Adipocyte最新文献

{"title":"An acute temperature rise to 40°C inhibits free fatty acid uptake into white adipocytes.","authors":"Federica Foti, Raoul S Schaepper, Daniel Konrad, Stephan Wueest","doi":"10.1080/21623945.2026.2626121","DOIUrl":"10.1080/21623945.2026.2626121","url":null,"abstract":"<p><p>Fever reflects a physiological rise in body temperature accompanied by elevated production of adrenaline. The increased body temperature in fever is caused by shivering thermogenesis in skeletal muscle and non-shivering thermogenesis in brown adipose tissue (BAT), the latter being mediated by uncoupled oxidation of free fatty acids (FFAs). We hypothesized that an acute temperature rise to 40°C increases adrenalin-induced lipolysis in white adipocytes, thereby potentially providing FFAs as an energy substrate to sustain fever-induced thermogenesis in skeletal muscle and BAT. In 3T3-L1 and primary murine white adipocytes, isoproterenol-induced extracellular FFA accumulation was significantly increased at 40°C compared to 37°C. In contrast, isoproterenol-induced increase in extracellular glycerol concentrations and the protein levels of phosphorylated hormone sensitive lipase were comparable at both temperatures, suggesting a similar degree of lipolysis. Moreover, incubation at 40°C did neither increase isoproterenol-induced oxygen consumption nor intracellular FFA concentrations, indicating that the elevated extracellular FFA accumulation was not due to reduced intracellular consumption. Conversely, isoproterenol blunted FFA uptake into adipocytes to a significantly higher extent at 40°C compared to 37°C. Hence, an acute temperature rise to 40°C reduces FFA uptake into white adipocytes, thereby increasing extracellular FFA availability.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2626121"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics integration reveals convergent extracellular matrix remodelling and lipid metabolic reprogramming as central axes of adipocyte differentiation from mouse embryonic stem cells.","authors":"M Al-Sayegh, M Khalili, M Alzaabi, M Sultana, L Ali, M Ali, M El-Hadidi","doi":"10.1080/21623945.2026.2680625","DOIUrl":"10.1080/21623945.2026.2680625","url":null,"abstract":"<p><p>Adipogenesis from mouse embryonic stem cells (mESCs) offers a tractable model for dissecting early adipocyte commitment, yet the mechanisms coordinating this transition across multiple biological layers remain incompletely understood. Here we present the first simultaneous five-layer multi-omics characterization of mESC-derived adipocyte differentiation, integrating transcriptomics, proteomics, secretomics, lipidomics, and metabolomics from matched adipogenic (Pos) and non-differentiating (Neg) cell populations at day 30. Applying Multi-Omics Factor Analysis (MOFA+), we identified a dominant shared latent axis that perfectly segregated Pos from Neg cells across all five views. Layer-specific functional enrichment converged on two principal biological axes: ECM remodeling - encompassing collagens, laminins, thrombospondins, and lysyl oxidases - and lipid metabolic reprogramming, with phospholipid and glycerolipid metabolic processes dominating the lipidomics/metabolomics layer. Ensemble Machine Learning Feature Ranking (EMFR) identified a secreted factor (Scpep1; importance score 0.90) as the top-ranked discriminatory feature. Network analysis revealed indirect ECM-lipid connectivity mediated by four bridging nodes (Plod1, Thbs2, Plg, Pmp22) through a hub subnetwork of phospholipid-metabolizing enzymes. Targeted qPCR validation of six candidate regulators (Itga5, Igfbp6, Pik3cg, Lpl, Acer3, Sirt1) confirmed RNA-seq concordance. These findings establish convergent ECM remodeling and lipid metabolic reprogramming as central axes of adipocyte identity acquisition from mESCs.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2680625"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13232875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148147871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When LXA4 meets white fat: browning via the miR-133a-3p/SIRT1 pathway in mouse models.","authors":"Dan Yu, Yuan Ruan, Yisu Wang, Xiaopei Chen, Dan Wang, Tianfeng Wu","doi":"10.1080/21623945.2026.2682679","DOIUrl":"10.1080/21623945.2026.2682679","url":null,"abstract":"<p><p>Given the established positive role of Lipoxin A4 (LXA4) in adipose browning at the cellular level, this study investigated its possible effect on white fat browning and the underlying molecular mechanisms. The obese insulin resistance mouse model was established. The body weight, subcutaneous and visceral fat, and food intake of the mice were observed. Haematoxylin-eosin staining was used to determine the effects of LXA4 on the morphology of inguinal white adipose tissue and brown adipose tissue, and to analyse the changes in fat mass and serum insulin levels, lipid metabolism and other indexes. The cellular experiments included the induction of browning in 3T3-L1 precursor adipocytes, the screening of miRNAs related to adipose browning and their downstream target genes using TargetScan, qRT-PCR, RNA immunoprecipitation and dual luciferase reporter assay. LXA4 attenuated weight gain, inhibited fat accumulation, and improved hyperlipidaemia and insulin resistance in high-fat diet-treated mice. LXA4 also promoted browning of 3T3-L1 precursor adipocytes. Activation of miR-133a-3p partially abrogated LXA4-induced promotion of white adipose browning. The effects of LXA4 and miR-133a-3p could be reversed by SIRT1. Collectively, LXA4 alleviates obesity-related metabolic disorders by promoting inguinal white adipose browning and improving insulin resistance possibly through the miR-133a-3p/SIRT1 pathway.