Obesity ‐induced skeletal muscle remodeling: A comparative analysis of exercise training and ACE‐inhibitory drug in male mice

Enalapril and aerobic exercise training have been found to shift the activity of the renin-angiotensin system (RAS) toward the counterregulatory arm and the kallikrein-kinin system (KKS) toward the bradykinin receptor subtype 2 (B2R), which in turn helps reduce apoptosis markers (BAX/Bcl-2 ratio) and improve PGC-1 α expression in muscle. However, it is worth noting that only exercise training mitigates obesity-induced myofiber atrophy. This is due to its ability to upregulate the mTOR/p70S6K pathway, boost muscle mitochondrial biogenesis marker (PGC-1α), and lower levels of muscle protein degradation marker s (MuRF-1 and Atrogin-1). It is important to note that AT1R (angiotensin type 1 receptor), MasR (Mas receptor), Bax (Bcl-2-associated X protein), Bcl-2 (B-cell lymphoma 2), and UPP (ubiquitin-proteasome pathway) are all relevant abbreviations in this context; also, green arrows represent activate re gulation, and red arrows represent the inhibitory regulation. AbstractObesity over-activates the classical arm of the renin-angiotensin system (RAS), impairing skeletal muscle remodeling. We aimed to compare the effect of exercise training and enalapril, an angiotensin-converting enzyme inhibitor, on RAS modulation in the skeletal muscle of obese animals. Thus, we divided C57BL/6 mice into two groups: standard chow (SC) and high-fat (HF) diet for 16  weeks. At the eighth week, the HF-fed animals were divided into four subgroups—sedentary (HF), treated with enalapril (HF-E...
Source: Physiological Reports - Category: Physiology Authors: Tags: ORIGINAL ARTICLE Source Type: research