5% reduction in percent body fat to 32% lower odds for 5% reductions in waist circumference and BMI. Associations were evident across subgroups defined by sex, diabetes duration, obesity status, and intervention assignment.

Reductions in adiposity are associated with stabilized and slightly lower HbA1c and a marked reduction in the need for insulin therapy. These benefits generalize across clinical subgroups.

Central obesity is a well-known risk factor of numerous disease. Numerous indicators are developed for central obesity measurement, among them, abdominal volume index (AVI), reflecting total volume of the abdomen, precisely estimates the visceral fat volume. As a relatively new health measure and potent prognostic marker of metabolic disturbances, no study is available to investigate its role in cardio-metabolic health and oxidized LDL among obese young adults. In the current study we aimed to evaluate the association between abdominal volume index (AVI) with cardio-metabolic profile including serum lipids, glycemic markers of serum glucose, hemoglobin (Hb) A1C, insulin, oxidized LDL and blood pressure among young obese adults.

Two hundred twenty young adults aged 18 to 25 years old with overweight or obesity were enrolled in the current study. Anthropometric measurements were done and AVI were calculated. Biochemical variables including serum total cholesterol (TC), low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL), triglyceride (TG), glycemic markers, including fasting serum glucose (FBS), insulin, hemoglobin (Hb) A1C and blood pressure were also measured with an automatic analyzer.

Participants in the third tertiles of AVI had higher body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) (p < 0.001 for all). Among biochemical variables, oxidized LDL, TG and HDL demonstrated significant associations across AVI tertiles in the first and second models, with higher oxidized LDL and TG and lower HDL levels observed in higher AVI tertiles (p < 0.05). Moreover, those at the highest AVI tertiles showed significantly higher odds ratios for elevated cardio-metabolic index and systolic and diastolic blood pressures compared to the first tertiles (p < 0.05).

In the current study, we comprehensively investigated the association between AVI with cardio-metabolic health in young obese adults and accordingly, AVI was unfavorably associated with metabolic health among obese adults. Further studies are needed to elaborate the underlying mechanisms.

Not applicable.

Adipose tissue plays a pivotal role in systemic metabolism and maintaining bodily homeostasis. Exosomes from adipose tissues, known as AT-Exos, are recognized as important messengers in the communication between adipose tissue and other organs. Despite this, the alterations in exosome composition and the functional disparities among depot-specific AT-Exos in obesity remain elusive.

In this work, we utilized lipidomics and microRNA (miRNA) sequencing to elucidate the lipid and miRNA profiles of AT-Exos in a diet-induced obesity model. We identified obesity-related miRNAs in AT-Exos and further explored their mechanisms using gain- and loss-of-function experiments. To evaluate the metabolic effects of AT-Exos on adipocytes, we conducted RNA-sequencing (RNA-seq) and confirmed our findings through Quantitative Real-time PCR (qPCR) and Western bolt analyses. Meanwhile, a mouse model with intraperitoneal injections was utilized to validate the role of exosomes derived from visceral white adipose tissue (vWAT-Exos) in obesity progression in vivo. Finally, we explored potential therapeutic intervention strategies targeting AT-Exos, particularly focusing on modulating the SIRPα-CD47 axis to enhance macrophage phagocytosis using Leptin-deficient (ob/ob) mice and SIRPα knock-out mice.

Our study revealed that obesity-related metabolism affects the biological processes of AT-Exos, with depot-specific secretion patterns. In obesity, the lipidome profile of AT-Exos was significantly altered, and diet can modify the miRNA content and function within these exosomes, influencing lipid metabolism and inflammatory pathways that contribute to metabolic dysregulation. Specifically, we identified that miR-200a-3p and miR-200b-3p promoted lipid accumulation in 3T3L1 cells partly through the PI3K/AKT/mTOR pathway. RNA-Seq analysis revealed that AT-Exos from different fat depots exerted distinct effects on adipocyte metabolism, with obese vWAT-Exos being notably potent in triggering inflammation and lipid accumulation in diet-induced obesity. Additionally, we found that inhibiting the SIRPα-CD47 axis can mitigate metabolic disorders induced by obese vWAT-Exos or ob/ob mice, partly due to the enhanced clearance of vWAT-Exos. Consistent with this, SIRPα-deficient mice exhibited a reduction in vWAT-Exos and displayed greater resistance to obesity.

