Abstract：
:Skeletal muscle atrophy is a debilitating response to several major diseases, muscle disuse and chronic steroid treatment for which currently no therapy is available. Since adiponectin signaling plays key roles in muscle energetics, we assessed if globular adiponectin (gAd) or the small molecule adiponectin mimetic 6-C-β-D-glucopyranosyl-(2S,3S)-(+)-5,7,3',4'-tetrahydroxydihydroflavonol (GTDF) could ameliorate muscle atrophy. Both GTDF and gAd induced C2C12 myoblast differentiation. GTDF and gAd effectively prevented reduction in myotube area and suppressed the expressions of atrophy markers; atrogin-1 and muscle ring finger protein-1 (MuRF1) in models of steroid, cytokine and starvation -induced muscle atrophy. The protective effects of GTDF and gAd were routed through AMPK and AKT activation and thereby stimulation of PPAR gamma coactivator 1α and inhibition of forkhead box O transcription factors. Finally, GTDF and gAd mitigated dexamethasone-induced muscle atrophy in vivo. Together, our results demonstrate that activating adiponectin signaling may be an effective therapeutic strategy against skeletal muscle atrophy.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Singh AK,Shree S,Chattopadhyay S,Kumar S,Gurjar A,Kushwaha S,Kumar H,Trivedi AK,Chattopadhyay N,Maurya R,Ramachandran R,Sanyal Sdoi
10.1016/j.mce.2016.09.013subject
Has Abstractpub_date
2017-01-05 00:00:00pages
273-285eissn
0303-7207issn
1872-8057pii
S0303-7207(16)30378-1journal_volume
439pub_type
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