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2682679"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148306586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of the safety and efficacy of sodium pentaborate pentahydrate in individuals with overweight and obesity: a randomized, double-blind, placebo-controlled, phase 1/2 dose-finding trial.","authors":"Fikrettin Şahin, Nahid Karamzad, Reza Aletaha, Fateme Tahmasbi, Fatemeh Amiri, Mark J M Sullman, Jessica A Grieger, Saeid Safiri","doi":"10.1080/21623945.2026.2716431","DOIUrl":"10.1080/21623945.2026.2716431","url":null,"abstract":"<p><p>The present study aimed to examine the short-term safety and tolerability of sodium pentaborate pentahydrate (NaB) and to explore preliminary efficacy and dose selection as secondary objectives in individuals with overweight or obesity. In this randomized, double-blind, placebo-controlled, phase 1/2 trial, conducted from July 2024 to January 2025, 177 adults with overweight or obesity were randomized, of whom 116 completed the 12-week trial. Participants received placebo or NaB at doses of 200, 400, 600, 800, or 1,000 mg for 12 weeks, alongside a standardized diet and exercise programme. The primary safety objective was to investigate short-term safety and tolerability through adverse events, hypoglycaemic episodes, gastrointestinal adverse events, and changes in haematological and biochemical parameters. The primary exploratory efficacy outcome was percentage change in body weight from baseline to week 12. Secondary and exploratory efficacy outcomes included body weight, body mass index (BMI), waist and hip circumferences, waist-to-hip ratio, glycaemic markers, lipid parameters, and blood pressure. Baseline characteristics were broadly similar across groups (all p ≥ 0.05), and no major short-term safety signal was observed. Mean body weight decreased in the 400 mg (-2.6 kg), 600 mg (-1.2 kg), and 1,000 mg groups (-3.1 kg). Compared with placebo, the 1,000 mg dose resulted in the largest reductions in body weight (mean difference, -2.30 kg; p = 0.01) and BMI (mean difference, -0.85 kg/m2; p = 0.02). The 1,000 mg dose showed preliminary efficacy for reducing body weight and BMI over 12 weeks compared with placebo, with no major short-term safety signal and no clinically meaningful changes in renal, hepatic, or haematological markers. All reported adverse events were mild. These short-term findings are exploratory and require confirmation in future phase 3 trials with extended follow-up to investigate long-term safety and efficacy.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2716431"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological inhibition of CLPP stabilizes LETMD1 to boost thermogenesis and alleviate obesity.","authors":"Huiwen Yuan, Yuqing Deng, Jingang Wang, Bing Luan, Zhen-Ning Zhang","doi":"10.1080/21623945.2026.2737917","DOIUrl":"10.1080/21623945.2026.2737917","url":null,"abstract":"<p><p>Obesity poses a severe global health burden, and activating adipose thermogenesis offers a promising therapeutic avenue. However, the contribution of mitochondrial proteostasis to thermogenic regulation remains elusive. Here, we identify mitochondrial protease CLPP as a negative regulator of adipose thermogenesis. Pharmacological suppression of CLPP activity enhances thermogenic programmes in adipocytes. Mechanistically, CLPP interacts with LETMD1 and promotes its degradation at the post-translational level, while LETMD1 stabilization is required for the thermogenic effects induced by CLPP suppression. <i>In vivo</i>, pharmacological suppression of CLPP activity using hinokiflavone significantly enhances energy expenditure, attenuates weight gain, and improves insulin sensitivity in obese mice. Collectively, our study identifies a CLPP-LETMD1 regulatory axis that regulates adipose thermogenesis and highlights CLPP suppression as a potential therapeutic strategy for obesity intervention.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2737917"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pro-obesity role of G3BP1 through altering adipogenic differentiation in mice via the PI3K/AKT pathway.","authors":"Haiyan Wang, Litong Sun, Haidan Mao, Yan Mei, Jinping Ni, Liren Wang","doi":"10.1080/21623945.2026.2743441","DOIUrl":"10.1080/21623945.2026.2743441","url":null,"abstract":"<p><p>As a growing but non-infectious epidemic, obesity is a common cause of several comorbidities. GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) is a central regulator of stress‑granule assembly that has significant implications in metabolic disorders. This article aims to explore the functional mechanism of G3BP1 in obesity, both in vitro and in vivo. Functional assays were used to detect cellular phenotypes. Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and western blotting were also used to test metastasis-, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling- and Wnt/β-catenin signalling-related genes. Oil‑red‑O staining and haematoxylin and eosin (H&E) staining were used to estimate lipid deposition. RT-qPCR, western blotting, and immunofluorescence staining were used to determine adipocyte differentiation and lipid metabolism. The TOPFlash/FOPFlash reporter assay was used to identify β-catenin activity. In a murine model fed a high-fat diet (HFD, 60% fat), body weight was measured prior to the detection of adipokine levels by enzyme‑linked immunosorbent assay (ELISA), triacylglycerol (TG) concentration using an assay kit, and adipogenic marker genes by western blotting. G3BP1 knockdown inhibited proliferation, migration, invasion, and adipogenesis, and induced cell cycle arrest in 3T3-L1 preadipocytes, and decreased body weight and adipogenesis and fat accumulation in obese mice. G3BP1 activated Wnt/β-catenin and PI3K/AKT pathways. LY294002 (PI3K inhibitor) and SC3036 (PI3K activator) reversed the in vitro effects of G3BP1 or silenced G3BP1 on preadipocyte invasion. G3BP1 may promote preadipocyte proliferation, migration, invasion, and adipogenesis to promote the progression of obesity, which might be relevant to the PI3K/AKT pathway.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2743441"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13671470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"cAMP-PKA/EPAC signaling pathways: crucial regulators of lipid homeostasis.","authors":"Caixia Chen, Hui Gao, Qi Tian, Junwei Cao","doi":"10.1080/21623945.2025.2603605","DOIUrl":"10.1080/21623945.2025.2603605","url":null,"abstract":"<p><p>Adipose omeostasishomoeostasis is maintained through the precise coordination of lipogenesis, lipolysis, and adipocyte differentiation, with microenvironmental components dynamically regulating lipid metabolism. Even though the classical cAMP-PKA pathway has been well-characterized for its function in lipid metabolism by phosphorylating transcription factors and lipolytic enzymes, little is known about how it collaborates with elements of the adipose tissue microenvironment, such as immune cells and the vascular endothelium, especially in pathological situations like obesity. EPAC, a newly discovered cAMP effector, has shown new signalingsignallingsignalling signalling pathways in the immune and cardiovascular systems by activating small G proteins. However, there are important understanding gaps regarding its roles in adipose metabolism, namely adipocyte development, microenvironmental interaction, and the pathophysiology of metabolic diseases. By bringing together disparate studies on PKA and EPAC, this review provides the first comprehensive synthesis of the cAMP-PKA/EPAC dual signaling signalling signallingcins signalling network, filling in knowledge gaps. The reciprocal regulation between this signaling signalling signalling signalling network and the adipose microenvironment establishes a novel 'signaling-microenvironment-systemic metabolism' framework for understanding metabolic disorders, including obesity, diabetes, and hepatic steatosis. Pharmacological modulation of the PKA/EPAC signalingsignalling signalling signalling pathways may therefore represent a viable therapeutic approach for restoring adipose tissue homeostasis homoeostasis.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2603605"},"PeriodicalIF":3.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12785204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of adiponectin in gestational diabetes mellitus: advances in mechanistic insights and early predictive potential.","authors":"Yuting Chen, Feiming He, Lili Zhang, Zhongying Zhang","doi":"10.1080/21623945.2026.2705620","DOIUrl":"10.1080/21623945.2026.2705620","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy and is associated with an increased risk of short-term adverse maternal and neonatal outcomes, as well as long-term metabolic disorders in both mothers and offspring. Exacerbated insulin resistance and inadequate compensatory pancreatic β-cell function constitute the core pathophysiological basis of GDM. Adiponectin is an insulin-sensitizing adipokine that plays important roles in glucose and lipid metabolism, inflammatory regulation, and energy homoeostasis. Changes in maternal circulating adiponectin levels during pregnancy are closely associated with reduced insulin sensitivity and increased risk of GDM. This review systematically summarizes the roles of adiponectin and its distinct isoforms, particularly high-molecular-weight adiponectin, in GDM development, metabolic regulation, and early risk assessment. We also integrate potential interactions between adiponectin and placental hormones, nutrient transport, local inflammation, oxidative stress, and exosome-related mechanisms. In addition, this review discusses the key issues related to adiponectin measurement standardization, gestational timing of blood sampling, population heterogeneity, combined prediction models, and their integration into the oral glucose tolerance test (OGTT). The current findings support adiponectin as a candidate biomarker for early GDM risk stratification and combined prediction models; however, adiponectin cannot replace OGTT as a diagnostic criterion.