This study elucidates that diet-induced obesity altered the lipid and miRNA profiles of AT-Exos, which involved in modulating adipocyte inflammation and metabolic balance. The SIRPα-CD47 axis emerges as a potential therapeutic target for obesity and its associated complications.

The circadian rhythm of cortisol, a key hormone essential for maintaining metabolic balance and stress homeostasis, is profoundly disrupted by night-shift work. This narrative review examines the physiological mechanisms underlying cortisol regulation, the effects of shift work on its circadian rhythm, the associated health risks, and potential mitigation strategies. Night-shift work alters the natural secretion pattern of cortisol, leading to dysregulation of the hypothalamic-pituitary-adrenal axis, which in turn can contribute to metabolic disorders, cardiovascular diseases, and impaired cognitive function. Understanding the physiological pathways mediating these changes is crucial for developing targeted interventions to mitigate the adverse effects of circadian misalignment. Potential strategies, such as controlled light exposure, strategic napping, and personalized scheduling, may help to stabilize cortisol rhythms and improve health outcomes. This review aims to provide insights that can guide future research and inform occupational health policies for night-shift workers by addressing these challenges.

Heart failure with preserved ejection fraction (HFpEF) represents a major clinical challenge with rising global prevalence. Women have a nearly double lifetime risk of developing HFpEF compared to heart failure with reduced ejection fraction (HFrEF). In HFpEF, sex differences emerge both in how traditional cardiovascular risk factors (such as hypertension, obesity, and diabetes) affect cardiac function and through distinct pathophysiological mechanisms triggered by sex-specific events like menopause and adverse pregnancy outcomes. These patterns influence not only disease development, but also therapeutic responses, necessitating sex-specific approaches to treatment. This review aims to synthesize existing knowledge regarding HFpEF in women including traditional and sex-specific risk factors, pathophysiology, presentation, and therapies, while outlining important knowledge gaps that warrant further investigation. The impact of HFpEF spans a woman's entire lifespan, requiring prevention and management strategies tailored to different life stages. While understanding of sex-based differences in HFpEF has improved, significant knowledge gaps persist. Through examination of current evidence and challenges, this review highlights promising opportunities for innovative research, therapeutic development, and clinical care approaches that could transform the management of HFpEF in women.

Brown adipose tissue (BAT) and thermogenic beige fat within white adipose tissue (WAT), collectively known as adaptive thermogenic fat, dissipate energy as heat, offering promising therapeutic potential to combat obesity and metabolic disorders. The specific biological functions of these fat depots are determined by their unique interaction with the microenvironments, composed of immune cells, endothelial cells, pericytes, and nerve fibers. Immune cells residing in these depots play a key role in regulating energy expenditure and systemic energy homeostasis. The dynamic microenvironment of thermogenic fat depots is essential for maintaining tissue health and function. Immune cells infiltrate both BAT and beige WAT, contributing to their homeostasis and activation through intricate cellular communications. Emerging evidence underscores the importance of various immune cell populations in regulating thermogenic adipose tissue, though many remain undercharacterized. This review provides a comprehensive overview of the immune cells that regulate adaptive thermogenesis and their complex interactions within the adipose niche, highlighting their potential to influence metabolic health and contribute to therapeutic interventions for obesity and metabolic syndrome.

