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Diet-induced obesity (DIO) is associated with glucose intolerance, insulin resistance (IR), and an increase in intramyocellular lipids (IMCL), which may lead to disturbances in glucose and protein metabolism. To this matter, it has been speculated that chronic obesity and elevated IMCL may contribute to skeletal muscle loss and deficits in muscle function and growth capacity. Thus, we hypothesized that diets with elevated fat content would induce obesity and insulin resistance, leading to a decrease in muscle mass and an attenuated growth response to increased external loading in adult male mice. Male C57BL/6 mice (8 wk of age) were subjected to five different diets, namely, chow, low-dat-diet (LFD), high-fat-diet (HFD), sucrose, or Western diet, for 28 wk. At 25 wk, HFD and Western diets induced a 60.4% and 35.9% increase in body weight, respectively. Interestingly, HFD, but not Western or sucrose, induced glucose intolerance and insulin resistance. Measurement of isometric torque (ankle plantar flexor and ankle dorsiflexor muscles) revealed no effect of DIO on muscle function. At 28 wk of intervention, muscle area and protein synthesis were similar across all diet groups, despite insulin resistance and increased IMCL being observed in HFD and Western diet groups. In response to 30 days of functional overload, an attenuated growth response was observed in only the HFD group. Nevertheless, our results show that DIO alone is not sufficient to induce muscle atrophy and contractile dysfunction in adult male C57BL/6 mice. However, diet composition does have an impact on muscle growth in response to increased external loading. The effects of diet-induced obesity on skeletal muscle mass are complex and dependent on diet composition and diet duration. The present study results show that chronic exposure to high levels of fatty acids does not affect muscle mass, contractile function, or protein synthesis in obese C57BL/6 mice compared with the consumption of chow. Obesity did result in a delay in load-induced growth; however, only a 45% HFD resulted in attenuated growth following 30 days of functional overload.
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http://dx.doi.org/10.1152/japplphysiol.00156.2020 | DOI Listing |
Drug Deliv Transl Res
September 2025
Department of Pharmacy, Birla Institute of Technology and Science, Pilani, Pilani Campus, Vidya Vihar, Pilani, Rajasthan, 333031, India.
Diabetes is a metabolic disorder of increasing global concern. Characterized by constantly elevated levels of glucose, severe β-cell dysfunction, and insulin resistance, it is the cause of a major burden on patients if not managed with therapeutic and lifestyle changes. The human body is slowly developing tolerance to many marketed antidiabetic drugs and the quest for the discovery of newer molecules continues.
View Article and Find Full Text PDFJ Nutr
September 2025
School of Medicine and Allied Health Sciences, University of The Gambia, Banjul, The Gambia; Shandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, 440 Jiyan Road, Jinan, Shandong 250
Background: Red and processed meat consumption is extensively linked to chronic disease risk in observational studies, with robust meta-analyses demonstrating significant positive associations for colorectal, breast, endometrial, and lung cancers, type 2 diabetes (T2DM), cardiovascular disease (CVD), and all-cause mortality. Dose-response relationships indicate elevated risks even at moderate intakes. Moreover, processed meats consistently show stronger detrimental effects than unprocessed red meats.
View Article and Find Full Text PDFMol Cell Endocrinol
September 2025
Department of Epidemiology, University of Michigan, Ann Arbor, USA. Electronic address:
Steroid hormones are integral to pregnancy and fetal development, regulating processes such as metabolism, inflammation, and immune responses. Excessive prenatal steroid exposure, through lifestyle choices or environmental chemicals, can lead to metabolic dysfunctions in offspring. The research focuses on how exposure to testosterone (T) and bisphenol A (BPA) affects the liver's DNA methylome, a key component of the epigenome influencing long-term health.
View Article and Find Full Text PDFCell Metab
August 2025
Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. Electronic address:
Diet and obesity contribute to insulin resistance and type 2 diabetes, in part via the gut microbiome. To explore the role of gut-derived metabolites in this process, we assessed portal/peripheral blood metabolites in mice with different risks of obesity/diabetes, challenged with a high-fat diet (HFD) + antibiotics. In diabetes/obesity-prone C57BL/6J mice, 111 metabolites were portally enriched and 74 were peripherally enriched, many of which differed in metabolic-syndrome-resistant 129S1/129S6 mice.
View Article and Find Full Text PDFMol Nutr Food Res
September 2025
Department of Clinical Medicine and Surgery, Physiology Unit, University of Naples "Federico II", Napoli, Italy.
This study evaluated the effect of a nutraceutical supplementation (NS) and Mediterranean hypocaloric diet (MHD) on hepatic steatosis indices (HSIs), γ-glutamyl transferase (γGT), and lipid profile in adults with hyperlipidemia and nonalcoholic fatty liver disease (NAFLD). In vitro study on HepG2 cells explored potential molecular mechanisms. A retrospective study was conducted on 45 overweight/obese subjects (19 M) prescribed MHD with/without NS.
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