Cinnamtannin A2, (−)-epicatechin tetramer, attenuates skeletal muscle wasting in disuse atrophy model mice induced by hindlimb suspension

Abstract

The impact of repeated administration of cinntamtannin A2 (A2, 25 μg/kg) on skeletal muscle disuse atrophy model mice induced by hindlimb suspension for 14 days was examined. In soleus, weight loss and a reduction in the average myofibre size with shifting to the smaller side of the peak were observed in the suspension-vehicle group, but A2 reduced these changes. Average myofibre size significantly increased in ground-A2 compared to ground-vehicle. A marked increase in the dephosphorylation of forkhead box O (FoxO) 3a by the suspension was reduced by A2. The phosphorylation of protein kinase B (Akt) and eukaryotic translation initiation factor 4E-binding protein (4EBP)-1 were significantly increased by the treatment of A2. In addition, a single dose of A2 increased dramatically in the 24-h excretion of catecholamines in urine. These results suggest that A2 administration results in sympathetic nerve activation and promotes hypertrophy while inhibiting the progress of disuse muscle atrophy.

Sensory Nutrition and Bitterness and Astringency of Polyphenols

“…This was characterized by multilocular lipid droplets, a marked reduction in adipocyte size and increased expression of the heat-producing protein, uncoupling protein 1 (UCP-1) [118]. Repeated administration of the flavanol cinnamtannin A2 (A2, epicatechin tetramer) for two weeks also resulted in significant activation of the Akt/mTOR pathway and a marked increase in the mean muscle cross-sectional area in the soleus muscle [119] as similar to adrenalin agonist clenbuterol [120]. It has also been observed that after a single dose of flavanol, blood catecholamine levels were significantly increased [121] and urinary catecholamine excretion was also elevated [118].…”