Previous evidence suggests that certain types of nuts, when included in a healthy diet pattern, may provide health benefits. Therefore, we hypothesize that the consumption of cashew nuts associated with a healthy diet may enhance antioxidant defenses and improve anthropometric and body composition parameters in individuals with obesity. We conducted a 12-week randomized clinical trial, divided into 4 sessions, involving adolescents randomly assigned to receive either 30 g of roasted cashew nuts together with nutrition education (cashew nut group-CNG) or only nutrition education (control group-CG). The total number of participants who started the study was 142, with 77 in the CNG and 65 in the CG. Data on anthropometry, body composition, and oxidative stress were collected at baseline (0-week) and endpoint (12-week). The main post-intervention findings in the CNG showed decreases in waist circumference (WC), thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) at 60 minutes in the CNG, while neck circumference (NC) increased. However, the CG showed an increase in TBARS and percentage of lean body mass (LBM), along with reduction in TAC at 60 minutes. After 12 weeks, the consumption of cashew nuts seemed to assist in WC reduction, even without a decrease in other anthropometric parameters, thereby decreasing the cardiometabolic risk. Furthermore, the consumption of cashew nuts demonstrated the ability to decrease overall oxidative damage as assessed by TBARS, a finding that reinforces the effects of this nut consumption against systemic oxidative stress associated with obesity.

Background and Objectives: The accumulation of fat in the body, especially visceral fat, is associated with various cardiometabolic conditions such as diabetes mellitus and fatty liver. The reasons for the accumulation of this fat are diverse. Some studies, also in the working population, have shown a clear association between sociodemographic variables and health habits with scales that assess overweight and obesity. This study aims to determine how certain sociodemographic variables, such as age, gender, and socioeconomic level, as well as certain healthy habits like physical activity and tobacco consumption, affect the levels of body and visceral fat. Materials and Methods: We conducted a descriptive and cross-sectional study involving 8590 Spanish workers. The percentage of body and visceral fat was measured using a bioimpedance analysis with a Tanita DC 430MA device. Results: Both the average values and the prevalence of elevated body and visceral fat increase with age and decrease with social class and lower levels of physical activity. These values are higher in smokers. A multivariate analysis shows that the variables most influential in increasing the risk of high levels of both body and visceral fat are age and low levels of physical activity. Conclusions: The profile of a person at high risk of having elevated body and visceral fat levels is an older male with a low socioeconomic status who smokes and leads a sedentary lifestyle.

Accurate body fat distribution assessment is essential for managing cardiovascular disease and metabolic disorders. Although several methods are available for segmental fat analysis, few studies have examined the validity of affordable methods such as Bioelectrical Impedance Analysis (BIA) against the reference method, Dual-Energy X-ray Absorptiometry (DXA). This study aimed to assess the validity of BIA as compared to DXA for segmental fat mass assessment, and to develop anthropometric multivariate regression models that offer a cost-effective alternative for health professionals in clinical and public health settings.

Cross-sectional study that included 264 young adults (161 males, mean age = 23.04 ± 5.61 years; and 103 females, mean age = 22.29 ± 5.98 years). Segmental fat mass was measured using DXA and BIA, and anthropometric measurements were collected following the ISAK protocol.

Significant differences were found between DXA and BIA for segmental fat mass (p < 0.001). Sex significantly influenced the results (p < 0.05), while BMI and hydration status had no significant impacts. The Bland-Altman analysis revealed significant differences (p < 0.001) between BIA and DXA for fat mass in the upper and lower limbs. Trunk fat mass also differed significantly in males and females (p < 0.001), except for the overall sample (p = 0.088). Anthropometric multivariate regression models showed a high predictive accuracy for both females (R²=0.766-0.910; p < 0.001) and males (R²=0.758-0.887; p < 0.001). Key predictors of segmental fat mass included body mass (r = 0.606-0.867; p < 0.001), skinfold thickness (r = 0.688-0.893; p < 0.001), and waist girth (r = 0.883 - 0.810; p < 0.001). Peripheral skinfolds were highly predictive for upper and lower limbs, while waist girth was relevant for trunk fat mass.

DXA and BIA are not interchangeable for segmental fat analysis due to the significant differences observed. However, the anthropometric multivariate regression models developed provide a cost-effective and reliable alternative for predicting segmental fat mass in clinical settings where DXA is unavailable.

Not applicable.

