bims-mimead Biomed News
on Adipose tissue and metabolic disease
Issue of 2026–02–01
six papers selected by
Rachel M. Handy, University of Guelph
  1. Blood-flow restriction resistance training improves skeletal muscle mitochondrial capacity and cardiovascular risk factors in type 2 diabetes.
  2. EBF2 variant identified in a patient with atypical partial lipodystrophy causes adipose fibrosis and dysfunction.
  3. Coenzyme Q10 supplementation raises plasma levels without improving mitochondrial function in older adults.
  4. Cardiometabolic Gains Unrelated to Weight Loss-Adjusted Body Fat or Distribution Changes in Adults With and Without Diabetes.
  5. Differential effects of the anti-obesity drug tirzepatide on adipose tissues: Brown fat as a key target.
  6. Kiss1-FASN participates fatty acid synthesis via high-fat diet in PgVAT of female mice.
  1. Cell Metab. 2026 Jan 28. pii: S1550-4131(25)00547-9. [Epub ahead of print]
    Blood-flow restriction resistance training improves skeletal muscle mitochondrial capacity and cardiovascular risk factors in type 2 diabetes.
    Nina Trinks, Sofiya Gancheva, Jennifer Pützer, Martin Schön, Maximilian Huttasch, Kalliopi Pafili, Lucia Mastrototaro, Bedair Dewidar, Yuliya Kupriyanova, Christian Herder, Klaus Strassburger, Oana P Zaharia, Philip M M Ruppert, Sander Kersten, Joris Hoeks, Sandra Trenkamp, Vera Schrauwen-Hinderling, Patrick Schrauwen, Michael Roden, Dominik H Pesta.
      Impaired muscle strength and mitochondrial functionality are hallmarks of type 2 diabetes (T2D). Conventional combined resistance/endurance exercise training has limited efficacy to simultaneously improve muscle function and metabolism. We examined whether low-load blood-flow restriction training (BFRT) increases both muscle strength and mitochondrial oxidative capacity in T2D. Over 12 weeks, BFRT and conventional resistance training (CREST) similarly improved muscle strength despite lower workload in BFRT. Uniquely, BFRT enhanced muscle and adipose tissue oxidative capacity and increased muscle mitochondrial content. Transcriptomic profiling revealed more pronounced changes, particularly in angiogenesis-linked pathways, upon BFRT. BFRT also preferentially led to reductions in visceral adipose tissue volume and waist circumference, whereas CREST more effectively decreased subcutaneous adipose tissue volume. Both interventions lowered resting heart rate and diastolic blood pressure. These findings position BFRT as a promising low-load exercising strategy to simultaneously improve mitochondrial oxidative capacity, muscle strength, and body composition in individuals with T2D.
    Keywords:  adipose tissue distribution; angiogenesis; blood-flow restriction training; cardiovascular function; mitochondrial respiration; resistance training; skeletal muscle function; type 2 diabetes
    DOI:  https://doi.org/10.1016/j.cmet.2025.12.016
  2. J Clin Invest. 2026 Jan 29. pii: e192737. [Epub ahead of print]
    EBF2 variant identified in a patient with atypical partial lipodystrophy causes adipose fibrosis and dysfunction.
    Maria C Foss-Freitas, Donatella Gilio, Lynn Pais, Eric D Buras, Romil Kaul Verma, Melanie O'Leary, Heidi L Rehm, Carmen Glaze, Kathryn Russell, Andre Monteiro da Rocha, Adam Neidert, Patrick Seale, Miriam S Udler, Elif A Oral, Tae-Hwa Chun.
      Lipodystrophy syndromes are marked by loss of adipose tissue (AT), which leads to insulin resistance and metabolic syndrome development. We identified a heterozygous nonsense variant in early B cell factor 2 (EBF2) (Chr8:26033143C>A, NM_022659.4: c.493G>T, p.E165X) in a patient with atypical partial lipodystrophy (PLD). The EBF family is crucial for the differentiation and function of various mesenchymal tissues. Through in vitro and in vivo disease models, we discovered that this variant limits adipocyte differentiation and hampers adipose tissue remodeling. Heterozygous knock-in (Ebf2E165X/+) mice showed restricted adipogenesis and defective extracellular matrix (ECM) remodeling during post-weaning and high-fat diet (HFD)-induced adipose tissue expansion. HFD caused abnormal adipocyte hypertrophy, decreased expression of adiponectin and leptin, and glucose intolerance in Ebf2E165X/+ mice. Furthermore, key mitochondrial genes involved in fatty acid metabolism and oxidation were specifically downregulated in the Ebf2E165X/+ adipose tissue. Our results suggest that EBF2 dysfunction driven by this nonsense variant drives disease pathology, establishing a connection between EBF2 disruption and an atypical form of lipodystrophy.
