R
Robert C. Noland
Researcher at Pennington Biomedical Research Center
Publications - 56
Citations - 4496
Robert C. Noland is an academic researcher from Pennington Biomedical Research Center. The author has contributed to research in topics: Insulin resistance & Skeletal muscle. The author has an hindex of 24, co-authored 50 publications receiving 3863 citations. Previous affiliations of Robert C. Noland include Pontifical Catholic University of Chile & Duke University.
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Journal ArticleDOI
Mitochondrial Overload and Incomplete Fatty Acid Oxidation Contribute to Skeletal Muscle Insulin Resistance
Timothy R. Koves,John R. Ussher,Robert C. Noland,Dorothy H. Slentz,Merrie Mosedale,Olga Ilkayeva,James R. Bain,Robert Stevens,Jason R.B. Dyck,Christopher B. Newgard,Gary D. Lopaschuk,Deborah M. Muoio +11 more
TL;DR: Target metabolomics finds that obesity-related insulin resistance in skeletal muscle is characterized by excessive beta-oxidation, impaired switching to carbohydrate substrate during the fasted-to-fed transition, and coincident depletion of organic acid intermediates of the tricarboxylic acid cycle.
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FGF21 is an endocrine signal of protein restriction
Thomas Laeger,Tara M. Henagan,Diana C. Albarado,Leanne M. Redman,George A. Bray,Robert C. Noland,Heike Münzberg,Susan M. Hutson,Thomas W. Gettys,Michael W. Schwartz,Christopher D. Morrison +10 more
TL;DR: FGF21 represents an endocrine signal of protein restriction, which acts to coordinate metabolism and growth during periods of reduced protein intake and that FGF21 is required for behavioral and metabolic responses to protein restriction.
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Muscle-Specific Deletion of Carnitine Acetyltransferase Compromises Glucose Tolerance and Metabolic Flexibility
Deborah M. Muoio,Robert C. Noland,Jean Paul Kovalik,Sarah E. Seiler,Michael N. Davies,Karen L. DeBalsi,Olga Ilkayeva,Robert Stevens,Indu Kheterpal,Jingying Zhang,Jeffrey D. Covington,Sudip Bajpeyi,Eric Ravussin,William E. Kraus,Timothy R. Koves,Randall L. Mynatt +15 more
TL;DR: An essential role is identified for the mitochondrial matrix enzyme, carnitine acetyltransferase (CrAT), in regulating substrate switching and glucose tolerance and offer therapeutically relevant insights into the molecular basis of metabolic inflexibility.
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Carnitine Insufficiency Caused by Aging and Overnutrition Compromises Mitochondrial Performance and Metabolic Control
Robert C. Noland,Timothy R. Koves,Sarah E. Seiler,Helen Lum,Robert M. Lust,Olga Ilkayeva,Robert Stevens,Fausto G. Hegardt,Deborah M. Muoio +8 more
TL;DR: The results implicate carnitine insufficiency and reduced CrAT activity as reversible components of the metabolic syndrome.
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Subsarcolemmal and intermyofibrillar mitochondria play distinct roles in regulating skeletal muscle fatty acid metabolism
Timothy R. Koves,Robert C. Noland,Andrew L. Bates,Sarah T. Henes,Deborah M. Muoio,Ronald N. Cortright +5 more
TL;DR: It is demonstrated that endurance exercise provokes subpopulation-specific changes in mitochondrial function that are characterized by enhanced fatty acid oxidation and modified CPT1beta-malonyl-CoA dynamics.