This study aimed to investigate the association of novel obesity indicators (lipid accumulation product [LAP] and cardiometabolic index [CMI]) with asymptomatic intracranial arterial stenosis (aICAS), particularly in different obesity statuses.

The study included 1994 participants (aged ≥ 40 years) from the Rose Asymptomatic Intracranial Artery Stenosis (RICAS) study, free of stroke or transient ischemic attack. Participants with aICAS were screened using transcranial Doppler ultrasound and diagnosed via magnetic resonance angiography. Multivariate logistic regression and receiver operating characteristic (ROC) curves were used to explore the association of LAP or CMI with aICAS.

A total of 146 participants were diagnosed with aICAS. Higher levels of LAP and CMI were associated with aICAS, particularly with moderate-to-severe aICAS. Notably, LAP was significantly associated with aICAS (OR 1.58; 95 % CI, 1.00-2.49; P = 0.048), and was showed the highest area under the curve (AUC, 0.654) among the three indicators (LAP, CMI, and BMI) in underweight and normal weight participants (Body mass index [BMI] ≤23.9 kg/m²). In the obesity population (BMI ≥28.0 kg/m2), CMI was significantly associated with aICAS (OR 1.40; 95 % CI, 1.11-1.77; P = 0.005), and was showed the highest AUC (0.610).

This study found a positive association between elevated levels of LAP or CMI and aICAS. Furthermore, LAP was significantly correlated with aICAS in underweight and normal weight individuals, while CMI was associated with aICAS in obesity individuals. Our findings may provide additional risk stratification information for aICAS.

Macrophages are critical immune cells present in virtually every tissue, where they contribute to tissue homeostasis beyond their traditional immune roles. Past and recent evidence highlights their involvement in endocrine regulation, particularly within the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. This review explores the ontogeny and function of macrophages residing in the hypothalamus, pituitary, adrenals, and gonads, emphasizing their contributions to hormonal output and endocrine homeostasis. Macrophages in the hypothalamus and pituitary modulate neuroendocrine signalling, impacting stress and reproductive hormone production. In the adrenal glands, distinct macrophage subsets regulate glucocorticoid and mineralocorticoid synthesis, influencing systemic metabolism and blood pressure. Gonadal macrophages contribute to steroidogenesis and fertility, with roles in testosterone production, ovarian folliculogenesis, and corpus luteum maintenance. The emerging understanding of macrophage regulation of endocrine function may seed novel therapeutic approaches for endocrine disorders. Future research should further elucidate the molecular mechanisms underlying macrophage regulation of hormone production and explore their implications for metabolic, immune, and reproductive health.

Lipid deposition is related to agricultural animal production and human health, and elucidating its molecular regulatory mechanisms is a topic of interest and a challenge in current scientific research. Musculoskeletal embryonic nuclear protein 1 (MUSTN1) regulates growth and development, including muscle tissue; however, its role in fat deposition remains unknown. Thus, our objective was to determine this role. Our new findings were as follows: MUSTN1 was highly expressed in the fat tissue of pigs with strong adipose deposition capacity; functionally, MUSTN1 promoted the proliferation and adipogenic differentiation of porcine and mouse preadipocytes. MUSTN1 knockout mice were protected against HFD-induced obesity, hepatic steatosis, and insulin resistance; and fatty acid binding protein 3 was identified as an interacting protein of MUSTN1, which facilitated preadipocyte proliferation and differentiation by activating the phosphatidylinositol 3 kinase/AKT signaling pathways. This study reveals a positive regulator for fat development, which suggests a novel approach for studying obesity and animal genetic improvement through the modulation of MUSTN1 expression.

Obesity, characterized by the excessive accumulation of white adipose tissue, is a significant global health burden and a major risk factor for a range of diseases, including malignancies and metabolic disorders. Individuals with high visceral fat content are particularly susceptible to severe complications such as type 2 diabetes, cardiovascular diseases, and liver disorders. However, the pathogenesis of obesity-related metabolic diseases extends beyond simple adiposity. Chronic obesity triggers a prolonged inflammatory response, which leads to tissue fibrosis and sustained organ damage, contributing to multi-organ dysfunction. This review explores the autoimmune mechanisms and inflammatory pathways underlying obesity-induced type 2 diabetes, atherosclerosis, and non-alcoholic fatty liver disease, with an emphasis on their interrelated pathophysiology and the potential for therapeutic interventions.

CXCR1/2 inhibitors are being implemented with immunotherapies in PDAC clinical trials. CXC-ligands are a family of cytokines responsible for stimulating these receptors; while typically secreted by activated immune cells, fibroblasts, and even adipocytes, they are also secreted by immune-evasive cancer cells. CXC-ligand release is known to occur in response to inflammatory stimuli. Adipose tissue is an endocrine organ and a source of inflammatory signaling peptides. Importantly, adipose-derived cytokines and chemokines are implicated as potential drivers of tumor cell immune evasion; cumulatively, these findings suggest that targeting CXC-ligands may be beneficial in the context of obesity.

RNA-sequencing of human PDAC cell lines was used to assess influences of adipose conditioned media on the cancer cell transcriptome. The adipose-induced secretome of PDAC cells was validated with ELISA for induction of CXCL5 secretion. Human tissue data from CPTAC was used to correlate IL-1β and TNF expression with both CXCL5 mRNA and protein levels. CRISPR-Cas9 was used to knockout CXCL5 from a murine PDAC KPC cell line to assess orthotopic tumor studies in syngeneic, diet-induced obese mice. Flow cytometry and immunohistochemistry were used to compare the immune profiles between tumors with or without CXCL5. Mice-bearing CXCL5 competent or deficient tumors were monitored for differential tumor size in response to anti-PD-1 immune checkpoint blockade therapy.

Human adipose tissue conditioned media stimulates CXCL5 secretion from PDAC cells via either IL-1β or TNF; neutralization of both is required to significantly block the release of CXCL5 from tumor cells. Ablation of CXCL5 from tumors promoted an enriched immune phenotype with an unanticipatedly increased number of exhausted CD8 T cells. Application of anti-PD-1 treatment to control tumors failed to alter tumor growth, yet treatment of CXCL5-deficient tumors showed response by significantly diminished tumor mass.

