title: Dietary pea protein stimulates bile acid excretion and lowers hepatic cholesterol concentration in rats.
abstract: It has been shown that some dietary plant proteins beneficially influence lipid metabolism in animals. The effect of pea protein in this respect however has not yet been investigated. Therefore, we studied the effect of purified pea protein on the lipid metabolism in rats. Twenty-four rats received diets with either 200 g/kg of casein or purified pea protein for 16 days. Concentrations of triacylglycerols in liver, plasma and lipoproteins did not differ between both groups of rats. However, rats fed the pea protein diet had a lower concentration of total cholesterol in the liver and the very low density lipoproteins (VLDL) fraction than rats fed the casein diet (p < 0.05); cholesterol concentration in plasma, low density lipoproteins (LDL) and high density lipoproteins (HDL) did not differ between both groups. Rats fed pea protein moreover had an increased mRNA concentration of cholesterol-7alpha-hydroxylase in the liver and an increased amount of bile acids excreted via faeces compared with rats fed casein (p < 0.05). Concomitantly, mRNA concentrations of sterol regulatory element-binding protein (SREBP)-2 and its target genes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and LDL receptor in the liver were increased in rats fed pea protein (p < 0.05). The data of this study suggests that pea protein stimulates formation and excretion of bile acids, which leads to a reduced hepatic cholesterol concentration and a reduced secretion of cholesterol via VLDL. An increased gene expression of SREBP-2 and its target genes HMG-CoA reductase and LDL receptor may be a means to compensate for the increased loss of cholesterol for bile acid synthesis.
authors.affiliation: Institute of Agricultural and Nutritional Sciences, Martin-Luther-University of Halle-Wittenberg, Halle, Saale, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Spielmann
authors.forename: G I
authors.initials: GI
authors.lastname: Stangl
authors.forename: K
authors.initials: K
authors.lastname: Eder
mesh_terms: D000821:Animal Feed; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D015243:Cholesterol, VLDL / Q000378:metabolism; D004044:Dietary Proteins / Q000008:administration & dosage; D005786:Gene Expression Regulation / Q000187:drug effects; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D018532:Pisum sativum / Q000737:chemistry*; D010940:Plant Proteins / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D001647:Bile Acids and Salts; D015243:Cholesterol, VLDL; D004044:Dietary Proteins; D010940:Plant Proteins; D012333:RNA, Messenger; D051782:Sterol Regulatory Element Binding Protein 2; D014280:Triglycerides; D002784:Cholesterol