Adiponectin suppresses gluconeogenic gene expression in mouse hepatocytes independent of LKB1-AMPK signaling
The adipocyte-derived hormone adiponectin signals from the fat storage depot to regulate metabolism in peripheral tissues. Inversely correlated with body fat levels, adiponectin reduction in obese individuals may play a causal role in the symptoms of metabolic syndrome. Adiponectin lowers serum gluc...
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| Veröffentlicht in: | The Journal of clinical investigation Jg. 121; H. 6; S. 2518 - 2528 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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United States
American Society for Clinical Investigation
01.06.2011
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| ISSN: | 0021-9738, 1558-8238, 1558-8238 |
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| Abstract | The adipocyte-derived hormone adiponectin signals from the fat storage depot to regulate metabolism in peripheral tissues. Inversely correlated with body fat levels, adiponectin reduction in obese individuals may play a causal role in the symptoms of metabolic syndrome. Adiponectin lowers serum glucose through suppression of hepatic glucose production, an effect attributed to activation of AMPK. Here, we investigated the signaling pathways that mediate the effects of adiponectin by studying mice with inducible hepatic deletion of LKB1, an upstream regulator of AMPK. We found that loss of LKB1 in the liver partially impaired the ability of adiponectin to lower serum glucose, though other actions of the hormone were preserved, including reduction of gluconeogenic gene expression and hepatic glucose production as assessed by euglycemic hyperinsulinemic clamp. Furthermore, in primary mouse hepatocytes, the absence of LKB1, AMPK, or the transcriptional coactivator CRTC2 did not prevent adiponectin from inhibiting glucose output or reducing gluconeogenic gene expression. These results reveal that whereas some of the hormone's actions in vivo may be LKB1 dependent, substantial LKB1-, AMPK-, and CRTC2-independent signaling pathways also mediate effects of adiponectin. |
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| AbstractList | The adipocyte-derived hormone adiponectin signals from the fat storage depot to regulate metabolism in peripheral tissues. Inversely correlated with body fat levels, adiponectin reduction in obese individuals may play a causal role in the symptoms of metabolic syndrome. Adiponectin lowers serum glucose through suppression of hepatic glucose production, an effect attributed to activation of AMPK. Here, we investigated the signaling pathways that mediate the effects of adiponectin by studying mice with inducible hepatic deletion of LKB1, an upstream regulator of AMPK. We found that loss of LKB1 in the liver partially impaired the ability of adiponectin to lower serum glucose, though other actions of the hormone were preserved, including reduction of gluconeogenic gene expression and hepatic glucose production as assessed by euglycemic hyperinsulinemic clamp. Furthermore, in primary mouse hepatocytes, the absence of LKB1, AMPK, or the transcriptional coactivator CRTC2 did not prevent adiponectin from inhibiting glucose output or reducing gluconeogenic gene expression. These results reveal that whereas some of the hormone's actions in vivo may be LKB1 dependent, substantial LKB1-, AMPK-, and CRTC2-independent signaling pathways also mediate effects of adiponectin. The adipocyte-derived hormone adiponectin signals from the fat storage depot to regulate metabolism in peripheral tissues. Inversely correlated with body fat levels, adiponectin reduction in obese individuals may play a causal role in the symptoms of metabolic syndrome. Adiponectin lowers serum glucose through suppression of hepatic glucose production, an effect attributed to activation of AMPK. Here, we investigated the signaling pathways that mediate the effects of adiponectin by studying mice with inducible hepatic deletion of LKB1, an upstream regulator of AMPK. We found that loss of LKB1 in the liver partially impaired the ability of adiponectin to lower serum glucose, though other actions of the hormone were preserved, including reduction of gluconeogenic gene expression and hepatic glucose production as assessed by euglycemic hyperinsulinemic clamp. Furthermore, in primary mouse hepatocytes, the absence of