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  • 1
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    Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta) (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-02
    Description: Glucose homeostasis depends on insulin responsiveness in target tissues, most importantly, muscle and liver. The critical initial steps in insulin action include phosphorylation of scaffolding proteins and activation of phosphatidylinositol 3-kinase. These early events lead to activation of the serine-threonine protein kinase Akt, also known as protein kinase B. We show that mice deficient in Akt2 are impaired in the ability of insulin to lower blood glucose because of defects in the action of the hormone on liver and skeletal muscle. These data establish Akt2 as an essential gene in the maintenance of normal glucose homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, H -- Mu, J -- Kim, J K -- Thorvaldsen, J L -- Chu, Q -- Crenshaw, E B 3rd -- Kaestner, K H -- Bartolomei, M S -- Shulman, G I -- Birnbaum, M J -- GM07229/GM/NIGMS NIH HHS/ -- P30 19525/PHS HHS/ -- P30 DK50306/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R01 DK56886/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 1;292(5522):1728-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11387480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Deoxyglucose/metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Female ; Gene Targeting ; Glucose/*metabolism ; Glucose Clamp Technique ; Glucose Tolerance Test ; Homeostasis ; Insulin/administration & dosage/blood/*metabolism ; *Insulin Resistance/genetics/physiology ; Islets of Langerhans/cytology/physiology ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle, Skeletal/enzymology/metabolism ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Quantitation of hepatic glycogenolysis and gluconeogenesis in fasting humans with 13C NMR (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: The rate of net hepatic glycogenolysis was assessed in humans by serially measuring hepatic glycogen concentration at 3- to 12-hour intervals during a 68-hour fast with 13C nuclear magnetic resonance spectroscopy. The net rate of gluconeogenesis was calculated by subtracting the rate of net hepatic glycogenolysis from the rate of glucose production in the whole body measured with tritiated glucose. Gluconeogenesis accounted for 64 +/- 5% (mean +/- standard error of the mean) of total glucose production during the first 22 hours of fasting. In the subsequent 14-hour and 18-hour periods of the fast, gluconeogenesis accounted for 82 +/- 5% and 96 +/- 1% of total glucose production, respectively. These data show that gluconeogenesis accounts for a substantial fraction of total glucose production even during the first 22 hours of a fast in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothman, D L -- Magnusson, I -- Katz, L D -- Shulman, R G -- Shulman, G I -- DK-34576/DK/NIDDK NIH HHS/ -- DK-40936/DK/NIDDK NIH HHS/ -- MO1-RR-00125-26/RR/NCRR NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948033" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Blood Glucose/metabolism ; Carbon Isotopes ; Fasting ; Female ; Glucagon/blood ; *Gluconeogenesis ; Humans ; Hydrocortisone/blood ; Insulin/blood ; Kinetics ; Liver/*metabolism ; Liver Glycogen/*metabolism ; Magnetic Resonance Spectroscopy/methods ; Male ; Nitrogen/*urine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Mitochondrial dysfunction in the elderly: possible role in insulin resistance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: Insulin resistance is a major factor in the pathogenesis of type 2 diabetes in the elderly. To investigate how insulin resistance arises, we studied healthy, lean, elderly and young participants matched for lean body mass and fat mass. Elderly study participants were markedly insulin-resistant as compared with young controls, and this resistance was attributable to reduced insulin-stimulated muscle glucose metabolism. These changes were associated with increased fat accumulation in muscle and liver tissue assessed by 1H nuclear magnetic resonance (NMR) spectroscopy, and with a approximately 40% reduction in mitochondrial oxidative and phosphorylation activity, as assessed by in vivo 13C/31P NMR spectroscopy. These data support the hypothesis that an age-associated decline in mitochondrial function contributes to insulin resistance in the elderly.