title: Dietary β-conglycinin prevents fatty liver induced by a high-fat diet by a decrease in peroxisome proliferator-activated receptor γ2 protein.
abstract: Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). Mice fed a high-fat diet, especially that of saturated-fat-rich oil, develop fatty liver with an increase in peroxisome proliferator-activated receptor (PPAR) γ2 protein in liver. The fatty liver induced by a high-fat diet is improved by knockdown of liver PPARγ2. In this study, we investigated whether β-conglycinin (a major protein of soy protein) could reduce PPARγ2 protein and prevent high-fat-diet-induced fatty liver in ddY mice. Mice were fed a high-starch diet (70 energy% [en%] starch) plus 20% (wt/wt) sucrose in their drinking water or a high-safflower-oil diet (60 en%) or a high-butter diet (60 en%) for 11 weeks, by which fatty liver is developed. As a control, mice were fed a high-starch diet with drinking water. Either β-conglycinin or casein (control) was given as dietary protein. β-Conglycinin supplementation completely prevented fatty liver induced by each type of diet, along with a reduction in adipose tissue weight. β-Conglycinin decreased sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP) messenger RNAs (mRNAs) in sucrose-supplemented mice, whereas it decreased PPARγ2 mRNA (and its target genes CD36 and FSP27), but did not decrease SREBP-1c and ChREBP mRNAs, in mice fed a high-fat diet. β-Conglycinin decreased PPARγ2 protein and liver triglyceride (TG) concentration in a dose-dependent manner in mice fed a high-butter diet; a significant decrease in liver TG concentration was observed at a concentration of 15 en%. In conclusion, β-conglycinin effectively prevents fatty liver induced by a high-fat diet through a decrease in liver PPARγ2 protein.
authors: Nutritional Science Program, National Institute of Health and Nutrition, Tokyo 162-8636, Japan. tomo0322@nih.go.jp
authors: Tomomi
authors: T
authors: Yamazaki
authors: Kyoko
authors: K
authors: Kishimoto
authors: Shinji
authors: S
authors: Miura
authors: Osamu
authors: O
authors: Ezaki
mesh_terms: D000818:Animals; D052179:Antigens, Plant / Q000494:pharmacology*; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D059305:Diet, High-Fat / Q000009:adverse effects*; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D004734:Energy Metabolism / Q000187:drug effects; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D005916:Globulins / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009687:Nuclear Proteins / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D019518:Postprandial Period; D012450:Safflower Oil / Q000494:pharmacology; D055314:Seed Storage Proteins / Q000494:pharmacology*; D030262:Soybean Proteins / Q000494:pharmacology*; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics; D013395:Sucrose / Q000494:pharmacology; D014157:Transcription Factors / Q000235:genetics; D014280:Triglycerides / Q000378:metabolism
chemical_list: D052179:Antigens, Plant; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D005916:Globulins; C506001:Mlxipl protein, mouse; D009687:Nuclear Proteins; D047495:PPAR gamma; D055314:Seed Storage Proteins; D030262:Soybean Proteins; C497388:Srebf1 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D014280:Triglycerides; C013894:beta-conglycinin protein, Glycine max; D013395:Sucrose; D012450:Safflower Oil