In summary, our findings show that both TNF and IL-1β can stimulate CXCL5 release from PDAC cells in vitro, which correlates with expression in patient data. CXCL5 depletion in vivo alone is sufficient to promote T cell infiltration into tumors, increasing efficacy and requiring checkpoint blockade inhibition to alleviate tumor burden.

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.

Overweight patients with cardiovascular disease (CVD) tend to survive longer than normal-weight patients, a phenomenon known as the "obesity paradox". The phenotypic characteristics of adipose distribution in these patients (who survive longer) often reveal a larger proportion of subcutaneous white adipose tissue (scWAT), suggesting that the presence of scWAT is negatively associated with all-cause mortality and that scWAT appears to provide protective benefits in patients facing unhealthy states. Exercise-mediated browning is a crucial aspect of the benign remodeling process of adipose tissue (AT). Reduced accumulation, reduced inflammation, and associated adipokine secretion are directly related to the reduction in CVD mortality. This paper summarized the pathogenetic factors associated with AT accumulation in patients with CVD and analyzed the possible role and pathway of exercise-mediated adipose browning in reducing the risk of CVD and CVD-related mortality. It is suggested that exercise-mediated browning may provide a new perspective on the "obesity paradox"; that is, overweight CVD patients who have more scWAT may gain greater cardiovascular health benefits through exercise.

Obesity-induced monocyte chemoattractant protein 1 (MCP-1) production leads to the infiltration of monocytes/macrophages into white adipose tissue (WAT), which contributes to systemic insulin resistance. Peroxisome proliferator-activated receptor gamma (PPARγ) agonists are known to reduce MCP-1 production in both humans and mice; however, the underlying mechanism in WAT remains unclear. Here, we propose a novel mechanism for the reduction in MCP-1 production in preadipocytes. The PPARγ agonist rosiglitazone (RSG) reduced MCP-1 production and secretion in response to lipopolysaccharide (LPS) in 3T3-L1 preadipocytes and mouse stromal vascular fraction-derived primary preadipocytes. Both RSG and SP600125 (a c-Jun N-terminal kinase (JNK) inhibitor) inhibited LPS-induced degradation of silent information regulator 2 homolog 1 (SIRT1), a negative regulator of MCP-1 production in 3T3-L1 preadipocytes. Furthermore, RSG inhibited LPS-induced activation of nuclear factor-κB. These effects of RSG were abolished in 3T3-L1 preadipocytes transfected with Pparg siRNA. These findings highlight a novel mechanism by which PPARγ activation inhibits JNK/SIRT1 signaling in preadipocytes and contributes to the reduction in MCP-1 production, suggesting that preadipocytes could be a potential therapeutic target for the treatment of insulin resistance.

Human adipose depots are functionally distinct. Yet, recent single-nucleus RNA sequencing (snRNA-seq) analyses largely uncovered overlapping or similar cell-type landscapes. We hypothesized that adipocyte subtypes, differentiation trajectories and/or intercellular communication patterns could illuminate this depot similarity-difference gap. For this, we performed snRNA-seq of human subcutaneous or visceral adipose tissues (five or ten samples, respectively). Of 27,665 adipocyte nuclei in both depots, most were 'classical', namely enriched in lipid metabolism pathways. However, we also observed 'nonclassical' adipocyte subtypes, enriched in immune-related, extracellular matrix deposition (fibrosis), vascularization or angiogenesis or ribosomal and mitochondrial processes. Pseudo-temporal analysis showed a developmental trajectory from adipose progenitor cells to classical adipocytes via nonclassical adipocytes, suggesting that the classical state stems from loss, rather than gain, of specialized functions. Last, intercellular communication routes were consistent with the different inflammatory tone of the two depots. Jointly, these findings provide a high-resolution view into the contribution of cellular composition, differentiation and intercellular communication patterns to human fat depot differences.

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.

Context Subfertility has a negative impact on the productivity of beef cow herds; thus, it is relevant to unravel the mechanisms. Aims To study follicular development, body composition, concentrations of progesterone and metabolic hormones and their gene expression in the endometrium during the oestrus cycle. Methods Fertile and subfertile Hereford cows were classified at 25 (n =84) and 60 (n =25) months old, as (1) fertile, pregnant at first insemination at 25months, that became pregnantmore than three of five times at 60months (n =5), or (2) subfertile, i.e. failed to became pregnant during three inseminations at 25months, that became pregnant at fewer than two of the five opportunities at 60months (n =6). Key results Fertile cows had greater concentrations of insuling-like growth factor 1 (IGF-1), leptin and adiponectin (P P P P P Conclusions Differences in progesterone and metabolic hormones in plasma and follicular fluid and their endometrial expression are associated with the success of pregnancy in beef cows. Implications Strategies to improve the follicle and endometrial microenvironments are needed to improve the productivity of beef herds.

Maintaining a well-developed vascular system alongside adipose tissue (AT) expansion significantly reduces the risk of metabolic complications. Although GSK3β (glycogen synthase kinase-3 beta) is known for its role in various cellular processes, its specific functions in AT and regulation of body homeostasis have not been reported.

GSK3β-floxed and GSK3α-floxed mice were crossed with adiponectin-Cre mice to generate GSK3β or GSK3α adipocyte-specific knockout mice (GSK3βADKO and GSK3αADKO). A comprehensive whole-body metabolism analysis was performed on obese GSK3βADKO mice induced by a high-fat diet. RNA sequencing was conducted on AT of both obese GSK3βADKO and GSK3αADKO mice. Various analyses, including vessel perfusion studies, lipolysis analysis, multiplex protein assays, in vitro protein phosphorylation assays, and whole-mount histology staining, were performed on AT of obese GSK3βADKO mice. Tube-formation experiments were performed using 3B-11 endothelial cells cultured in the conditional medium of matured adipocytes under hypoxic conditions. Chromatin precipitation and immunofluorescence studies were conducted using cultured adipocytes with GSK3 inhibition.