Central body fat distribution affects kidney function. Abdominal fat measurements using computed tomography (CT) may prove superior in assessing body composition-related kidney risk in living kidney donors. This retrospective cohort study including 550 kidney donors aimed to determine the association between CT-measured abdominal fat areas and kidney function before and after donor nephrectomy. Donors underwent glomerular filtration rate measurements (125I-Iothalamate, mGFR) before and 3 months after donation. Linear regression analyses with body surface area (BSA)-standardized and crude mGFR were performed to assess the association of height-indexed tomographic fat measurements with kidney function. In age-, and sex-adjusted analyses higher levels of total abdominal, visceral, subcutaneous, and intramuscular adipose tissue index were significantly associated with lower mGFR levels before donation (BSA-standardized mGFR: visceral adipose tissue index: Βeta=-0.11, p < 0.001, subcutaneous: Βeta=-0.10, p < 0.001, intramuscular: Βeta=-1.18, p < 0.001, total abdominal: Βeta=-0.07, p < 0.001). Higher tomographic abdominal fat is associated with lower BSA-standardized mGFR after donation and a greater decrease in mGFR between screening and 3 months post-donation. This study shows that CT-measured abdominal fat area is associated with kidney function before and after living kidney donation.

Time-restricted feeding (TRF), an intermittent fasting approach involving a shortened eating window within 24 h, has gained popularity as a weight management approach. This review addresses how TRF may favor fat redistribution and the function of the adipose organ. TRF trials (mainly 16:8 model, with a duration of 5-48 weeks) reported a significant weight loss (1.2-10.2%, ~ 1.4-9.4 kg), with a considerable decrease in total fat mass (1.6-21%, ~ 0.5-7 kg) and visceral adipose compartment (VAC, 11-27%) in overweight and obese subjects. Experimental TRF in normal-fed and obesogenic-diet-fed mice and rats (with a fasting duration ranging between 9 and 21 h within 1-17 weeks) reported a significant reduction in body weight (~ 7-40%), total fat mass (~ 17-71%), and intrahepatic fat (~ 25-72%). TRF also improves VAC and subcutaneous adipose compartment (SAC) function by decreasing adipocyte size, macrophage infiltration, M1-macrophage polarity, and downregulating inflammatory genes. In conclusion, beyond its effect on body weight loss, total fat mass, and intrahepatic fat accumulation, TRF favors adipose organ fat redistribution in overweight and obese subjects by decreasing VAC and improving the function of VAC and SAC.

Metabolic syndrome (MetS) is a cluster of metabolic abnormalities, including visceral obesity, dyslipidemia, and insulin resistance. In this regard, visceral white adipose tissue (vWAT) plays a critical role, influencing energy metabolism, immunomodulation, and oxidative stress. Adipose-derived stem cells (ADSCs) are key players in these processes within vWAT. While second-generation antipsychotics (SGAs) have significantly improved treatments for mental health disorders, their chronic use is associated with an increased risk of MetS. In this study, we explored the impact of SGAs on ADSCs to better understand their role in MetS and identify potential therapeutic targets. Our findings reveal that olanzapine disrupts lipid droplet formation during adipogenic differentiation, impairing insulin receptor endocytosis, turnover, and signaling. SGAs also alter the endolysosomal compartment, leading to acidic vesicle accumulation and increased lysosomal biogenesis through TFEB activation. PKCζ is crucial for the SGA-induced nuclear translocation of TFEB and acidic vesicle formation. Notably, inhibiting PKCζ restored insulin receptor tyrosine phosphorylation, normalized receptor turnover, and improved downstream signaling following olanzapine treatment. This activation of PKCζ by olanzapine is driven by increased phosphatidic acid synthesis via phospholipase D (PLD), following G protein-coupled receptor (GPCR) signaling activation. Overall, olanzapine and clozapine disrupt endolysosomal homeostasis and insulin signaling in a PKCζ-dependent manner. These findings highlight SGAs as valuable tools for uncovering cellular dysfunction in vWAT during MetS and may guide the development of new therapeutic strategies to mitigate the metabolic side effects of these drugs.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a refined categorization of non-alcoholic fatty liver disease (NAFLD), highlighting the intricate relationship between hepatic steatosis and metabolic dysfunction. Abdominal obesity (AO), a key diagnostic criterion for metabolic dysfunction, predominantly results from inappropriate diet and unhealthy dietary habits. To comprehensively investigate which dietary factors contribute to MASLD through AO and to understand the underlying biological mechanisms, we initially conducted a systematic review of meta-analysis articles in the PubMed database from the past decade, summarizing dietary factors that affect AO. Subsequently, we conducted targeted searches in the PubMed database for these dietary factors and provided a narrative review of the mechanisms of how these dietary factors lead to AO and how AO exacerbates MASLD. A diet characterized by excessive intake of energy, carbohydrates, fructose, or ultra-processed foods (UPFs) is considered inappropriate. Inappropriate diet leads to the formation of MASLD and AO by enhancing pathways such as de novo lipid synthesis (DNL) in the liver, insulin resistance (IR), gut-liver dysfunction, and inflammation. Dietary interventions for inappropriate diets can effectively intervene in and improve MASLD and AO. The mechanism of inappropriate diet on abdominal fat deposition is through excessive energy or the activation of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) to increase endocortisol secretion. Then, the excessive accumulation of visceral fat facilitates a rapid and augmented flux of free fatty acids (FFAs) to the liver and initiates a series of deleterious effects, including oxidative stress (OS), endoplasmic reticulum stress (ERS), activation of protein kinase C (PKC) pathways, and inflammation. Additionally, FFAs may mediate excessive lipid deposition and hepatocellular damage through the action of hormones. These pathways to liver damage exacerbate MASLD and progression to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis. Furthermore, investigating other potential mechanisms by which AO may influence MASLD could offer new recommendations for the treatment guidelines of MASLD.

