This study evaluated the effects of dietary myo-inositol (MI) on growth performance, antioxidant status and lipid metabolism of juvenile Chinese mitten crab (Eriocheir sinensis) fed different percentage of lipid. Crabs (4·58 (sem 0·05) g) were fed four diets including a normal lipid diet (N, containing 7 % lipid and 0 mg/kg MI), N with MI supplementation (N + MI, containing 7 % lipid and 1600 mg/kg MI), a high lipid diet (H, containing 13 % lipid and 0 mg/kg MI) and H with MI supplementation (H + MI, containing 13 % lipid and 1600 mg/kg MI) for 8 weeks. The H + MI group showed higher weight gain and specific growth rate than those in the H group. The dietary MI could improve the lipid accumulations in the whole body, hepatopancreas and muscle as a result of feeding on the high dietary lipid (13 %) in crabs. Besides, the crabs fed the H + MI diets increased the activities of antioxidant enzymes but reduced the malondialdehyde content in hepatopancreas compared with those fed the H diets. Moreover, dietary MI enhanced the expression of genes involved in lipid oxidation and exportation, yet reduced lipid absorption and synthesis genes expression in the hepatopancreas of crabs fed the H diet, which might be related to the activation of inositol 1,4,5-trisphosphate receptor (IP3R)/calmodulin-dependent protein kinase kinase-β (CaMKKβ)/adenosine 5’-monophosphate-activated protein kinase (AMPK) signalling pathway. This study demonstrates that MI could increase lipid utilisation and reduce lipid deposition in the hepatopancreas of E. sinensis fed a high lipid diet through IP3R/CaMKKβ/AMPK activation. This work provides new insights into the function of MI in the diet of crustaceans.

The development and maintenance of body composition and functions require an adequate protein intake with a continuous supply of amino acids (AA) to tissues. Body pool and AA cellular concentrations are tightly controlled and maintained through AA supply (dietary intake, recycled from proteolysis and de novo synthesis), AA disposal (protein synthesis and other AA-derived molecules) and AA losses (deamination and oxidation). Different molecular regulatory pathways are involved in the control of AA sufficiency including the mechanistic target of rapamycin complex 1, the general control non-derepressible 2/activating transcription factor 4 system or the fibroblast growth factor 21. There is a tight control of protein intake, and human subjects and animals appear capable of detecting and adapting food and protein intake and metabolism in face of foods or diets with different protein contents. A severely protein deficient diet induces lean body mass losses and ingestion of sufficient dietary energy and protein is a prerequisite for body protein synthesis and maintenance of muscle, bone and other lean tissues and functions. Maintaining adequate protein intake with age may help preserve muscle mass and strength but there is an ongoing debate as to the optimal protein intake in older adults. The protein synthesis response to protein intake can also be enhanced by prior completion of resistance exercise but this effect could be somewhat reduced in older compared to young individuals and gain in muscle mass and function due to exercise require regular training over an extended period.

The present study evaluated the effects of dietary Zn level on growth performance, serum and hepatopancreas metabolites, expression of genes involved in lipid and energy metabolism, and the signalling pathway of dietary Zn-induced lipolysis. Five isonitrogenous and isolipidic diets were formulated to contain different Zn levels: 46·4 (basal diet), 77·2, 87·0, 117·1 and 136·8 mg/kg, respectively. The results indicated that shrimp fed the diet containing Zn at 117·1 mg/kg had higher weight gain and specific growth rate, and the lowest feed intake and feed conversion rate, than shrimp fed the other diets. The deposition rate of Zn in whole body significantly decreased with increasing dietary Zn level. Dietary Zn prevented the accumulation of free radicals and improved antioxidant activities by increasing Cu/Zn superoxide dismutase and reducing malondialdehyde in hepatopancreas. Dietary Zn supplementation enhanced lipase activity and adiponectin, which could promote TAG breakdown and fatty acid oxidation and lead to reduced lipid in hepatopancreas. The mRNA expressions of ob-rb, adipor, camkkβ, ampk, cd36, mcd and cpt1 involved in Zn-induced lipid catabolism were up-regulated, and the expressions of srebp, acc, fas and scd1 were down-regulated. The mRNA levels of SLC39 family genes (zip3, zip9, zip11 and zip14) in hepatopancreas were up-regulated with increasing dietary Zn level. The results demonstrated that dietary Zn level could significantly affect growth performance, tissue deposition of Zn, lipid metabolites and expression of genes involved in lipogenesis and lipolysis in Litopenaeus vannamei.