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2705620"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13418717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148597576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β2-adrenergic receptor stimulation drives differentiation of human adipose-derived mesenchymal stem cells into beige adipocytes.","authors":"Kazuki Maekawa, Fumika Yokoyama, Rie Tsutsumi, Akiko Tateishi, Akifumi Maeda, Norifumi Tateishi","doi":"10.1080/21623945.2026.2682671","DOIUrl":"10.1080/21623945.2026.2682671","url":null,"abstract":"<p><p>β-Adrenergic receptors (β-ARs) drive the induction of beige adipocytes in rodents and humans, yet the dominant human subtype, β2-AR or β3-AR, remains debated. This study aimed to confirm whether human adipose-derived mesenchymal stem cell (hADSCs)-derived adipocytes can serve as a beiging-competent model under human-relevant browning stimuli and to compare the involvement of β2-AR and β3-AR in hADSCs-derived beige adipocyte differentiation. hADSCs were differentiated into adipocytes using an adipogenic cocktail in the presence or absence of human-relevant browning stimuli or β2-AR/β3-AR-selective agonists with or without β2-AR/β3-AR-selective antagonists. Non-selective β-AR activation induces beige adipogenesis along with mRNA and/or protein expression of beiging markers, including uncoupling protein 1 (UCP1), appearance of multilocular adipocytes, and enhanced mitochondrial respiratory readouts. Moreover, norepinephrine, forskolin, and trigonelline increased mRNA and/or protein expression of UCP1. Pharmacological dissection with subtype-selective agonists and antagonists revealed that activation of β2-AR, but not β3-AR, is necessary and sufficient for inducing UCP1. The β2-AR blockade abolished UCP1 upregulation, whereas the β3-AR blockade had minimal effects. β2-selective stimulation recapitulated the beiging response. This study establishes hADSCs-derived adipocytes as a practicable, human-relevant platform for screening pharmacological agents and food-derived compounds and identifies β2-AR as a translationally actionable target for inducing beige adipocytes in humans.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2682671"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depot-specific differences in visceral and subcutaneous adipose tissue from patients with obesity.","authors":"Mathis Neuhaus, Claes Fryklund, Min Cai, Johan Fernø, Gunnar Mellgren, Carolina E Hagberg, Karin G Stenkula","doi":"10.1080/21623945.2026.2708374","DOIUrl":"10.1080/21623945.2026.2708374","url":null,"abstract":"<p><p>Factors limiting fat cell expandability remain scarcely explored, and comprehensive functional comparisons of adipose depots in humans are limited. In the present study, we collected visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) paired-samples from 22 patients with obesity undergoing elective Roux-en-Y gastric bypass surgery. Whole tissue samples were used to determine adipocyte cell size using a coulter counter and gene expression levels using bulk mRNA sequencing. Isolated adipocytes from the same tissue samples were used to functionally assess glucose uptake using glucose tracer assay, and lipolysis by measuring glycerol release. Western blotting was used to determine Caveolin 1 levels in adipocytes. The relationship between <i>COL3A1</i> expression and systemic health outcomes was assessed using data from the Adipose Tissue Knowledge Portal. We found that SAT adipocytes were larger in size, displayed higher basal lipolysis and higher lipolysis-related gene expression than VAT adipocytes. Isoprenaline-induced lipolytic responsiveness, as well as basal and insulin-stimulated glucose uptake were higher in VAT than in SAT adipocytes. SAT displayed higher levels of extracellular matrix components associated with cellular flexibility and higher cellular Caveolin 1 levels than VAT. Further, we identified subcutaneous adipose tissue <i>COL3A1</i> as a potential contributor to insulin resistance in obesity, positively associated with BMI, HOMA-IR and adipocyte size. In summary, our findings underscore distinct metabolic properties of subcutaneous and visceral adipocytes in obesity, with SAT adipose tissue exhibiting characteristics that possibly promote greater cellular expandability.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"15 1","pages":"2708374"},"PeriodicalIF":3.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13418479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}