RESUMO
Aim To study the effects of melatonin on glucose output in insulin resistant HepG2 cells and the related mechanism. Methods Insulin resistant HepG2 cells were induced by high glucose and insulin (HGI) (25 mmol • L"1 and 1 (irnol • L"1 respectively) co-culture for 24 h,and then melatonin (10 nmol • L"1) was supplied. The glucose uptake and the gly-cogen content were measured. Levels of protein p-Akt, p-FoxOl as well as p-GSK-30 were evaluated by Western blot. The nuclear export of FoxOl and its intracellular localization were detected by immunofluorescence. Results HGI incubation led to significant decrease in insulin-stimulated glucose uptake and glyco-gen synthesis in HepG2 cells (P < 0. 0( ). However, melatonin reversed these inhibitory effects by increasing glucose uptake and glycogen synthesis significantly (P<0. 01). The results also showed that melatonin not only up-regulated levels of protein p-GSK-3 (3, p-Akt and p-FoxOl but also promoted cytoplasm translocation of FoxOl. Conclusions Melatonin could regulate glycogenesis and gluconeogenesis ih insulin resistant HepG2 cells via Akt/GSK-3(3 and Akt/FoxOl pathway. It thus suppresses the endogenous glucose output and improves the glucose metabolism.
RESUMO
Significant differences were observed in glycogen metabolism of Anabas testudineus exposed to an acute lethal (1.56 mg/litre) and a sublethal (0.56 mg/litre) concentration of furadan. At sublethal concentration, the muscle glycogen which was utilized during the early periods of exposure, was replenished in the later period of exposure and at 120 h, the muscle glycogen levels were higher than the control. At higher concentration, the liver glycogen levels showed an increase presumably at the expense of fuel reserves of the muscle.