Chronic kidney disease (CKD) is a serious health concern with an estimated prevalence of about 13.4% worldwide. It is cause and consequence of various comorbidities, including cardiovascular diseases. In parallel, common pathological conditions closely related to ageing and unhealthy dietary habits increase the risk of CKD development and progression, including type 2 diabetes and obesity. Among these, obesity is either independent risk factor for new onset kidney disease or accelerates the rate of decline of kidney function by multiple mechanisms. Therefore, the role of diets aimed at attaining weight loss in patients with obesity is clearly essential to prevent CKD as to slow disease progression. Various dietary approaches have been licensed for the medical dietary therapy in CKD, including low-protein diet and Mediterranean diet. Interestingly, emerging evidence also support the use of low-carbohydrate/ketogenic diet (LCD/KD) in these patients. More specifically, LCD/KDs may efficiently promote weight loss, improve metabolic parameters, and reduce inflammation and oxidative stress, resulting in a dietary strategy that act globally in managing collateral conditions that are directly and indirectly related to the kidney function.

This consensus statement from the Italian Society of Endocrinology (SIE), working group of the Club Nutrition - Hormones and Metabolism; the Italian Society of Nutraceuticals (SINut), Club Ketodiets and Nutraceuticals "KetoNut-SINut"; and the Italian Society of Nephrology (SIN) is intended to be a guide for Endocrinologist, Nutritionists and Nephrologist who deal with the management of patients with obesity with non-dialysis CKD providing a practical guidance on assessing nutritional status and prescribing the optimal diet in order to best manage obesity to prevent CKD and its progression to dialysis.

The study assesses the metabolic impact of dietary whey proteins across generations.

Virgin females are fed 20% energy whey proteins with 70% energy carbohydrates, which reduces body weight gain and visceral adipose compared to controls fed dietary casein. In contrast, the males are unresponsive. The effect is accentuated in reproductive females that also have reduced plasma levels of glucose. The responsive females have increased cecal levels of pyruvic and lactic acid, suggesting a greater catabolism of carbohydrates in the gut. While the male and female offspring born to mothers on whey proteins continue to reduce body weight gain, the female offspring further decreases the visceral and subcutaneous tissues and increases the gut capacity to breakdown dietary carbohydrates and proteins, whereas the male offspring are able to only decrease the visceral and increase protein catabolism in the gut. The ileum of male mice responded by reducing the gene expression for fibroblast growth factor 15 and increasing the expression of chymotrypsinogen B1.

The effect of whey proteins on growth can be passed from the mother to the offspring without a sex preference, whereas the transmission of gut activity and adiposity are dependent on the sex of the offspring.