Dietary β-conglycinin prevents fatty liver induced by a high-fat diet by a decrease in peroxisome...

Area of Science:

• Nutrition Science
• Metabolic Research

Background:

• High sucrose/fructose or fat diets induce hepatic steatosis (fatty liver).
• Fatty liver in mice fed high-fat diets correlates with increased liver peroxisome proliferator-activated receptor (PPAR) γ2 protein.
• Liver-specific PPARγ2 knockdown ameliorates high-fat diet-induced fatty liver.

Purpose of the Study:

• To investigate if β-conglycinin, a soy protein component, can reduce PPARγ2 protein.
• To determine if β-conglycinin prevents high-fat diet-induced fatty liver in ddY mice.
• To elucidate the molecular mechanisms by which β-conglycinin exerts its effects.

Main Methods:

• Mice were fed high-starch/sucrose, high-safflower oil, or high-butter diets for 11 weeks.
• Dietary protein was either β-conglycinin or casein (control).
• Gene expression (mRNAs for SREBP-1c, ChREBP, PPARγ2, CD36, FSP27) and protein levels (PPARγ2) were analyzed, along with liver triglyceride (TG) content and adipose tissue weight.

Main Results:

• β-Conglycinin supplementation completely prevented fatty liver and reduced adipose tissue weight across all tested diets.
• In sucrose-fed mice, β-conglycinin decreased sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP) mRNAs.
• In high-fat diet-fed mice, β-conglycinin decreased PPARγ2 mRNA and its target genes but not SREBP-1c or ChREBP mRNAs; it dose-dependently reduced PPARγ2 protein and liver TG.

Conclusions:

• β-Conglycinin effectively prevents high-fat diet-induced fatty liver.
• The preventive effect is mediated by a reduction in liver PPARγ2 protein.
• β-Conglycinin demonstrates potential as a dietary intervention for fatty liver disease.