Our findings provide the first evidence that adipocyte-specific knockout of GSK3β expands AT vascularization and mitigates obesity-related metabolic disorders. GSK3β deficiency, but not GSK3α, in adipocytes activates AMPK (AMP-activated protein kinase), leading to increased phosphorylation and nuclear accumulation of HIF-2α, resulting in enhanced transcriptional regulation. Consequently, adipocytes increased VEGF (vascular endothelial growth factor) expression, which engages VEGFR2 on endothelial cells, promoting angiogenesis, expanding the vasculature, and improving vessel perfusion within obese AT. GSK3β deficiency promotes AT remodeling, shifting unhealthy adipocyte function toward a healthier state by increasing insulin-sensitizing hormone adiponectin and preserving healthy adipocyte function. These effects lead to reduced fibrosis, reactive oxygen species, and ER (endoplasmic reticulum) stress in obese AT and improve metabolic disorders associated with obesity.

Deletion of GSK3β in adipocytes activates the AMPK/HIF-2α/VEGF/VEGFR2 axis, promoting vasculature expansion within obese AT. This results in a significantly improved local microenvironment, reducing inflammation and effectively ameliorating metabolic disorders associated with obesity.

Cardiovascular diseases are the major cause of death globally. The primary risk factors are high blood lipid levels, hypertension, diabetes, and obesity. Phytosterols are naturally occurring plant bioactive substances. Short-term clinical trials have demonstrated phytosterols' cholesterol-lowering potential, but their effects on cardiovascular risk factors remain controversial, and relevant meta-analyses are limited and incomplete. We conducted a systematic and comprehensive search of PubMed, Web of Science, Embase and Cochrane Library up to December 22, 2023. A total of 109 randomized controlled trials (RCTS) of phytosterols (PS) intervention on cardiovascular risk factor outcomes were included in a preliminary screening of the retrieved literature by Endnote 20. We assessed the quality of all included randomized controlled trials using the Cochrane Collaboration's Risk of Bias tool. Cochrane data conversion tool was used for data conversion, and finally Stata was used for meta-analysis, egger test and sensitivity analysis of the included studies. The results indicated that dietary phytosterols intake could significantly decrease total cholesterol (TC) level (mean difference = -13.41; 95% confidence interval [CI]: -15.19, -11.63, p < 0.001), low density lipoprotein cholesterol (LDL-C) level (mean difference = -12.57; 95% CI: -13.87, -11.26, p < 0.001), triglycerides (TG) level (mean difference = -6.34; 95% CI: -9.43, -3.25, p < 0.001), C-reactive protein (CRP) level (mean difference = -0.05; 95% CI: -0.08, -0.01, p = 0.671), systolic blood pressure (SBP) level (mean difference = -2.10; 95% CI: -3.27, -0.9, p < 0.001), diastolic blood pressure (DBP) level (mean difference = -0.83; 95% CI: -0.58, -0.07, p = 0.032), increased high-density lipoprotein cholesterol (HDL-C) level (mean difference = 0.46; 95% CI: 0.13, 0.78, p = 0.005), but did not alter the levels of blood glucose (GLU) (mean difference = -0.44; 95% CI: -1.64, 0.76, p = 0.471), glycosylated hemoglobin, Type A1C (HbA1c) (mean difference = -0.28; 95% CI: -0.75, 0.20, p = 0.251), interleukin-6 (IL-6) (mean difference = 0.00; 95% CI: -0.02, 0.02, p = 0.980), tumor necrosis factor (TNF-α) (mean difference = 0.08; 95% CI: -0.08, 0.24, p = 0.335), oxidized low-density lipoprotein cholesterol (OXLDL-C) (standard mean difference = 0.16; 95% CI: -0.38, 0.06, p = 0.154), body mass index (BMI) (mean difference = 0.01; 95% CI: -0.07, 0.09, p = 0.886), waist circumference (WC) (mean difference = -0.10; 95% CI: -0.50, 0.30, p = 0.625) and body weight (mean difference = 0.03; 95% CI: -0.18, 0.24, p = 0.787). Our results suggest that phytosterols may be beneficial in reducing the levels of TC, LDL-C, TG, CRP, SBP, and DBP, but have no significant effect on GLU, HbA1c, TNF-α, IL-6, OXLDL-C, BMI, WC, and Weight. However, there were a small number of RCTS included in this study and their small population size may have reduced the quality of the study. And most of the included studies were short-term intervention trials. Therefore, higher quality studies need to be designed in future studies to establish more accurate conclusions.

Current research has found that adipose tissue is not only involved in energy metabolism, but also a highly active endocrine organ that secretes various adipokines, including adiponectin, leptin, resistin and apelin, which are involved in the regulation of physiology and pathology of tissues and organs throughout the body. With the yearly increasing incidence, obesity has become a risk factor for a variety of pathological changes, including inflammation and metabolic syndrome in various system (endocrine, circulatory, locomotor and central nervous system). Thus these symptoms lead to multi-organ dysfunctions, including the heart, liver, kidneys, brain and joints. An in-depth summary of the roles of adipokines in the regulation of other tissues and organs can help to provide more effective therapeutic strategies for obesity-related diseases and explore potential therapeutic targets. Therefore, this review has retrospected the endocrine function of adipose tissue under obesity and the role of dysregulated adipokine secretion in related diseases and the underlying mechanisms, in order to provide a theoretical basis for targeting adipokine-mediated systemic dysregulation.

This study aimed to investigate the relationship between PET and CT parameters and sarcopenia, adipose tissue, and tumor metabolism in esophageal carcinoma (EC) and its impact on survival in EC.

Our study included 122 EC patients who underwent PET/CT for staging. Muscle and adipose tissue characteristics were evaluated, including lumbar (L3) and cervical (C3) muscle areas, psoas major (PM) and sternocleidomastoid muscle (SCM) parameters, and PET parameters for visceral and subcutaneous adipose tissue (SAT). Sarcopenia was determined using CT images, with a threshold for muscle tissue at the L3 vertebral level, and its impact on overall survival (OS) was investigated.

