Dietary l-arginine supplementation of tilapia (Oreochromis niloticus) alters the microbial population and activates intestinal fatty acid oxidation

Currently, little is known about the function of l-arginine in the homeostasis of intestinal lipid metabolism. This study was conducted to test the hypothesis that dietary l-arginine supplementation may alter intestinal microbiota and lipid metabolism in tilapia. Tilapia were fed a basal diet (containing 16.9 g l-arginine per kilogram diets) or the basal diet supplemented with 1% or 2% l-arginine for 8 wks. In the present study, we found that dietary supplementation with 1% or 2% l-arginine induced a shift in the community structure of gut microbiota, as showed by increased (p < 0.05) alpha-diversity, altered (p < 0.05) beta-diversity and function profile. This finding coincided with decreased lipid accretion in the intestine of tilapia, which was associated with an enhancement in mRNA levels for peroxisome proliferator-activated receptor alpha (Ppar alpha), acyl-coenzyme a oxidase 1 (Acox1), and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (Pgc-1 alpha). Using intestinal epithelial cell culture, we demonstrated that the lipid-lowering effect of l-arginine was mainly mediated by activating the AMP-activated protein kinase (AMPK) signaling pathway, carnitine palmitoyltransferase 1 (CPT1), and PPAR alpha, as well as mRNA levels for Acox1 and Acox2. Collectively, our results suggest that dietary l-arginine supplementation of tilapia changed the intestinal microbiota and activated intestinal fatty acid oxidation. However, future studies are warranted to determine the relationship between microbiota and lipid metabolism in the intestine.

Automated summary

This study found that dietary supplementation of l-arginine in tilapia altered the gut microbiota, activated intestinal fatty acid oxidation, and reduced lipid accretion in the intestine. The mechanism behind this effect may involve activation of the AMPK signaling pathway, CPT1, PPARα, as well as increased mRNA levels of Acox1 and Acox2. Further studies are needed to explore the relationship between microbiota and lipid metabolism in the intestine.