Impact of Dietary Crude Protein Level on Hepatic Lipid Metabolism in Weaned Female Piglets

SIMPLE SUMMARY: It has been reported that a high crude protein diet could reverse the diet-induced lipid accumulation in the liver of mice and rodents. However, in vivo data supporting a functional role of a high crude protein diet on hepatic lipid metabolism-associated genes and proteins in weaned piglets is not available. In the present study, we aimed to provide a mechanistic insight into alterations in the hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis in response to different dietary crude protein levels. Our results demonstrated that dietary crude protein could regulate hepatic lipid metabolism through regulating hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis. The result indicated an important role of dietary crude protein in regulating hepatic lipid metabolism in weaned piglets. ABSTRACT: Amino acids serve not only as building blocks for proteins, but also as substrates for the synthesis of low-molecular-weight substances involved in hepatic lipid metabolism. In the present study, eighteen weaned female piglets at 35 days of age were fed a corn- and soybean meal-based diet containing 20%, 17%, or 14% crude protein (CP), respectively. We found that 17% or 20% CP administration reduced the triglyceride and cholesterol concentrations, while enhanced high-density lipoprotein cholesterol (HDL-C) concentration in serum. Western blot analysis showed that piglets in the 20% CP group had higher protein abundance of hormone-sensitive triglyceride lipase (HSL) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), as compared with other groups. Moreover, the mRNA expression of sterol regulatory element binding transcription factor 1 (SREBPF1), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD) were lower in the 17% or 20% CP group, compared with those of the piglets administered with 14% CP. Of note, the mRNA level of acetyl-CoA carboxylase alpha (ACACα) was lower in the 17% CP group, compared with other groups. Additionally, the mRNA level of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor alpha α (PPARα), glucose-6-phosphatase catalytic subunit (G6PC), and phosphoenolpyruvate carboxykinase 1 (PKC1) in the liver of piglets in the 20% CP group were higher than those of the 14% CP group. Collectively, our results demonstrated that dietary CP could regulate hepatic lipid metabolism through altering hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis.