Dietary inositol improved glucose and lipid metabolism mediated by the Insulin-PI3K-Akt signaling pathway in Pacific white shrimp (Litopenaeus vannamei)

The present study aimed to evaluate the effects of dietary inositol level (0.86, 1.34, 1.40, 2.30, 3.88 and 7.50 g kg−1) on glucose and lipid homeostasis in Litopenaeus vannamei. The results indicated that the contents of inositol, phosphatidyl inositol (PI) and glycogen in hepatopancreas and muscle, very low-density lipoprotein (VLDL) in hepatopancreas and hemolymph, the activity of carnitine palmitoyl-transferase (CPT1) and the expression of hmit and inox were positively related to the dietary inositol levels, while the contents of glucose (GLU), crustacean hyperglycemic hormone (CHH), triglyceride (TG), cholesterol (CHO) and non-esterified fatty acid (NEFA) in hemolymph and the expression of imp, pepck, g6pc and fbp were negatively correlated with the dietary inositol level. TG content, phosphoenolpyruvate carboxykinase (PEPCK) activity and the expression levels of srebp, fas, acc1, g6pd and 6gpd in shrimp fed 3.88 and 7.50 g kg−1 inositol diets were significantly lower compared with shrimp fed the basal diet, while the expression of cpt1, aco, fabp, fatp and idir were showed the reverse change trend (P < 0.05). The activities of hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK) and the expression levels of ir, irs1, pi3k and akt were significantly increased as dietary inositol levels ranged from 1.40 to 7.50 g kg−1, while the expression levels of gsk-3β and foxo1 significantly down-regulated. Hepatopancreas R cells number in shrimp fed 2.30, 3.88 and 7.50 g kg−1 inositol diets were significantly increased compared with shrimp fed 0.86 g kg−1 inositol diet, while the diameters and areas showed an opposite trend. In addition, dietary inositol supplementation significantly increased hemolymph insulin like peptide (ILP) content but had no significant effect on high density lipoprotein cholesterol (HLDC) content in hemolymph, hepatic lipase (HL) activity and the ratio of n-3/ n-6 PUFA and DHA/EPA in hepatopancreas. In conclusion, appropriate dietary inositol could positively regulate the Insulin-PI3K-Akt pathway to promote glucose utilization and maintain the normal accumulation of glycogen and lipids required for development, while high dietary inositol could promote lipid mobilization and prevent hepatopancreas lipids deposition by negatively regulating the Insulin-PI3K-Akt pathway, improving ILP sensitivity and enhancing VLDL synthesis, which may therefore be an important mechanism in the action of inositol on glucose and lipid metabolism. These findings provided further insight and understanding of mechanisms by which dietary inositol regulated glucose and lipid metabolism in L. vannamei.