LKB1, AMPK, or the transcriptional coactivator CRTC2 did not prevent adiponectin from inhibiting glucose output or reducing gluconeogenic gene expression. These results reveal that whereas some of the hormone's actions in vivo may be LKB1 dependent, substantial LKB1-, AMPK-, and CRTC2-independent signaling pathways also mediate effects of adiponectin.The adipocyte-derived hormone adiponectin signals from the fat storage depot to regulate metabolism in peripheral tissues. Inversely correlated with body fat levels, adiponectin reduction in obese individuals may play a causal role in the symptoms of metabolic syndrome. Adiponectin lowers serum glucose through suppression of hepatic glucose production, an effect attributed to activation of AMPK. Here, we investigated the signaling pathways that mediate the effects of adiponectin by studying mice with inducible hepatic deletion of LKB1, an upstream regulator of AMPK. We found that loss of LKB1 in the liver partially impaired the ability of adiponectin to lower serum glucose, though other actions of the hormone were preserved, including reduction of gluconeogenic gene expression and hepatic glucose production as assessed by euglycemic hyperinsulinemic clamp. Furthermore, in primary mouse hepatocytes, the absence of LKB1, AMPK, or the transcriptional coactivator CRTC2 did not prevent adiponectin from inhibiting glucose output or reducing gluconeogenic gene expression. These results reveal that whereas some of the hormone's actions in vivo may be LKB1 dependent, substantial LKB1-, AMPK-, and CRTC2-independent signaling pathways also mediate effects of adiponectin. |
| Audience | Academic |
| Author | Chu, Qingwei Kaestner, Klaus H. Miller, Russell A. Foretz, Marc Ahima, Rexford S. Birnbaum, Morris J. Le Lay, John Scherer, Philipp E. Viollet, Benoit |
| AuthorAffiliation | 1 The Institute of Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 2 Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA. 3 Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris, France. 4 Inserm U1016, Paris, France |
| AuthorAffiliation_xml | – name: 1 The Institute of Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 2 Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA. 3 Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris, France. 4 Inserm U1016, Paris, France |
| Author_xml | – sequence: 1 givenname: Russell A. surname: Miller fullname: Miller, Russell A. – sequence: 2 givenname: Qingwei surname: Chu fullname: Chu, Qingwei – sequence: 3 givenname: John surname: Le Lay fullname: Le Lay, John – sequence: 4 givenname: Philipp E. surname: Scherer fullname: Scherer, Philipp E. – sequence: 5 givenname: Rexford S. surname: Ahima fullname: Ahima, Rexford S. – sequence: 6 givenname: Klaus H. surname: Kaestner fullname: Kaestner, Klaus H. – sequence: 7 givenname: Marc surname: Foretz fullname: Foretz, Marc – sequence: 8 givenname: Benoit surname: Viollet fullname: Viollet, Benoit – sequence: 9 givenname: Morris J. surname: Birnbaum fullname: Birnbaum, Morris J. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21606593$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Adiponectin - pharmacology Adiponectin - physiology Aminoimidazole Carboxamide - analogs & derivatives Aminoimidazole Carboxamide - pharmacology AMP-Activated Protein Kinases - deficiency AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - physiology Animals Biomedical research Blood Glucose - analysis Body fat Cardiovascular disease Dextrose Fasting - blood Fatty acids Gene Deletion Gene expression Gene Expression Regulation - drug effects Genetic research Gluconeogenesis - drug effects Gluconeogenesis - genetics Glucose Glucose Clamp Technique Hepatocytes - drug effects Hepatocytes - metabolism Insulin - blood Insulin resistance Kinases Liver Metabolic syndrome Mice Organ Specificity Oxidation Phosphorylation Physiological aspects Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - physiology Proteins Recombinant Fusion Proteins - physiology Ribonucleotides - pharmacology Signal transduction Signal Transduction - drug effects Signal Transduction - physiology Trans-Activators - deficiency Trans-Activators - genetics Trans-Activators - physiology Transcription Factors Transcription, Genetic - drug effects |
| Title | Adiponectin suppresses gluconeogenic gene expression in mouse hepatocytes independent of LKB1-AMPK signaling |
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