    Keywords:  Adipose tissue; Genetic variation; Genetics; Metabolism; Transcription
    DOI:  https://doi.org/10.1172/JCI192737
  3. Geroscience. 2026 Jan 28.
    Coenzyme Q10 supplementation raises plasma levels without improving mitochondrial function in older adults.
    Malte Schmücker, Cathrine Tranberg, Jacob Borch, Mette Killerup Kaae, Michelle Damgaard, Mathias Flensted-Jensen, Ida Blom, Marco Morosetti, Sara Barbarossa, Patrick Orlando, Luca Tiano, Flemming Dela, Jørn Wulff Helge, Steen Larsen.
      Mitochondrial function is important to healthy aging, as it influences energy metabolism, oxidative stress, and physical performance. With age, mitochondrial function and biosynthesis of coenzyme Q10 (CoQ10) may change. CoQ10 serves as a key antioxidant and component of the electron transport system. Supplementation with CoQ10 may help preserve mitochondrial function and support healthy aging. Forty older community-dwelling adults (74 ± 4 years) received either daily oral CoQ10 supplementation (400 mg daily) or a placebo in a 12-week double-blinded, randomized, placebo-controlled design. Before and after the supplementation period, muscle biopsies were obtained. Subsequently, oral glucose tolerance tests (OGTT) and VO2max tests were conducted. Mitochondrial respiratory capacity (MRC), mitochondrial H2O2 emission, and mitochondrial content were assessed in both isolated mitochondria and permeabilized muscle fibers. Levels and redox status of CoQ10 were measured in plasma, muscle tissue, and isolated skeletal muscle mitochondria. Additionally, resting metabolic rate, cognitive function, and body composition were investigated. Plasma levels of CoQ10 increased significantly without changes in redox status after the intervention. No changes between groups or time were observed in muscle and isolated mitochondria regarding MRC, H2O2 emission, mitochondrial content, and levels of CoQ10. Glucose homeostasis, VO2max, and body composition were also unchanged. Twelve weeks of supplementation led to increased plasma levels of CoQ10, with unchanged levels in muscle tissue and isolated mitochondria. No differences in mitochondrial function, glucose homeostasis, and physical performance were found in a cohort of robust older adults.
    Keywords:  Antioxidant; Healthy aging; Mitochondrial function; Reactive oxygen species
    DOI:  https://doi.org/10.1007/s11357-025-02068-9
  4. Obesity (Silver Spring). 2026 Jan 25.
    Cardiometabolic Gains Unrelated to Weight Loss-Adjusted Body Fat or Distribution Changes in Adults With and Without Diabetes.
    Jose E Galgani, Gabriela Carrasco, Gonzalo Pons, Fernando Carrasco, Víctor Cortés, Rodrigo Fernández-Verdejo, Eric Ravussin.
       OBJECTIVE: This study assessed whether changes in body composition or fat distribution after weight loss are associated with cardiometabolic improvements, independent of weight loss magnitude.
    METHODS: We analyzed data from a 1-year lifestyle intervention in adults with obesity and type 2 diabetes (Study I) and a 12-week hypocaloric diet intervention in adults with overweight/obesity without diabetes (Study II). Body composition was assessed by DXA and fat distribution by either abdominal computed tomography (Study I) or DXA-derived trunk to total fat ratio (Study II). Insulin sensitivity was assessed by glucose clamp (Study I) and HOMA-IR (both studies). Additional markers included glucose, lipids, and blood pressure. Changes in body composition and fat distribution were adjusted for baseline values and weight loss using regression analysis.
    RESULTS: Body weight decreased by 9.8% in Study I and 5.3% in Study II, with fat mass accounting for 64% (95% CI: 0.51%-0.77%) and 77% (95% CI: 0.68%-0.86%) of weight lost, respectively. Clamp-derived insulin sensitivity increased by 50% (Study I), and HOMA-IR decreased by 26% in both studies. No cardiometabolic changes were associated with weight loss-adjusted changes in body fat percentage or fat distribution.