Sarcopenia was detected in 48 patients. SULmax in the primary tumor (PT) was significantly higher in sarcopenic patients (SP). The frequency of distant metastasis was higher in SP and OS was significantly lower. In the locally advanced stage, sarcopenia status decreased survival. L3, PM, C3, and SCM muscle areas were highly correlated. Subcutaneous adipose tissue SUVmax was significantly increased in SP and those with distant metastasis. Univariate analysis identified PT SULmax, PT SUVmean, PT TLG, lymph node and distant metastasis, SAT SUVmax, and sarcopenia as poor prognostic factors, while multivariate analysis confirmed BMI, distant metastasis, PT SUVmean, PT TLG as independent predictors of OS.

This study demonstrated that sarcopenia, linked to reduced survival, correlates with primary tumor SULmax, distant metastasis, and subcutaneous tissue PET parameters, exerting a notable impact on survival, particularly in locally advanced stages. Attenuation-corrected CT can be used instead of diagnostic CT, and sarcopenia can be diagnosed using not only L3 but also C3 slices.

Chronic liver disease is a major cause of morbidity and mortality worldwide. Epidemiology, clinical phenotype and response to therapies for gastrointestinal and liver diseases are commonly different between women and men due to sex-specific hormonal, genetic and immune-related factors. The hepatic immune system has unique regulatory functions that promote the induction of intrahepatic tolerance, which is key for maintaining liver health and homeostasis. In liver diseases, hepatic immune alterations are increasingly recognized as a main cofactor responsible for the development and progression of chronic liver injury and fibrosis. In this Review, we discuss the basic mechanisms of sex disparity in hepatic immune regulation and how these mechanisms influence and modify the development of autoimmune liver diseases, genetic liver diseases, portal hypertension and inflammation in chronic liver disease. Alterations in gut microbiota and their crosstalk with the hepatic immune system might affect the progression of liver disease in a sex-specific manner, creating potential opportunities for novel diagnostic and therapeutic approaches to be evaluated in clinical trials. Finally, we identify and propose areas for future basic, translational and clinical research that will advance our understanding of sex disparities in hepatic immunity and liver disease.

Convergent data suggest that advanced prostate cancer and coronary heart disease (CHD) share biological vulnerabilities that may be linked to adiposity. Here we explore whether leptin, as a marker and mediator of adiposity, could link prostate cancer to CHD.

Patients with metastatic castration-resistant prostate cancer (mCRPC) enrolled in a phase II trial (NCT02703623) studying androgen deprivation therapy, abiraterone, prednisone, and apalutamide were eligible if they had plasma and a chest CT scan available. Coronary artery calcium (CAC) scores and adipokine levels were measured upon enrollment.

Of 164 patients, 87% were white. The mean age was 65.6 ± 7.5 years, 88% were either overweight or obese, 59% had hypertension, 48% had hyperlipidemia (HLD), 20% had type 2 diabetes mellitus, and 41% were former or current smokers. Coronary calcifications were found in 115 patients (70%). Among 47 patients with non-contrast chest CT scans, the median total CAC score was 133 AU (IQR 22.6-704.6). Four patients (9%) had a score of 0 AU (low risk) and 24 (51%) scores ≥100 AU, associated with high risk for major adverse cardiovascular events. Leptin levels correlated positively with the right coronary artery (RCA) CAC score [Pearson correlation coefficient (ρ) = 0.3715 (P = .0142)]. In a multivariate logistic regression analysis, older age, HLD, and higher leptin levels were independently associated with RCA calcification and a higher number of calcified coronary arteries.

Among men with mCRPC, there was a high burden of CHD, and higher leptin levels were associated with coronary atherosclerosis independently of traditional cardiac risk factors.

Emerging evidence on cirrhosis suggests a close correlation between abnormality in body composition characteristics and poor prognosis. This study aimed to evaluate the impact of dynamic changes in body composition on the prognostic outcomes in patients with cirrhosis.

This retrospective analysis included 158 patients diagnosed as cirrhosis from January 2018 to August 2023. Skeletal muscle mass, muscle quality, visceral and subcutaneous adiposity were evaluated using computed tomography (CT) imaging at the third lumbar vertebra level. Competing risk model was performed four different body composition status (i.e., normal, only sarcopenia, only myosteatosis, and combined status) for liver-related mortality. We also explored the relationship between the dynamic change in body composition and long-term prognosis by applying Gray's test.

Of the 158 cirrhotic patients (mean [SD] age, 57.1 [12.6] years), sarcopenia was present in 85 (60.1 %) patients, while 22 (13.9 %) patients had sarcopenic obesity and 68 (43.0 %) had myosteatosis. Patients solely diagnosed with sarcopenia exhibited a higher mortality rate compared to those with normal body composition (Gray's test, P=0.006), while patients solely diagnosed with myosteatosis or with a combination of sarcopenia and myosteatosis did not reach statistical significance (Gray's test, P=0.076; P=0.140). Multivariable analysis also revealed that VSR (HR=1.10 [1.01∼1.20]; P=0.028), sarcopenia (HR=2.73 [1.20∼6.22], P=0.017) and myosteatosis (HR=2.39 [1.10∼5.18], P=0.028) were significant independent predictors of liver-related deaths. Otherwise, patients exhibiting aggravating body composition during follow-up period were associated with a significantly higher mortality risk compared to those with normal or remission body composition status (HR=7.63 [1.12∼51.14]; P=0.036).

Progressive alterations in body composition status appears to be associated with liver-related mortality in individuals with liver cirrhosis. Focusing on the management of skeletal muscle, along with visceral and subcutaneous adiposity, may contribute to improving the prognosis of cirrhotic patients.

Adipose tissue accumulation around non-adipose tissues is associated with obesity and metabolic disease. One relatively unstudied depot is peripancreatic adipose tissue (PAT) that accumulates in obesity and insulin resistance and may impact beta cell function. Pancreatic lipid accumulation and PAT content are negatively related to metabolic outcomes in humans, but these studies are limited by the inability to pursue mechanisms.

We obtained PAT from human donors through the Human Pancreas Analysis Program to evaluate differences in paracrine signaling compared to subcutaneous adipose tissue (SAT), as well as effects of the PAT secretome on aortic vasodilation, human islet insulin secretion, and gene transcription using RNAseq.

