| The Role of GH in Adipose Tissue: Lessons from Adipose-Specific GH Receptor Gene-Disrupted Mice. | |
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MedLine Citation:
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PMID: 23349524 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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GH receptor (GHR) gene-disrupted mice (GHR-/-) have provided countless discoveries as to the numerous actions of GH. Many of these discoveries highlight the importance of GH in adipose tissue. For example GHR-/- mice are insulin sensitive yet obese with preferential enlargement of the sc adipose depot. GHR-/- mice also have elevated levels of leptin, resistin, and adiponectin, compared with controls leading some to suggest that GH may negatively regulate certain adipokines. To help clarify the role that GH exerts specifically on adipose tissue in vivo, we selectively disrupted GHR in adipose tissue to produce Fat GHR Knockout (FaGHRKO) mice. Surprisingly, FaGHRKOs shared only a few characteristics with global GHR-/- mice. Like the GHR-/- mice, FaGHRKO mice are obese with increased total body fat and increased adipocyte size. However, FaGHRKO mice have increases in all adipose depots with no improvements in measures of glucose homeostasis. Furthermore, resistin and adiponectin levels in FaGHRKO mice are similar to controls (or slightly decreased) unlike the increased levels found in GHR-/- mice, suggesting that GH does not regulate these adipokines directly in adipose tissue in vivo. Other features of FaGHRKO mice include decreased levels of adipsin, a near-normal GH/IGF-1 axis, and minimal changes to a large assortment of circulating factors that were measured such as IGF-binding proteins. In conclusion, specific removal of GHR in adipose tissue is sufficient to increase adipose tissue and decrease circulating adipsin. However, removal of GHR in adipose tissue alone is not sufficient to increase levels of resistin or adiponectin and does not alter glucose metabolism. |
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Authors:
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Edward O List; Darlene E Berryman; Kevin Funk; Elahu S Gosney; Adam Jara; Bruce Kelder; Xinyue Wang; Laura Kutz; Katie Troike; Nicholas Lozier; Vincent Mikula; Ellen R Lubbers; Han Zhang; Clare Vesel; Riia K Junnila; Stuart J Frank; Michal M Masternak; Andrzej Bartke; John J Kopchick |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2013-1-24 |
Journal Detail:
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Title: Molecular endocrinology (Baltimore, Md.) Volume: - ISSN: 1944-9917 ISO Abbreviation: Mol. Endocrinol. Publication Date: 2013 Jan |
Date Detail:
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Created Date: 2013-1-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8801431 Medline TA: Mol Endocrinol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Edison Biotechnology Institute (E.O.L., D.E.B., K.F., E.S.G., A.J., B.K., X.W., L.K, K.T., N.L., V.M., E.R.L., H.Z., C.V, R.K.J., J.J.K.), Department of Specialty Medicine (E.O.L.), School of Applied Health Sciences and Wellness (D.E.B.), Department of Biomedical Sciences (D.E.B., A.J., J.J.K.), Department of Pediatrics (B.K.), Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701; Department of Medicine (S.J.F.), Division of Endocrinology, Diabetes and Metabolism, University of Alabama at Birmingham, Birmingham, Alabama; College of Medicine (M.M.M.), Burnett School of Biomedical Sciences, University of Central Florida, Orlando, Florida 32827; Institute of Human Genetics (M.M.M.), Polish Academy of Sciences, Strzeszyńska 32, 60-479 Poznań, Poland; and Department of Internal Medicine (A.B.), Geriatrics Research, Southern Illinois University School of Medicine, Springfield, Illinois 62702. |
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