title: Dietary L-arginine supplementation differentially regulates expression of lipid-metabolic genes in porcine adipose tissue and skeletal muscle.
abstract: Obesity is a major health crisis worldwide and new treatments are needed to fight this epidemic. Using the swine model, we recently reported that dietary L-arginine (Arg) supplementation promotes muscle gain and reduces body-fat accretion. The present study tested the hypothesis that Arg regulates expression of key genes involved in lipid metabolism in skeletal muscle and white adipose tissue. Sixteen 110-day-old barrows were fed for 60 days a corn- and soybean-meal-based diet supplemented with 1.0% Arg or 2.05% L-alanine (isonitrogenous control). Blood samples, longissimus dorsi muscle and overlying subcutaneous adipose tissue were obtained from 170-day-old pigs for biochemical studies. Serum concentrations of leptin, alanine and glutamine were lower, but those for Arg and proline were higher in Arg-supplemented pigs than in control pigs. The percentage of oleic acid was higher but that of stearic acid and linoleic acid was lower in muscle of Arg-supplemented pigs, compared with control pigs. Dietary Arg supplementation increased mRNA levels for fatty acid synthase in muscle, while decreasing those for lipoprotein lipase, glucose transporter-4, and acetyl-coenzyme A carboxylase-α in adipose tissue. Additionally, mRNA levels for hormone sensitive lipase were higher in adipose tissue of Arg-supplemented pigs compared with control pigs. These results indicate that Arg differentially regulates expression of fat-metabolic genes in skeletal muscle and white adipose tissue, therefore favoring lipogenesis in muscle but lipolysis in adipose tissue. Our novel findings provide a biochemical basis for explaining the beneficial effect of Arg in improving the metabolic profile in mammals (including obese humans).
authors.affiliation: Laboratory of Animal Nutrition and Human Health and Key Laboratory of Agro-ecology, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, Hunan 410125, China.
authors.forename: Bie
authors.initials: B
authors.lastname: Tan
authors.forename: Yulong
authors.initials: Y
authors.lastname: Yin
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Liu
authors.forename: Wenjie
authors.initials: W
authors.lastname: Tang
authors.forename: Haijun
authors.initials: H
authors.lastname: Xu
authors.forename: Xiangfeng
authors.initials: X
authors.lastname: Kong
authors.forename: Xinguo
authors.initials: X
authors.lastname: Li
authors.forename: Kang
authors.initials: K
authors.lastname: Yao
authors.forename: Wanting
authors.initials: W
authors.lastname: Gu
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Smith
authors.forename: Guoyao
authors.initials: G
authors.lastname: Wu
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000032:analysis; D052436:Adipose Tissue, White / Q000187:drug effects* / Q000378:metabolism; D000409:Alanine / Q000097:blood; D000818:Animals; D001120:Arginine / Q000008:administration & dosage* / Q000378:metabolism; D055598:Chemical Phenomena; D019587:Dietary Supplements; D051275:Glucose Transporter Type 4 / Q000032:analysis; D005973:Glutamine / Q000097:blood; D020738:Leptin / Q000097:blood; D019787:Linoleic Acid / Q000032:analysis; D050356:Lipid Metabolism; D050155:Lipogenesis / Q000187:drug effects; D008066:Lipolysis; D008071:Lipoprotein Lipase / Q000032:analysis; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D013229:Stearic Acids / Q000032:analysis; D013552:Swine
chemical_list: D051275:Glucose Transporter Type 4; D020738:Leptin; D012333:RNA, Messenger; D013229:Stearic Acids; D005973:Glutamine; D001120:Arginine; D019787:Linoleic Acid; D008071:Lipoprotein Lipase; D000103:Acetyl-CoA Carboxylase; D000409:Alanine