PAT had greater secretion of IFN-γ and most inflammatory eicosanoids compared to SAT. Secretion of adipokines negatively related to metabolic health were also increased in PAT compared to SAT. We found no overall effects of PAT compared to SAT on human islet insulin secretion, however, insulin secretion was suppressed after PAT exposure from men compared to women. Vasodilation was significantly dampened by PAT conditioned media, an effect explained almost completely by PAT from men and not women. Islets treated with PAT showed selective changes in lipid metabolism pathways while SAT altered cellular signaling and growth. RNAseq analysis showed changes in islet gene transcription impacted by PAT compared to SAT, with the biggest changes found between PAT based on sex.

The PAT secretome is metabolically negative compared to SAT, and impacts islet insulin secretion, blood flow, and gene transcription in a sex dependent manner.

White adipose tissue (WAT) and the gut are involved in the development of neuroinflammation when an organism detects any kind of injury, thereby triggering metainflammation. In fact, the autonomous nervous system innervates both tissues, although the complex role played by the integrated sympathetic, parasympathetic, and enteric nervous system functions have not been fully elucidated. Our aims were to investigate the participation of inflamed WAT and the gut in neuroinflammation. Firstly, we conducted an analysis into how inflamed peripheral WAT plays a key role in the triggering of metainflammation. Indeed, this included the impact of the development of local insulin resistance and its metabolic consequences, a serious hypothalamic dysfunction that promotes neurodegeneration. Then, we analyzed the gut-brain axis dysfunction involved in neuroinflammation by examining cell interactions, soluble factors, the sensing of microbes, and the role of dysbiosis-related mechanisms (intestinal microbiota and mucosal barriers) affecting brain functions. Finally, we targeted the physiological crosstalk between cells of the brain-WAT-gut axis that restores normal tissue homeostasis after injury. We concluded the following: because any injury can result not only in overall insulin resistance and dysbiosis, which in turn can impact upon the brain, but that a high-risk of the development of neuroinflammation-induced neurodegenerative disorder can also be triggered. Thus, it is imperative to avoid early metainflammation by applying appropriate preventive (e.g., lifestyle and diet) or pharmacological treatments to cope with allostasis and thus promote health homeostasis.

The Systemic Immune-Inflammatory Index (SII) and Systemic Inflammatory Response Index (SIRI) are novel composite inflammatory markers. Previous studies suggest that obesity in individuals correlates with persistently low levels of chronic inflammation. This study aims to explore the association between SII and SIRI and Body Mass Index (BMI) among children and adolescents.

A cross-sectional survey was conducted using the National Health and Nutrition Examination Survey (NHANES) dataset from 2 consecutive cycles from 2017-2020. Multivariate linear regression models were employed to examine the linear relationships between BMI and SII and SIRI. Non-linear associations were explored using smooth curve fitting and threshold effect analysis.

A total of 2980 children and adolescents aged 6-19 years were included in this population-based study. In the population description of body mass index categories, we found progressively higher levels of SII and SIRI, notably peaking among obese children (SII mean ± SD: 528.83 ± 285.46; SIRI mean ± SD: 1.12 ± 0.79). Weighted multivariate linear regression confirmed a significant positive association between BMI and both inflammatory indices (P < 0.0001). Subgroup analyses revealed consistent correlations across gender divisions and highlighted a non-linear relationship between BMI and SII.

SII and SIRI are positively associated with BMI in children and adolescents, indicating their potential as markers for assessing systemic inflammation in pediatric obesity. Further large-scale prospective studies are required to substantiate these findings.

Central obesity is a well-recognized risk factor for diabetes, yet the potential role of lipids in the diabetes risk associated with central obesity remains unclear. This study aimed to explore the possible mediating role of 11 lipid parameters [high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), non-high-density lipoprotein cholesterol (Non-HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), remnant cholesterol (RC), and ratios of Non-HDL-C/HDL-C, RC/HDL-C, LDL/HDL-C, TG/HDL-C, TC/HDL-C] in the association of central obesity with diabetes risk.

We utilized data from 15,453 participants in the NAGALA longitudinal cohort to assess the association of baseline central obesity indicators [waist-height ratio (WHtR), waist circumference (WC)] and the 11 lipid parameters with diabetes risk. Mediation analysis models were constructed to explore the mediating role of lipid parameters in the association of WC/WHtR with diabetes.

Confirmatory associative analysis using multivariable Cox regression showed that, except for Non-HDL-C, TC and LD-C, the remaining eight lipid parameters were significantly associated with WC/WHtR and diabetes risk. Mediation analysis indicated that TG, RC, HDL-C, and lipid ratios such as Non-HDL-C/HDL-C ratio, RC/HDL-C ratio, TG/HDL-C ratio, TC/HDL-C ratio and LDL/HDL-C ratio are potential lipids affecting the diabetes risk related to central obesity. Among these, the RC/HDL-C ratio seemed to contribute the most in the WC/WHtR-related diabetes risk association, with a mediation percentage of about 37%. Additionally, lipid ratio parameters appeared to play a more mediating role in the association of central obesity-related diabetes risk than individual lipids.

In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.

Atherogenesis starts during childhood, making childhood and adolescence an important window of opportunity to prevent atherosclerotic cardiovascular disease later in life.

To identify early-life risk factors for preclinical atherosclerosis in adolescence.

This cohort study is part of the ongoing Wheezing Illness Study in Leidsche Rijn (WHISTLER) prospective birth cohort study, which includes 3005 healthy newborns born between December 2001 and December 2012 in the Leidsche Rijn area of Utrecht, the Netherlands. Eligible participants included those from the WHISTLER cohort who visited the clinic between March 2019 and October 2020 for adolescent follow-up. This study's analyses were performed in January 2024.

Early-life growth was assessed at birth to 6 months, 5 years, and 12 to 16 years. Abdominal ultrasonography determined abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) depth. Blood pressure (BP) percentiles and body mass index (BMI) z scores were used.

Carotid ultrasonography was performed at age 12 to 16 years to assess carotid intima-media thickness (cIMT) and the distensibility coefficient (DC), established measures of preclinical atherosclerosis. Multivariable linear regression models were used to identify early-life risk factors for cIMT and DC in adolescence.