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004429/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Kitt Falk -- Befroy, Douglas -- Dufour, Sylvie -- Dziura, James -- Ariyan, Charlotte -- Rothman, Douglas L -- DiPietro, Loretta -- Cline, Gary W -- Shulman, Gerald I -- K-23 DK-02347/DK/NIDDK NIH HHS/ -- K23 DK002734/DK/NIDDK NIH HHS/ -- K23 DK002734-04/DK/NIDDK NIH HHS/ -- M01 RR-00125/RR/NCRR NIH HHS/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P60 AG-10469/AG/NIA NIH HHS/ -- R01 AG-09872/AG/NIA NIH HHS/ -- R01 AG023686/AG/NIA NIH HHS/ -- R01 AG023686-01A1/AG/NIA NIH HHS/ -- R01 DK-49230/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 May 16;300(5622):1140-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750520" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging/metabolism ; Blood Glucose/metabolism ; Body Mass Index ; Female ; Humans ; Insulin/metabolism ; *Insulin Resistance ; Liver/metabolism ; Male ; Middle Aged ; Mitochondria/*metabolism ; Mitochondrial Diseases/blood/*complications/metabolism ; Muscle, Skeletal/metabolism ; Nuclear Magnetic Resonance, Biomolecular ; Oxidation-Reduction ; Oxygen Consumption ; Phosphorylation ; Triglycerides/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Cyclin D1-Cdk4 controls glucose metabolism independently of cell cycle progression (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-05-30
    Description: Insulin constitutes a principal evolutionarily conserved hormonal axis for maintaining glucose homeostasis; dysregulation of this axis causes diabetes. PGC-1alpha (peroxisome-proliferator-activated receptor-gamma coactivator-1alpha) links insulin signalling to the expression of glucose and lipid metabolic genes. The histone acetyltransferase GCN5 (general control non-repressed protein 5) acetylates PGC-1alpha and suppresses its transcriptional activity, whereas sirtuin 1 deacetylates and activates PGC-1alpha. Although insulin is a mitogenic signal in proliferative cells, whether components of the cell cycle machinery contribute to its metabolic action is poorly understood. Here we report that in mice insulin activates cyclin D1-cyclin-dependent kinase 4 (Cdk4), which, in turn, increases GCN5 acetyltransferase activity and suppresses hepatic glucose production independently of cell cycle progression. Through a cell-based high-throughput chemical screen, we identify a Cdk4 inhibitor that potently decreases PGC-1alpha acetylation. Insulin/GSK-3beta (glycogen synthase kinase 3-beta) signalling induces cyclin D1 protein stability by sequestering cyclin D1 in the nucleus. In parallel, dietary amino acids increase hepatic cyclin D1 messenger RNA transcripts. Activated cyclin D1-Cdk4 kinase phosphorylates and activates GCN5, which then acetylates and inhibits PGC-1alpha activity on gluconeogenic genes. Loss of hepatic cyclin D1 results in increased gluconeogenesis and hyperglycaemia. In diabetic models, cyclin D1-Cdk4 is chronically elevated and refractory to fasting/feeding transitions; nevertheless further activation of this kinase normalizes glycaemia. Our findings show that insulin uses components of the cell cycle machinery in post-mitotic cells to control glucose homeostasis independently of cell division.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076706/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076706/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Yoonjin -- Dominy, John E -- Choi, Yoon Jong -- Jurczak, Michael -- Tolliday, Nicola -- Camporez, Joao Paulo -- Chim, Helen -- Lim, Ji-Hong -- Ruan, Hai-Bin -- Yang, Xiaoyong -- Vazquez, Francisca -- Sicinski, Piotr -- Shulman, Gerald I -- Puigserver, Pere -- DK059635/DK/NIDDK NIH HHS/ -- F32 DK083871/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 CA083688/CA/NCI NIH HHS/ -- R01 CA108420/CA/NCI NIH HHS/ -- R01 DK069966/DK/NIDDK NIH HHS/ -- R01 DK089098/DK/NIDDK NIH HHS/ -- R01069966/PHS HHS/ -- R03 DA032468/DA/NIDA NIH HHS/ -- R03 MH092174/MH/NIMH NIH HHS/ -- R24 DK080261/DK/NIDDK NIH HHS/ -- R24DK080261-06/DK/NIDDK NIH HHS/ -- U24 DK059635/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 Jun 26;510(7506):547-51. doi: 10.1038/nature13267. Epub 2014 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Department of Chemistry and Chemical Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Yale's Mouse Metabolic Phenotyping Center and Departments of Internal Medicine and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA. ; Chemical Biology Platform, Broad Institute of Harvard and MIT, 7 Cambridge Center, Cambridge, Massachusetts 02141, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870244" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acids/pharmacology ; Animals ; *Cell Cycle ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclin D1/deficiency/genetics/*metabolism ; Cyclin-Dependent Kinase 4/antagonists & inhibitors/*metabolism ; Diabetes Mellitus/metabolism ; Enzyme Activation ; Fasting ; Gene Deletion ; Gluconeogenesis/genetics ; Glucose/*metabolism ; Glycogen Synthase Kinase 3/metabolism ; Hepatocytes/cytology/drug effects/metabolism ; Histone Acetyltransferases/metabolism ; Homeostasis ; Humans ; Hyperglycemia/metabolism ; Hyperinsulinism/metabolism ; Insulin/*metabolism ; Male ; Mice ; Phosphorylation ; RNA, Messenger/analysis/genetics ; *Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: Fibroblast growth factor (FGF) 19 