Long-Term Protein Restriction Modulates Lipid Metabolism in White Adipose Tissues and Alters Colonic Microbiota of Shaziling Pigs

Abstract

Obesity is a matter of concern to the public. Abundant evidence has been accumulated that nutritional intervention is a promising strategy to address this health issue. The objective of this study is to investigate alterations in the lipid metabolism in white adipose tissues and the gut microbiota of Shaziling pigs challenged by long-term protein restriction. Results showed that compared with the control group, reducing the protein level by 20% (−20%) increased the mRNA abundance of FABP4 in white adipose tissues (P < 0.05). This occurred in conjunction with increases in PPARγ protein expression. Conversely, the protein expression of C/EBPα was reduced in the −20% group (P < 0.05). Moreover, the −20% group had increased/decreased phosphorylation of AMPKα/mTOR, respectively (P < 0.05). As for the colonic gut microbiota, a 20% reduction in the protein level led to increased Lachnospiraceae XPB1014 group abundance at the genus level (P < 0.01). Collectively, these results indicated that a 20% protein reduction could modulate lipid metabolism and alter the colonic microbiota of Shaziling pigs, an approach which might be translated into a treatment for obesity.

β-Hydroxy-β-methyl Butyrate Regulates the Lipid Metabolism, Mitochondrial Function, and Fat Browning of Adipocytes

“…Cell samples were collected by using RIPA Lysis Buffer (Beyotime Biotechnology, Shanghai, China) containing protease inhibitor cocktail tablets and phosphatase inhibitor cocktail tablets (Sigma-Aldrich Trading Co., Ltd., Shanghai, China). The next procedures were conducted as previously described [26]. The primary antibodies used were the following: CCAAT/enhancer-binding protein alpha (C/EBPα, 18311-1-AP, Proteintech, Chicago, IL, USA, 1:500); peroxisome proliferator-activated receptor gamma (PPARγ, 2435S, CST, Boston, MA, USA, 1:1000); phosphorylated (p)-AMP-activated protein kinase AMPK (p-AMPK, 2535S, CST, Boston, MA, USA, 1:1000); phosphorylated (p)-silent information regulator 2 related enzyme 1 (p-Sirt1, 2314S, CST, Boston, MA, USA, 1:2000); hormonesensitive lipase (HSL, 4107S, CST, Boston, MA, USA, 1:1000); lipoprotein lipase (LPL, ab137821, Abcam, Cambridge, Cambs, UK, 1:1000); uncoupled protein 3 (UCP3, 10750-1-AP, Proteintech, Chicago, IL, USA, 1:500); PGC-1α (ab54481, Proteintech, Chicago, IL, USA, 1:3000); PRDM16 (ab106410, Abcam, Cambridge, Cambs, UK, 2 µg/mL); UCP1 (14670, CST, Boston, MA, USA, 1:1000); glyceraldehyde-3-phosphate dehydrogenase (GAPDH, 60004-1-Ig, Proteintech, Chicago, IL, USA, 1:7000).…”