In total, 232 adolescents (median [IQR] age, 14.9 [13.7-15.8] years; 121 female [52.2%]) were included. More postnatal weight gain (B = 12.34; 95% CI, 2.39 to 22.39), higher systolic BP at 5 years (B = 0.52; 95% CI, 0.02 to 1.01), more VAT at 5 years (B = 3.48; 95% CI, 1.55 to 5.40), and a larger change in VAT between 5 and 12 to 16 years (B = 3.13; 95% CI, 1.87 to 4.39) were associated with a higher cIMT in adolescence. A higher BMI (B = -2.70, 95% CI,-4.59 to -0.80) and VAT at 5 years (B = -0.56; 95% CI, -0.87 to -0.25), as well as a larger change in BMI between 5 and 12 to 16 years (B = -3.63; 95% CI, -5.66 to -1.60) were associated with a higher carotid stiffness in adolescence. On the contrary, a larger change in SAT between 5 and 12 to 16 years (B = 0.37; 95% CI, 0.16 to 0.58) was associated with a higher carotid DC in adolescence.

In this cohort study of 232 participants, early-life growth parameters, and particularly abdominal VAT development, were associated with a higher cIMT and carotid stiffness in adolescence. These findings suggest that assessment of adipose tissue development during childhood can aid characterization of lifetime risk trajectories and tailoring of cardiovascular prevention and risk management strategies.

Obesity poses a significant global health challenge, necessitating effective prevention and treatment strategies. Exercise and diet are recognized as pivotal interventions in combating obesity. This study reviews the literature concerning the impact of exercise-induced cytokines, dietary factors, and inflammation on adipose tissue metabolism, shedding light on potential pathways for therapeutic intervention.

A comprehensive review of relevant literature was conducted to elucidate the role of exercise-induced cytokines, including interleukin-6 (IL-6), interleukin-15 (IL-15), brain-derived neurotrophic factor (BDNF), irisin, myostatin, fibroblast growth factor 21 (FGF21), follistatin (FST), and angiopoietin-like 4 (ANGPTL4), in adipose tissue metabolism. Various databases were systematically searched using predefined search terms to identify relevant studies. Articles selected for inclusion underwent thorough analysis to extract pertinent data on the mechanisms underlying the influence of these cytokines on adipose tissue metabolism.

Exercise-induced cytokines exert profound effects on adipose tissue metabolism, influencing energy expenditure (EE), thermogenesis, fat loss, and adipogenesis. For instance, IL-6 activates AMP-activated protein kinase (AMPK), promoting fatty acid oxidation and reducing lipogenesis. IL-15 upregulates peroxisome proliferator-activated receptor delta (PPARδ), stimulating fatty acid catabolism and suppressing lipogenesis. BDNF enhances AMPK-dependent fat oxidation, while irisin induces the browning of white adipose tissue (WAT), augmenting thermogenesis. Moreover, myostatin, FGF21, FST, and ANGPTL4 each play distinct roles in modulating adipose tissue metabolism, impacting factors such as fatty acid oxidation, adipogenesis, and lipid uptake. The elucidation of these pathways offers valuable insights into the complex interplay between exercise, cytokines, and adipose tissue metabolism, thereby informing the development of targeted obesity management strategies.

Understanding the mechanisms by which exercise-induced cytokines regulate adipose tissue metabolism is critical for devising effective obesity prevention and treatment modalities. Harnessing the therapeutic potential of exercise-induced cytokines, in conjunction with dietary interventions, holds promise for mitigating the global burden of obesity. Further research is warranted to delineate the precise mechanisms underlying the interactions between exercise, cytokines, and adipose tissue metabolism.

Owing to the global obesity epidemic, understanding the regulatory mechanisms of glucose and lipid metabolism has become increasingly important. The dopaminergic system, including dopamine, dopamine receptors, dopamine transporters, and other components, is involved in numerous physiological and pathological processes. However, the mechanism of action of the dopaminergic system in glucose and lipid metabolism is poorly understood. In this review, we examine the role of the dopaminergic system in glucose and lipid metabolism.

The dopaminergic system regulates glucose and lipid metabolism through several mechanisms. It regulates various activities at the central level, including appetite control and decision-making, which contribute to regulating body weight and energy metabolism. In the pituitary gland, dopamine inhibits prolactin production and promotes insulin secretion through dopamine receptor 2. Furthermore, it can influence various physiological components in the peripheral system, such as pancreatic β cells, glucagon-like peptide-1, adipocytes, hepatocytes, and muscle, by regulating insulin and glucagon secretion, glucose uptake and use, and fatty acid metabolism.

The role of dopamine in regulating glucose and lipid metabolism has significant implications for the physiology and pathogenesis of disease. The potential therapeutic value of dopamine lies in its effects on metabolic disorders.

Adipose-derived mesenchymal stromal cells (AD-MSCs) are an essential issue in modern medicine. Extensive preclinical and clinical studies have shown that mesenchymal stromal/stem cells, including AD-MSCs, have specific properties (ability to differentiate into other cells, recruitment to the site of injury) of particular importance in the regenerative process. Ongoing research aims to elucidate factors supporting AD-MSC culture and differentiation in vitro. Angiopoietin-like proteins (ANGPTLs), known for their pleiotropic effects in lipid and glucose metabolism, may play a significant role in this context. Regeneration is a complex and dynamic process controlled by many factors. ANGPTL6 (Angiopoietin-related growth factor, AGF), among many activities modulated the biological activity of stem cells. This study examined the influence of synthesized AGF-derived peptides, designated as AGF9 and AGF27, on AD-MSCs. AGF9 and AGF27 enhanced the viability and migration of AD-MSCs and acted as a chemotactic factor for these cells. AGF9 stimulated chondrogenesis and lipid synthesis during AD-MSCs differentiation, influenced AD-MSCs cytokine secretion and modulated transcriptome for such basic cell activities as migration, transport of molecules, and apoptosis. The ability of AGF9 to modulate the biological activity of AD-MSCs warrants the consideration of this peptide a noteworthy therapeutic agent that deserves further investigation for applications in regenerative medicine.

