Chronic AICAR treatment enhances anabolic signaling in sarcopenic skeletal muscle
AMP-Activated Protein Kinase
Muscle Atrophy
DOI:
10.1096/fasebj.2022.36.s1.r5697
Publication Date:
2022-05-03T08:19:46Z
AUTHORS (7)
ABSTRACT
Many fields of study have grappled with the challenge decelerating effects aging. Physical exercise plays a vital role in attenuating impact aging process. While many exercise-induced chemical signaling pathways are not fully understood, AMP-activated protein kinase mediates beneficial adaptations to training. AMPK is activated by accumulation AMP (and ADP) during muscle contraction-induced ATP breakdown. The prodrug AICAR mimics and leads activation increasing concentration analog, ZMP. primary purpose present determine effect chronic (31 days) treatment on anabolic old (24 mo.) mice. improved treadmill running performance attenuated atrophy aged Surprisingly, given AICAR's known acute signaling, increased skeletal concentrations insulin-like growth factor-1 apelin, both which activate through mechanistic target rapamycin complex 1 (mTORC1). Accordingly, ribosomal S6 phosphorylation was also elevated AICAR-treated muscles. Our results suggest that addition its other well-established metabolic effects, may enhance anabolism sarcopenic potentially muscle-wasting conditions.
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