title: Supplementing obese Zucker rats with niacin induces the transition of glycolytic to oxidative skeletal muscle fibers.
abstract: In the present study, we tested the hypothesis that niacin increases the oxidative capacity of muscle by increasing the oxidative type I muscle fiber content. Twenty-four obese Zucker rats were assigned to 2 groups of 12 rats that were fed either a control diet (O group) or a diet supplemented with 750 mg/kg diet niacin (O+N group) for 4 wk. In addition, one group of lean rats (L group) was included in the experiment and fed the control diet for 4 wk. Plasma and liver concentrations of TG were markedly greater in obese groups than in the L group but markedly lower in the O+N group than in the O group (P < 0.05). Rats of the O+N group had a higher percentage of oxidative type I fibers and higher mRNA levels of genes encoding regulators of muscle fiber composition (Ppard, Ppargc1a, Ppargc1b), angiogenic factors (Vegfa, Vegfb), and genes involved in fatty acid utilization (Cpt1b, Slc25a20, Slc22a4, Slc22a5, Slc27a1) and oxidative phosphorylation (Cox4i1, Cox6a2) and a higher activity of the mitochondrial oxidative enzyme succinate dehydrogenase in muscle than rats of the O and L groups (P < 0.05). These niacin-induced changes in muscle metabolic phenotype are indicative of an increased capacity of muscle for oxidative utilization of fatty acids and are likely mediated by the upregulation of Ppard, Ppargc1a, and Ppargc1b, which are key regulators of muscle fiber composition, mitochondrial biogenesis, angiogenesis, and genes involved in fatty acid catabolism and oxidative phosphorylation. The increased utilization of fatty acids by muscle might contribute to the strong TG-lowering effect of niacin treatment.
authors.affiliation: Institute of Animal Nutrition and Nutrition Physiology, Justus-Liebig-University, Giessen,Germany.
authors.forename: Robert
authors.initials: R
authors.lastname: Ringseis
authors.forename: Susann
authors.initials: S
authors.lastname: Rosenbaum
authors.forename: Denise K
authors.initials: DK
authors.lastname: Gessner
authors.forename: Lea
authors.initials: L
authors.lastname: Herges
authors.forename: Johanna F
authors.initials: JF
authors.lastname: Kubens
authors.forename: Frank-Christoph
authors.initials: FC
authors.lastname: Mooren
authors.forename: Karsten
authors.initials: K
authors.lastname: Krüger
authors.forename: Klaus
authors.initials: K
authors.lastname: Eder
mesh_terms: D000818:Animals; D019587:Dietary Supplements; D005786:Gene Expression Regulation; D006019:Glycolysis; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008053:Lipid Mobilization; D008099:Liver / Q000378:metabolism; D008297:Male; D063269:Mitochondrial Turnover; D018657:Muscle Fibers, Slow-Twitch / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D009525:Niacin / Q000627:therapeutic use*; D009765:Obesity / Q000178:diet therapy* / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D011924:Rats, Zucker; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D000960:Hypolipidemic Agents; D009124:Muscle Proteins; D012333:RNA, Messenger; D014280:Triglycerides; D009525:Niacin