Chronic kidney disease (CKD) causes specific hormonal disturbances, such as variations in leptin and testosterone levels and function. These disturbances can promote errors in signaling interaction and cellular information processing and can be implicated in the pathogenesis of atherosclerosis. This study investigates the factors that affect leptin in CKD patients and examines how leptin is related to markers of vascular disease. We conducted a cross-sectional study of 162 patients with CKD in pre-dialysis and dialysis stages. We recorded clinical and laboratory data, including leptin, testosterone, and subclinical atherosclerosis markers like brachial-ankle pulse wave velocity (ba PWV) in pre-dialysis CKD patients and flow-mediated vasodilation (FMD) and nitroglycerin-mediated vasodilation (NMD) in hemodialysis (HD) patients. Leptin was significantly correlated with testosterone in CKD pre-dialysis stages (p < 0.001) and also in HD (p = 0.026), with adipose tissue mass in pre-dialysis stages (p < 0.001), and also in HD (p < 0.001). In women HD patients, leptin correlated with NMD (p = 0.039; r = -0.379); in all HD patients, leptin correlated with C reactive protein (p = 0.007; r = 0.28) and parathormone (p = 0.039; r = -0.220). Our research emphasizes the connection between leptin, adipose tissue, and testosterone in all stages of CKD. Leptin was associated with NMD in HD women and correlated with inflammatory syndrome and parathyroid hormone in all HD patients.

T-Lymphocyte activation is modulated by the adipokine leptin and serum concentrations of this hormone can be reduced with short-term calorie restriction. The aim of this study was to understand whether leptin per se is important in determining levels of T-lymphocyte activation in humans, by investigating whether the reduction in leptin concentration following calorie restriction is associated with a decrease in T-Lymphocyte activation in blood and adipose tissue.

Twelve men with overweight and obesity (age 35-55 years, waist circumference 95-115 cm) reduced their calorie intake by 50% for 3 consecutive days. Blood and subcutaneous adipose tissue were obtained for isolation of immune cells and cytokine analysis. CD4+ and CD8 + T-Lymphocytes were identified and characterised according to their expression of activation markers CD25 and CD69 by flow cytometry.

Serum leptin was reduced by (mean ± SEM) 31 ± 16% (p < 0.001) following calorie restriction. The percentage of blood CD4 + CD25 + T-lymphocytes and level of CD25 expression on these lymphocytes were significantly reduced by 8 ± 10% (p = 0.016) and 8 ± 4% (p = 0.058), respectively. After calorie restriction, ex vivo leptin secretion from abdominal subcutaneous adipose tissue explants was not changed, and this corresponded with a lack of change in adipose tissue resident T-Lymphocyte activation.

Serum leptin was reduced after calorie restriction and this was temporally associated with a reduction in activation of blood CD4 + CD25 + T-Lymphocytes. In abdominal subcutaneous adipose tissue, however, leptin secretion was unaltered, and there were no observed changes in adipose resident T-Lymphocyte activation.

The growing obesity epidemic necessitates increased research on adipocyte and adipose tissue function and disease mechanisms that progress obesity. Historically, adipocytes were viewed simply as storage for excess energy. However, recent studies have demonstrated that adipocytes play a critical role in whole-body homeostasis, are involved in cell communication, experience forces in vivo, and respond to mechanical stimuli. Changes to the adipocyte mechanical microenvironment can affect function and, in some cases, contribute to disease. The aim of this review is to summarize the current literature on the mechanobiology of adipocytes. We reviewed over 100 papers on how mechanical stress is sensed by the adipocyte, the effects on cell behavior, and the use of cell culture scaffolds, particularly those with tunable stiffness, to study adipocyte behavior, adipose cell and tissue mechanical properties, and computational models. From our review, we conclude that adipocytes are responsive to mechanical stimuli, cell function and adipogenesis can be dictated by the mechanical environment, the measurement of mechanical properties is highly dependent on testing methods, and current modeling practices use many different approaches to recapitulate the complex behavior of adipocytes and adipose tissue. This review is intended to aid future studies by summarizing the current literature on adipocyte mechanobiology.

Hypertension is a highly prevalent cardiovascular disease risk factor that may be related to inflammation. Whether adverse levels of specific inflammatory cytokines relate to hypertension is unknown. The present study sought to determine whether higher levels of IL (interleukin)-1β, IL-6, TNF (tumor necrosis factor)-α, IFN (interferon)-γ, IL-17A, and CRP (C-reactive protein) are associated with a greater risk of incident hypertension.

The REGARDS study (Reasons for Geographic and Racial Difference in Stroke) is a prospective cohort study that recruited 30 239 community-dwelling Black and White adults from the contiguous United States in 2003 to 2007 (visit 1), with follow-up 9 years later in 2013 to 2016 (visit 2). We included participants without prevalent hypertension who attended follow-up 9 years later and had available laboratory measures and covariates of interest. Poisson regression estimated the risk ratio of incident hypertension by level of inflammatory biomarkers.

Among 1866 included participants (mean [SD] aged of 62 [8] years, 25% Black participants, 55% women), 36% developed hypertension. In fully adjusted models comparing the third to first tertile of each biomarker, there was a greater risk of incident hypertension for higher IL-1β among White (1.24 [95% CI, 1.01-1.53]) but not Black participants (1.01 [95% CI, 0.83-1.23]) and higher TNF-α (1.20 [95% CI, 1.02-1.41]) and IFN-γ (1.22 [95% CI, 1.04-1.42]) among all participants. There was no increased risk with IL-6, IL-17A, or CRP.

Higher levels of IL-1β, TNF-α, and IFN-γ, representing distinct inflammatory pathways, are elevated in advance of hypertension development. Whether modifying these cytokines will reduce incident hypertension is unknown.

