Endocrine Abstracts

Skeletal muscle is a central player in locomotion and systemic metabolism, particularly in glucose regulation. Type 2 diabetes and obesity are associated with insulin resistance and muscle dysfunction, often exacerbated by sarcopenic obesity. Exercise is a proven intervention to counteract these declines, yet the molecular mechanisms underlying its benefits remain incompletely understood. Emerging research highlights the dynamic and time-dependent molecular responses in skeletal muscle following exercise, including waves of transcriptional, proteomic, and metabolic changes. Integration of multi-omics approaches is revealing new insights into how skeletal muscle interacts with other organs to maintain energy homeostasis. However, individual variability in exercise responses underscores the need for precision exercise strategies tailored to genetic, epigenetic, environmental, and phenotypic factors. By mapping the molecular landscape of exercise adaptation, researchers aim to identify therapeutic targets to enhance insulin sensitivity, prevent metabolic dysfunction, and inform personalized interventions. Despite ongoing challenges, understanding the intricate biology of exercise holds promise for innovative strategies to combat Type 2 diabetes and related disorders, supporting the mantra that "exercise is medicine."

Acknowledgements: This work is supported by unconditional donations from the Novo Nordisk Foundation (NNF) to NNF Center for Basic Metabolic Research (Grant number NNF18CC0034900; NNF23SA0084103), as well as the Swedish Diabetes Foundation (DIA2021-645), the Swedish Research Council 2015-00165, the Novo Nordisk Foundation (NNF17OC0030088), the EFSD/Novo Nordisk Programme for Diabetes Research in Europe and the Strategic Research Program in Diabetes at Karolinska Institutet.