Compared with Milk Protein, a Wheat and Pea Protein Blend Reduces High-Fat, High-Sucrose Induced Metabolic Dysregulations while Similarly Supporting Tissue Protein Anabolism in Rats.

ABSTRACT

BACKGROUND: Plant proteins (PPs) have been associated with better cardiovascular health than animal proteins (APs) in epidemiological studies. However, the underlying metabolic mechanisms remain mostly unknown. OBJECTIVES: Using a combination of cutting-edge isotopic methods, we aimed to better characterize the differences in protein and energy metabolisms induced by dietary protein sources (PP compared with AP) in a prudent or western dietary context. METHODS: Male Wistar rats (n = 44, 8 wk old) were fed for 4.5 mo with isoproteic diets differing in their protein isolate sources, either AP (100% milk) or PP (50%50% pea wheat) and being normal (NFS) or high (HFS) in sucrose (6% or 15% kcal) and saturated fat (7% or 20% kcal), respectively. We measured body weight and composition, hepatic enzyme activities and lipid content, and plasma metabolites. In the intestine, liver, adipose tissues, and skeletal muscles, we concomitantly assessed the extent of amino acid (AA) trafficking using a 15N natural abundance method, the rates of macronutrient routing to dispensable AA using a 13C natural abundance method, and the metabolic fluxes of protein synthesis (PS) and de novo lipogenesis using a 2H labeling method. Data were analyzed using ANOVA and Mixed models. RESULTS: At the whole-body level, PP limited HFS-induced insulin resistance (-27% in HOMA-IR between HFS groups, P < 0.05). In the liver, PP induced lower lipid content (-17%, P < 0.01) and de novo lipogenesis (-24%, P < 0.05). In the different tissues studied, PP induced higher AA transamination accompanied by higher routings of dietary carbohydrates and lipids toward dispensable AA synthesis by glycolysis and ß-oxidation, resulting in similar tissue PS and protein mass. CONCLUSIONS: In growing rats, compared with AP, a balanced blend of PP similarly supports protein anabolism while better limiting whole-body and tissue metabolic dysregulations through mechanisms related to their less optimal AA profile for direct channeling to PS.