bims-mimead 2026-08-02 papers

Adipocyte. 2026 Dec;15(1): 2708374

Depot-specific differences in visceral and subcutaneous adipose tissue from patients with obesity.

Mathis Neuhaus, Claes Fryklund, Min Cai, Johan Fernø, Gunnar Mellgren, Carolina E Hagberg, Karin G Stenkula.

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 COL3A1 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 COL3A1 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.

Keywords: Adipose tissue biology; adipose depot differences; cell size; collagen; extracellular matrix; glucose transport; lipolysis

DOI: https://doi.org/10.1080/21623945.2026.2708374

Trends Endocrinol Metab. 2026 Jul 31. pii: S1043-2760(26)00177-3. [Epub ahead of print]

Is glutamate an adipose redox signal that regulates lipolysis?

Martina Beretta, Elizabeth J New, Kelsey H Fisher-Wellman, James R Krycer.

Uncontrolled adipose lipolysis is a defining feature of insulin resistance and metabolic disease. Although insulin potently suppresses lipolysis, the mechanisms that override antilipolytic control in insulin resistance remain poorly defined. Building on recent advances in metabolic tracing, redox biology, and adipose-neuronal crosstalk, we propose that adipocyte metabolism actively regulates lipolysis. We outline a model whereby redox imbalance within adipocytes promotes the diversion of glucose-derived carbon towards glutamate synthesis. This, in turn, may activate sympathetic drive within white adipose tissue, derepressing lipolysis even under fed conditions. This could reposition 'selective insulin resistance' as a consequence of metabolic rewiring rather than solely due to defective insulin signalling. This suggests that future studies should explore adipose redox balance and neurometabolic signalling as avenues for treating metabolic disease.

Keywords: adipose tissue; glutamate; insulin resistance; lipolysis; sympathetic neurons

DOI: https://doi.org/10.1016/j.tem.2026.07.006

Nat Commun. 2026 Jul 28. pii: 7110. [Epub ahead of print]17(1):

Fractionated proteomics identifies a protein network mitigating resistance exercise-induced damage in human skeletal muscle.

Maithreyan Kuppusamy, Daniel Jacko, Yamini Gupta, Sandro Sieger, Kirill Schaaf, Martin Matijass, Käthe Bersiner, Jonas Zacher, Sara Bonini, Miguel Cosenza-Contreras, Peter van der Ven, Wilhelm Bloch, Dieter O Fürst, Dominic Winter, Jörg Höhfeld, Pitter F Huesgen, Sebastian Gehlert.

Resistance exercise (RE) improves strength and muscle mass, with multiple benefits for human health. However, intense RE also induces acute myofibrillar damage. The molecular mechanisms that preserve, mark, degrade, and restore damaged proteins to keep skeletal muscle working under RE are incompletely understood. Based on repeated sampling of human skeletal muscle, we show here that acute, repeated and interrupted RE induce dynamic changes of the protein landscape associated with the sarcomeric cytoskeleton. These changes correlate with changes in phosphorylation indicative of adaptation and deadaptation signaling footprints. Regulation mainly affects the protein network linked to the muscle maintenance protein BAG3, which includes mechanosensory proteins, small heat shock proteins, and a lipid droplet associated protein. All network components exhibit altered phosphorylation and increased cytoskeletal association after damaging RE. Moreover, network components cooperate to recognize strained skeletal muscle structures and mediate their degradation through chaperone-assisted selective autophagy (CASA). Our study thus identifies key regulators of skeletal muscle homeostasis in humans.

DOI: https://doi.org/10.1038/s41467-026-75501-y

J Appl Physiol (1985). 2026 Jul 28.

Sex Hormones and Menopause Hormone Therapy Predict Muscle Strength Across the Lifespan.

Rachel N Logue Cook, Adina F Turcu, Carrie A Karvonen-Gutierrez, Sandra K Hunter.

Aging is associated with declines in muscle strength, yet after menopause the relative rate of decline is greater in females than males. Whether sex hormones are predictive of strength across the lifespan and with aging is largely unknown. This study assessed the impact of sex hormone concentrations and menopause hormone therapy (MHT) on muscle strength in aging. Hand grip strength, sex hormone concentrations (total testosterone, bioavailable testosterone (FAI), estradiol, bioavailable estradiol (FEI)), and history of female MHT use were extracted or calculated from the National Health and Nutrition Examination Survey (NHANES) for 4,330 participants (2,194 females). Males were 36-40% stronger than females throughout adulthood. One-year averages of total testosterone (r=0.48, p<0.01), FAI (r=0.86, p<0.001), and FEI (r=0.71, p<0.001) were associated with strength in males. All hormones were correlated with strength in females, with estradiol (r=0.81, p<0.001) and FEI correlations (r=0.82, p<0.001) the strongest. Multiple linear regressions demonstrated that the FAI was a predictor of strength, while total testosterone was not, in both males and females and that estradiol and FEI were indicative of female strength in later adulthood. Hand grip strength in older females with a history of MHT use was 1.9kg greater than those with no MHT history (p<0.01) and this advantage widened with age (2.4% at 60 yrs to 14.3% at ≥80 yrs). This study strongly suggests (1) age-related declines in endogenous sex hormones, particularly bioavailable hormones, contribute to strength reductions with aging; and (2) MHT may have the potential to offset meaningful strength reductions with advanced aging.

Keywords: aging; estradiol; grip strength; sex difference; testosterone

DOI: https://doi.org/10.1152/japplphysiol.00366.2026