Meat Protein in High-Fat Diet Induces Adipogensis and Dyslipidemia by Altering Gut Microbiota and Endocannabinoid Dysregulation in the Adipose Tissue of Mice.

Abstract

Endocannabinoids modulate insulin and adipokine expression in adipocytes through cannabinoid receptors and their levels are elevated during hyperglycemia and obesity, but little is known about how diets affect them. We assessed the effects of dietary casein, chicken, beef, and pork proteins in a high-fat diet mode, on endocannabinoids, adipogenesis, and biomarkers associated with dyslipemdia. A high-fat beef or chicken diet upregulated cannabinoid 1 receptor, N-acyl phosphatidylethanolamine-selective phospholipase-D and diacylglycerol lipase α in adipose tissue and reduced the immunoreactivity of mitochondrial uncoupling protein 1 in brown adipose tissue. In addition, the high-fat diets with beef and chicken protein had a significant impact on adipocyte differentiation and mitochondrial biogenesis in obese mice. A 16S rRNA gene sequencing indicated that high-fat diets, regardless of the protein source, significantly enhanced the ratio of Firmicutes to Bacteroidetes in colon. Meat proteins in a high-fat diet significantly decreased the relative abundances of Akkermansia and Bifidobacteria but enhanced the lipopolysaccharides level in the serum, which promoted the adipogenesis process by causing dysregulation in the endocannabinoid receptors. Consumption of meat protein with high-fat-induced adiposity, visceral obesity, and dyslipidemia reduced the thermogenesis and had a distinctive effect on the mitochondrial biogenesis compared with casein protein.