    CONCLUSIONS: Cardiometabolic improvements from weight loss appear independent of changes in body fat percentage or fat distribution.
    Keywords:  body composition; insulin sensitivity; lifestyle intervention; metabolic health; obesity
    DOI:  https://doi.org/10.1002/oby.70123
  5. Biomed Pharmacother. 2026 Jan 26. pii: S0753-3322(26)00089-2. [Epub ahead of print]195 119057
    Differential effects of the anti-obesity drug tirzepatide on adipose tissues: Brown fat as a key target.
    Alberto Mestres-Arenas, Tania Quesada-López, Albert Blasco-Roset, Marta Giralt, Francesc Villarroya, Anna Planavila, Marion Peyrou.
      Tirzepatide is an anti-obesity drug based on dual agonism of the incretin receptors GLP-1R and GIPR. Its anti-obesity effect is largely based on its action of reducing food intake. However, there are indications that tirzepatide exerts effects on adipose tissues beyond those resulting from fat loss due to reduced food intake. To investigate this, we treated mice, previously been made obese through high-fat diet, with tirzepatide. We also established an experimental group of mice pair-fed with those treated with tirzepatide, key to distinguish the specific effect of tirzepatide from food intake reduction-mediated effects. Both groups experienced similar reduction in body weight, with a trend toward greater loss in visceral and subcutaneous white fat in mice under tirzepatide treatment. Glucose tolerance improved in tirzepatide-treated obese mice, independently of reduced food intake. Tirzepatide treatment also lowered the inflammatory status of obese mice, which in this case, was attributable to decreased food consumption. Tirzepatide exerted distinct effects on brown adipose tissue relative to white adipose tissues, significantly boosting thermogenic activity and modifying its gene expression pattern, including the upregulation of genes linked to thermogenesis and substrate oxidation. White adipose tissues responded differently, being primarily affected in their lipid metabolism. These effects were specific to tirzepatide treatment and not attributable to reduced food intake. Our results indicate that tirzepatide affects the function and metabolism of adipose tissues and especially induces activation of brown adipose tissue in mice, which may be relevant for future human studies to ascertain the mechanisms of tirzepatide metabolic benefits.
    Keywords:  Obesity; Thermogenesis; Tirzepatide; adipose tissue; brown adipose tissue; mitochondria
    DOI:  https://doi.org/10.1016/j.biopha.2026.119057
  6. J Lipid Res. 2026 Jan 27. pii: S0022-2275(26)00012-X. [Epub ahead of print] 100986
    Kiss1-FASN participates fatty acid synthesis via high-fat diet in PgVAT of female mice.
    Xuehan Li, Chunyu Liang, Ge Song, Yihusan Lin, Yue Chen, Jiani Zhao, Hongtao Sui, Xinliang Pan, Lingyu Sun, Jianhao Chen, Jiaqi Li, Zhen Ni, Yi Yan.
      Long-term consumption of high-fat diet (HFD) leads to energy surplus, resulting in excessive adipose tissue (AT) accumulation and dysfunction. Kiss1 is known to play a role in the metabolic regulation of AT. To explore the involvement of Kiss1 in mediating the effects of energy surplus induced by HFD, we conducted an 8-week intervention combining aerobic exercise and HFD in mice with AT-specific knockout (KO) and overexpression of Kiss1, along with HFD treatment in Kiss1-KO 3T3-L1 cells. Our results revealed that in perigonadal visceral AT (PgVAT) of female mice, the expression of Kiss1 and FASN is positively correlated. Additionally, Kiss1 participate the fatty acid (FA) synthesis pathway in PgVAT of female mice. When we overexpressed Kiss1 in AT of female mice, we found that Aerobic exercise reduced FASN levels by downregulating Kiss1 expression in PgVAT, thereby may suppressing the FA synthesis capacity. This study provides novel insights for developing targeted therapeutic strategies against obesity and associated metabolic disorders.
    Keywords:  Adipose tissue; FASN; High-fat diet; Kiss1; aerobic exercise
    DOI:  https://doi.org/10.1016/j.jlr.2026.100986
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