The regulation of AMPK pathway in liver abnormal lipid deposition caused by high carbohydrate diet in rice field eel

Abstract

AMP-activated protein kinase-alpha 1 (AMPKα1) plays a vital role in glucose and lipid metabolism. Five isonitrogenous and isolipid diets with starch levels (15%, 20%, 25%, 30% and 35%) were formulated to study the modulation of AMPKα1 in hepatic lipid deposition induced by high gelatinized starch diet in rice field eel (Monopterus albus) (initial body weight, 30.00 ± 0.10 g) and the growth trial lasted for 8 weeks. The results showed that dietary gelatinized starch did not affect the growth performance of rice filed eel compared with S15 group. High gelatinized starch could induce AMPKα1 expression and glucose catabolism, and inhibit hepatic glycogen synthesis without effecting glucose content. Dietary ≥ 30% gelatinized starch began to dramatically suppress gluconeogenesis and promote the lipid synthesis, followed by a higher triglyceride (TG) and hepatic crude lipid. Dietary 20–30% gelatinized starch induced phosphorylation of AMPKα compared to 15% gelatinized starch diet, whereas 35% starch dramatically suppressed AMPKα phosphorylation together with unnormal increase in phosphorylation of forkhead box O1 A (FOXO1A) and acetyl-CoA carboxylase (ACC), TG content compared to 30% starch. In short, high gelatinized starch could induce AMPKα1 expression and promoted systemic metabolism, whereas dietary ≥ 25% gelatinized starch initially suppressed AMPKα1 activation and caused abnormal lipid deposition in liver of rice field eel.