Effects of Dietary Carbohydrate Level on Growth Performance, Immune Response, and Antioxidant Capacity of the Male Giant Freshwater Prawn Macrobrachium rosenbergii
Abstract
This study examined the effects of dietary carbohydrate levels on growth performance, immune response, and antioxidant capacity of male giant freshwater prawn Macrobrachium rosenbergii. Prawns with an initial body weight of 15.04 ± 0.08 g were fed for 9 weeks on five isonitrogenous, isolipidic diets formulated to contain 10%, 15%, 20%, 25%, and 30% carbohydrate (designated CHO10–CHO30). Weight gain rate and specific growth rate rose from CHO10 to CHO20 and then declined (peak in CHO20); broken-line regression of weight gain rate estimated the optimal dietary carbohydrate level at approximately 19.36% under the present experimental conditions. Moderate carbohydrate inclusion (15–20%) enhanced hepatopancreatic total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and catalase (CAT) activities together with the transcription of cu/znsod, cat and glutathione peroxidase (gsh-px), whereas levels ≥ 25% lowered these defenses and raised hepatopancreatic malondialdehyde (MDA). High-carbohydrate diets also increased hemolymph glucose, triglyceride, total cholesterol and low-density lipoprotein cholesterol, progressively altered the mRNA expression of genes involved in the Toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) signaling pathway (upregulated tlr, myd88, relish and tumor necrosis factor; downregulated inhibitor of NF-κB alpha (IκB-α)), and altered the expression of apoptosis-related genes (downregulated B-cell lymphoma 2 (bcl-2), upregulated caspase-3). These results suggest that M. rosenbergii has an estimated optimal dietary carbohydrate level of approximately 19.36% under the present experimental conditions; intakes at or above 25% are associated with compromised hepatopancreatic health and growth, likely through the induction of oxidative stress, altered transcription of TLR/MyD88 pathway-related genes, and changes in apoptosis-related gene expression.