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Time-restricted feeding (TRF) and aerobic exercise are lifestyle interventions to prevent or manage different metabolic diseases. How these interventions interact, including the impact of meal timing, is not well understood. The aim of this study was to examine the influence of TRF on fat oxidation during exercise, whereby participants performed an 8-week fat-training program either in the fasted state or after a carbohydrate-based snack. 36 participants were randomized into three groups. (1) Training sessions were performed in the fasted state; (2) Training sessions were performed after consuming a standardized carbohydrate-based snack; (3) Exercise training with an ad libitum diet as a control group. Pre- and post-tests included anthropometric measurements and a fat-cycle-ergometry protocol to measure substrate oxidation. Data were analyzed as workload-matched and maximal fat oxidation using a series of mixed ANOVAs. Workload-matched (p = 0.038) and maximal (p < 0.001) fat oxidation improved in all groups. No significant group × time interactions were found in substrate utilization. Time had a significant effect on body weight (p = 0.011), fat mass (p < 0.001), and muscle mass (p < 0.001). Results suggest that fat exercise training leads to improvements in fat oxidative capacity independent of fed or fasted state.
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http://dx.doi.org/10.14814/phy2.70194 | DOI Listing |
J Nutr Biochem
September 2025
Oil Crops Research Institute, Chinese Academy of Agricultural Sciences, Hubei Key Laboratory of Lipid Chemistry and Nutrition, Oil Crops and Lipids Process Technology National & Local Joint Engineering Laboratory, Key Laboratory of Oilseeds Processing, Ministry of Agriculture, Wuhan 430062, PR CHINA
Increasing evidence indicates that ferroptosis contributes to the occurrence and development of metabolic dysfunction-associated fatty liver disease (MAFLD). This study aimed to investigate the improvement effect of plant sterol ester of α-linolenic acid (PS-ALA) on ferroptosis in hepatocytes and further elucidate the underlying molecular mechanism, focusing on the regulation of Nrf2 signaling. We found that PS-ALA ameliorated liver iron overload and reduced ROS generation and lipid peroxides (MDA and 4-HNE) production both in mice fed a high-fat diet and HepG2 cells induced by oleic acid/erastin.
View Article and Find Full Text PDFJ Hepatol
September 2025
National Research Council (CNR), Institute of Clinical Physiology (IFC), Pisa, Italy. Electronic address:
Cell 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 PDFPhytomedicine
August 2025
School of Chinese Materia Medica, Beijing University of Chinese Medicine, 102488, China. Electronic address:
Background: Diabetic nephropathy (DN), a serious diabetic complication, currently has limited treatment options. Yulan Jiangtang capsules (YL) are a clinically approved traditional Chinese medicine formula for glycemic control and diabetes-related complications. Nevertheless, the underlying mechanisms of their therapeutic effects remain incompletely elucidated.
View Article and Find Full Text PDFCell Rep
September 2025
Department of Pathology, University of Iowa, Iowa City, IA, USA. Electronic address:
High fat diet (HFD)-induced obesity increases the risk and severity of psoriasis. However, the immunoregulatory effects of different HFDs on psoriasis pathogenesis remains poorly understood. Here, mimicking human dietary fat profiles, four HFDs-saturated, monounsaturated, omega-6, and omega-3 fats-were designed and used to induce obesity in mice.
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