Background & objectives Acute pancreatitis (AP) is a well known gastrointestinal cause of hospital admissions. There is a proven association between the severity of AP and obesity due to increased rates of local complications, multiple organ failure and mortality. Increased visceral adiposity is reported to be a better predictor of severe pancreatitis than body mass index (BMI) in many studies. This study aimed to assess the relationship between visceral adiposity and the severity of AP by measuring the visceral adipose tissue (VAT) area. Methods This single-centre, prospective study was conducted on consecutive individuals admitted with AP. The severity of AP was correlated with the VAT area, as estimated between 48 and 72 h of admission. Results Seventy-four individuals with AP were recruited during the study period. The overall study cohort's mean±SD for VAT area was 128.06±34.22 cm2. The VAT area was significantly larger in individuals with severe pancreatitis (141.01±33.75cm2) than in those with mild or moderate pancreatitis (115.11±29.85 cm2). The sensitivity, specificity and area under the receiver operating characteristics (AUROC) of VAT were 78.4 per cent, 54.1 per cent and 0.722 in predicting severe AP, respectively. Interpretation & conclusions There is a significant association between severe AP and VAT. With the worldwide increase in obesity incidences, incorporating VAT into one of the prognostic indices for AP needs to be further explored.

Deciphering lipid metabolism in white adipose tissue (WAT) depots during weight gain is important to understand the heterogeneity of WAT and its roles in obesity. Here, we examined the expression of key enzymes of lipid metabolism and changes in the morphology of representative visceral (epididymal) and subcutaneous (inguinal) WAT (eWAT and iWAT, respectively)-in adult male rats acclimated to cold (4 ± 1 °C) for 45 days and reacclimated to room temperature (RT, 22 ± 1 °C) for 1, 3, 7, 12, 21, or 45 days. The relative mass of both depots decreased to a similar extent after cold acclimation. However, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), and medium-chain acyl-CoA dehydrogenase (ACADM) protein level increased only in eWAT, whereas adipose triglyceride lipase (ATGL) expression increased only in iWAT. During reacclimation, the relative mass of eWAT reached control values on day 12 and that of iWAT on day 45 of reacclimation. The faster recovery of eWAT mass is associated with higher expression of FAS, acetyl-CoA carboxylase (ACC), G6PDH, and ACADM during reacclimation and a delayed increase in ATGL. The absence of an increase in proliferating cell nuclear antigen suggests that the observed depot-specific mass increase is predominantly due to metabolic adjustments. In summary, this study shows a differential rate of visceral and subcutaneous adipose tissue weight regain during post-cold reacclimation of rats at RT. Faster recovery of the visceral WAT as compared to subcutaneous WAT during reacclimation at RT could be attributed to observed differences in the expression patterns of lipid metabolic enzymes.

This manuscript summarizes novel clinical and interventional approaches in the management of chronic, nociceptive, and neuropathic pain.

Pain can be defined as a feeling of physical or emotional distress caused by an external stimulus. Pain can be grouped into distinct types according to characteristics including neuropathic pain, which is a pain caused by disease or lesion in the sensory nervous system; nociceptive pain, which is pain that can be sharp, aching, or throbbing and is caused by injury to bodily tissues; and chronic pain, which is long lasting or persisting beyond 6 months. With improved understanding of different signaling systems for pain in recent years, there has been an upscale of methods of analgesia to counteract these pathological processes. Novel treatment methods such as use of cannabinoids, stem cells, gene therapy, nanoparticles, monoclonal antibodies, and platelet-rich plasma have played a significant role in improved strategies for therapeutic interventions. Although many management options appear to be promising, extensive additional clinical research is warranted to determine best practice strategies in the future for clinicians.

Obesity is a major health problem that affects millions of individuals, and it is associated with metabolic diseases including insulin resistance (IR), type 2 diabetes (T2D), and cardiovascular diseases (CVDs). However, Body fat distribution (BFD) rather than crude obesity is now considered as a more accurate factor associated with these diseases. The factors affecting BFD vary, from genetic background, epigenetic factors, ethnicity, aging, hormonal changes, to lifestyle and medication consumptions. The main goal of controlling BFD comes from the fact that fat accumulation in different depots has a different effect on the overall health and metabolic health of individuals. It is well established that fat storage in the abdominal visceral depot is associated with metabolic disorder occurrence, while gluteal-femoral subcutaneous fat depot seems to be protective against these diseases. In this paper, we will summarize the factors affecting fat distribution. Then, we will present evidence connecting gluteal-femoral fat depot with protection against metabolic disorders including IR, T2D, and CVDs. Finally, we will list the suggested mechanisms that lead to this protective effect. The abstract is visualized in Graphical Abstract.

A better understanding of adipose tissue (AT) dysfunction, which includes morphological and functional changes such as adipocyte hypertrophy as well as impaired adipogenesis, lipid storage/mobilization, endocrine and inflammatory responses, is needed in the context of obesity. One dimension of AT dysfunction, secretory adiposopathy, often assessed as a low plasma adiponectin (A)/leptin (L) ratio, is commonly observed in obesity. The aim of this study was to examine markers of AT development and metabolism in 67 women of varying age and adiposity (age: 40-62 years; body mass index, BMI: 17-41 kg/m2) according to levels of adiponectinemia, leptinemia or the plasma A/L ratio.

Body composition, regional AT distribution and circulating adipokines were determined. Lipolysis was measured from glycerol release in subcutaneous abdominal (SCABD) and omental (OME) adipocytes under basal, isoproterenol-, forskolin (FSK)- and dibutyryl-cyclic AMP (DcAMP)-stimulated conditions. Adipogenesis (C/EBP-α/β/δ, PPAR-γ2 and SREBP-1c) and lipid metabolism (β2-ARs, HSL, FABP4, LPL and GLUT4) gene expression (RT-qPCR) was assessed in both fat depots. Participants in the upper versus lower tertile of adiponectin, leptin or the A/L ratio were compared.

Basal lipolysis was similar between groups. Women with a low plasma A/L ratio were characterized by higher adiposity and larger SCABD and OME adipocytes (p<0.01) compared to those with a high ratio. In OME adipocytes, women in the low adiponectinemia tertile showed higher isoproterenol-stimulated lipolysis (0.01

CONCLUSIONS

Secretory adiposopathy assessed as the plasma A/L ratio, more so than adiponectin or leptin levels alone, discriminates low and elevated lipolysis in OME and SCABD adipocytes despite similar AT expression of selected genes involved in lipid metabolism.

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