is an enterokine synthesized and released when bile acids are taken up into the ileum. We show that FGF19 stimulates hepatic protein and glycogen synthesis but does not induce lipogenesis. The effects of FGF19 are independent of the activity of either insulin or the protein kinase Akt and, instead, are mediated through a mitogen-activated protein kinase signaling pathway that activates components of the protein translation machinery and stimulates glycogen synthase activity. Mice lacking FGF15 (the mouse FGF19 ortholog) fail to properly maintain blood concentrations of glucose and normal postprandial amounts of liver glycogen. FGF19 treatment restored the loss of glycogen in diabetic animals lacking insulin. Thus, FGF19 activates a physiologically important, insulin-independent endocrine pathway that regulates hepatic protein and glycogen metabolism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076083/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076083/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kir, Serkan -- Beddow, Sara A -- Samuel, Varman T -- Miller, Paul -- Previs, Stephen F -- Suino-Powell, Kelly -- Xu, H Eric -- Shulman, Gerald I -- Kliewer, Steven A -- Mangelsdorf, David J -- DK40936/DK/NIDDK NIH HHS/ -- DK62434/DK/NIDDK NIH HHS/ -- DK67158/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R01 DK040936-23/DK/NIDDK NIH HHS/ -- R01 DK067158/DK/NIDDK NIH HHS/ -- R01 DK067158-09/DK/NIDDK NIH HHS/ -- R24 DK085638/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-10/DK/NIDDK NIH HHS/ -- U24 DK059635/DK/NIDDK NIH HHS/ -- U24 DK059635-05/DK/NIDDK NIH HHS/ -- U24 DK076169/DK/NIDDK NIH HHS/ -- U24 DK076169-05/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Mar 25;331(6024):1621-4. doi: 10.1126/science.1198363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Medical Center, 6001 Forest Park Road, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Eukaryotic Initiation Factors/metabolism ; Fibroblast Growth Factors/*metabolism/*pharmacology ; Glucose/metabolism ; Glycogen Synthase/metabolism ; Glycogen Synthase Kinase 3/metabolism ; Hep G2 Cells ; Humans ; Insulin/*metabolism/pharmacology ; Liver/drug effects/*metabolism ; Liver Glycogen/*biosynthesis ; MAP Kinase Signaling System ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; *Protein Biosynthesis ; Proto-Oncogene Proteins c-akt/metabolism ; Ribosomal Protein S6/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-28
    Description: Nonalcoholic fatty liver disease (NAFLD) is a major factor in the pathogenesis of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH). The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effects on NAFLD, insulin resistance, and obesity in preclinical models but is too toxic for clinical use. We developed a controlled-release oral formulation of DNP, called CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial uncoupling. In rat models, CRMP reduced hypertriglyceridemia, insulin resistance, hepatic steatosis, and diabetes. It also normalized plasma transaminase concentrations, ameliorated liver fibrosis, and improved hepatic protein synthetic function in a methionine/choline-deficient rat model of NASH. Chronic treatment with CRMP was not associated with any systemic toxicity. These data offer proof of concept that mild hepatic mitochondrial uncoupling may be a safe and effective therapy for the related epidemics of metabolic syndrome, T2D, and NASH.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495920/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perry, Rachel J -- Zhang, Dongyan -- Zhang, Xian-Man -- Boyer, James L -- Shulman, Gerald I -- P30 DK-34989/DK/NIDDK NIH HHS/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- R01 DK-40936/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R24 DK-085638/DK/NIDDK NIH HHS/ -- T32 DK-101019/DK/NIDDK NIH HHS/ -- U24 DK-059635/DK/NIDDK NIH HHS/ -- UL1 TR-000142/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1253-6. doi: 10.1126/science.aaa0672. Epub 2015 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Yale Liver Center, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. gerald.shulman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25721504" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4-Dinitrophenol/*administration & dosage/toxicity ; Animals ; Blood Glucose/metabolism ; Delayed-Action Preparations/*administration & dosage ; Diabetes Mellitus, Type 2/*drug therapy/metabolism ; Glucose Tolerance Test ; Insulin Resistance ; Lipid Metabolism ; Liver Cirrhosis/drug therapy ; Male ; Mice ; Mitochondria, Liver/drug effects/metabolism ; Muscle, Skeletal/metabolism ; Non-alcoholic Fatty Liver Disease/*drug therapy/metabolism ; Oxidation-Reduction ; Proton Ionophores/*administration & dosage/toxicity ; Random Allocation ; Rats ; Rats, Zucker
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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