(−)-Epigallocatechin-3-O-gallate or (−)-epicatechin enhances lipid catabolism and antioxidant defense in common carp (Cyprinus carpio L.) fed a high-fat diet: Mechanistic insights from the AMPK/Sirt1/PGC-1α signaling pathway

Long-term high-fat diets (HF) lead to lipid accumulation and an oxidative stress response, which deteriorates the chemical and physical characteristics of fish muscle. Green tea extracts, such as (−)-epigallocatechin-3-O-gallate (EGCG) and (−)-epicatechin (EC), have been found to regulate antioxidant ability and lipid metabolism. However, the effects of EGCG and EC on alleviating oxidative stress and lipid metabolism disorders caused by HF are unclear. Furthermore, the underlying mechanisms remain unknown. In this study, a total of 360 carp (average weight: 9.75 ± 0.09 g) were provided with four experimental diets: a control diet (CN, 6.15% dietary lipids), a high-fat diet (HF, 14.05% dietary lipids), HF supplemented with EGCG (HF + EGCG, 14.05% dietary lipids +50 mg/kg EGCG), and a HF diet supplemented with EC (HF + EC, 14.05% dietary lipids +1000 mg/kg EC) for a duration of 84 days. The results indicated that EGCG or EC ameliorated the negative effects of the HF diet on muscle tissue. Apart from muscle physical characteristics, EGCG decreased yellowness (b*), redness (a*), and dripping loss (P < 0.05). Apart from muscle nutritional composition and antioxidant status, EC mitigated the reduction in protein levels in the muscle induced by the HF diet. Similarly, EGCG and EC mitigated the excessive accumulation of lipids and reactive oxygen species (ROS) in the muscle induced by the HF diet (P < 0.05). Further study showed that EGCG or EC facilitated the phosphorylation of AMP-activated protein kinase (AMPK) and increased silent information regulator 1 (Sirt1) and PPARγ coactivator-1 alpha (PGC-1α) expression in muscle. Taken together, the results of this study revealed that EGCG or EC enhance lipid metabolism and antioxidant capacity in the muscle of common carp (Cyprinus carpio L.) via the AMPK/Sirt1/PGC-1α pathway.