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Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence
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DOI：10.1038/s42255-024-01130-8.png)
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Abstract
En 中文
Beta (beta)-cell senescence contributes to type 2 diabetes mellitus (T2DM). While exercise is vital for T2DM management and significantly affects cellular ageing markers, its effect on beta-cell senescence remains unexplored. Here, we show that short-term endurance exercise training (treadmill running, 1 h per day for 10 days) in two male and female mouse models of insulin resistance decreases beta-cell senescence. In vivo and in vitro experiments revealed that this effect is mediated, at least in part, by training-induced increases in serum glucagon, leading to activation of 5 '-AMP-activated protein kinase (AMPK) signalling in beta-cells. AMPK activation resulted in the nuclear translocation of NRF2 and decreased expression of senescence markers and effectors. Remarkably, human islets from male and female donors with T2DM treated with serum collected after a 10-week endurance exercise training programme showed a significant decrease in the levels of senescence markers. These findings indicate that exercise training decreases senescence in pancreatic islets, offering promising therapeutic implications for T2DM. Exercise training decreases pancreatic islet senescence through glucagon and AMPK signalling in mouse and human islets, which could have implications for T2DM therapeutics.
Keywords:
PROTEIN-KINASE
SECRETORY PHENOTYPE
MECHANISMS
STRESS
MUSCLE
EXPRESSION
RESISTANCE
HALLMARKS
DISEASE
MARKERS
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ShareSaveCellular senescence in aging and age-related disease: from mechanisms to therapy.png)
NATURE MEDICINE
OAAI
NATURE MEDICINEIF50
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CIRCULATIONIF38.6
OAAIShareSaveβ Cell Aging Markers Have Heterogeneous Distribution and Are Induced by Insulin ResistanceCELL METABOLISMOAAI
CELL METABOLISMIF30.9
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