دورية أكاديمية
أعرض في EDS

Hypermetabolism, hyperphagia, and reduced adiposity in tankyrase-deficient mice.

التفاصيل البيبلوغرافية
العنوان: Hypermetabolism, hyperphagia, and reduced adiposity in tankyrase-deficient mice.
المؤلفون: Yeh TY; Department of Medicine, Endocrine Division, University of California, San Diego, La Jolla, California, USA., Beiswenger KK, Li P, Bolin KE, Lee RM, Tsao TS, Murphy AN, Hevener AL, Chi NW
المصدر: Diabetes [Diabetes] 2009 Nov; Vol. 58 (11), pp. 2476-85. Date of Electronic Publication: 2009 Aug 03.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Diabetes Association Country of Publication: United States NLM ID: 0372763 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1939-327X (Electronic) Linking ISSN: 00121797 NLM ISO Abbreviation: Diabetes Subsets: MEDLINE
أسماء مطبوعة: Publication: Alexandria, VA : American Diabetes Association
Original Publication: [New York, American Diabetes Association]
مواضيع طبية MeSH: Adipose Tissue/*enzymology , Energy Metabolism/*genetics , Hyperphagia/*genetics , Tankyrases/*deficiency, Adipose Tissue, Brown/metabolism ; Animals ; Blastocyst ; Chromosome Mapping ; Chromosomes, Human, Pair 8 ; Embryonic Stem Cells/metabolism ; Fatty Acids/metabolism ; Female ; Glycolysis/drug effects ; Heterozygote ; Humans ; Insulin/pharmacology ; Leptin/blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Mitochondria, Muscle/metabolism ; Muscle, Skeletal/metabolism ; Oxygen Consumption ; Tankyrases/genetics
مستخلص: Objective: Tankyrase (TNKS) is a Golgi-associated poly-ADP-ribose polymerase that is implicated in the regulation of GLUT4 trafficking in 3T3-L1 adipocytes. Its chromosomal locus 8p23.1 is linked to monogenic forms of diabetes in certain kindred. We hypothesize that TNKS is involved in energy homeostasis in mammals.
Research Design and Methods: Gene-trap techniques were used to ablate TNKS expression in mice. Homozygous and wild-type littermates maintained on standard chow were compared.
Results: Wild-type mice express the TNKS protein abundantly in adipose tissue, the brain, and the endocrine pancreas but scarcely in the exocrine pancreas and skeletal muscle. TNKS-deficient mice consume increased amounts of food (by 34%) but have decreased plasma leptin levels and a >50% reduction in epididymal and perirenal fat pad size. Their energy expenditure is increased as assessed by metabolic cage studies and core body temperatures. These changes are not attributable to an increase in physical activity or uncoupled respiration (based on oxygraph analyses of mitochondria isolated from brown fat and skeletal muscle). The heightened thermogenesis of TNKS-deficient mice is apparently fueled by increases in both fatty acid oxidation (based on muscle and liver gene expression analyses and plasma ketone levels) and insulin-stimulated glucose utilization (determined by hyperinsulinemic-euglycemic clamps). Although TNKS deficiency does not compromise insulin-stimulated GLUT4 translocation in primary adipocytes, it leads to the post-transcriptional upregulation of GLUT4 and adiponectin in adipocytes and increases plasma adiponectin levels.
Conclusions: TNKS-deficient mice exhibit increases in energy expenditure, fatty acid oxidation, and insulin-stimulated glucose utilization. Despite excessive food intake, their adiposity is substantially decreased.
References: Mol Cell Biol. 2007 May;27(10):3716-31. (PMID: 17353260)
Nucleic Acids Res. 2002 May 1;30(9):e36. (PMID: 11972351)
J Biol Chem. 2000 Dec 8;275(49):38437-44. (PMID: 10988299)
J Clin Invest. 1996 Nov 15;98(10):2244-50. (PMID: 8941640)
J Clin Invest. 2006 Jul;116(7):1784-92. (PMID: 16823476)
Diabetes. 2004 Feb;53(2):486-91. (PMID: 14747302)
Biochimie. 2008 Jan;90(1):83-92. (PMID: 17825467)
Endocr Rev. 2002 Feb;23(1):38-89. (PMID: 11844744)
Mol Cell Biol. 2007 Jul;27(13):4698-707. (PMID: 17452443)
Kidney Int. 1999 Aug;56(2):461-70. (PMID: 10432384)
J Biol Chem. 2004 Sep 10;279(37):38236-48. (PMID: 15208325)
Physiol Rev. 2006 Apr;86(2):435-64. (PMID: 16601266)
J Biol Chem. 2002 Aug 30;277(35):31887-92. (PMID: 12080061)
Annu Rev Nutr. 2002;22:459-82. (PMID: 12055354)
Proc Natl Acad Sci U S A. 2000 Feb 1;97(3):1125-30. (PMID: 10655495)
Neurosci Biobehav Rev. 1994 Fall;18(3):435-47. (PMID: 7984361)
Cell Metab. 2007 Sep;6(3):181-94. (PMID: 17767905)
J Lipid Res. 2002 Dec;43(12):1997-2006. (PMID: 12454259)
J Pharmacol Exp Ther. 1994 Aug;270(2):752-60. (PMID: 8071868)
Cell Metab. 2009 Mar;9(3):277-86. (PMID: 19254572)
PLoS One. 2008 Jul 09;3(7):e2639. (PMID: 18612384)
Mol Cell Biochem. 2005 Aug;276(1-2):183-92. (PMID: 16132700)
Biochem J. 2007 Mar 1;402(2):279-90. (PMID: 17059388)
Anal Biochem. 1974 Aug;60(2):405-12. (PMID: 4844560)
Diabetes. 2004 May;53(5):1375-84. (PMID: 15111509)
Biochem J. 2008 Feb 1;409(3):623-33. (PMID: 18177270)
Lancet. 1975 Dec 20;2(7947):1243-4. (PMID: 53729)
Nat Rev Mol Cell Biol. 2002 Apr;3(4):267-77. (PMID: 11994746)
Prog Lipid Res. 2002 May;41(3):197-239. (PMID: 11814524)
Ann Hum Genet. 2006 Sep;70(Pt 5):587-93. (PMID: 16907705)
Biochem J. 2006 Nov 1;399(3):415-25. (PMID: 16884355)
Nature. 2005 Jul 21;436(7049):356-62. (PMID: 16034410)
Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3444-9. (PMID: 16492734)
Nat Med. 2002 Nov;8(11):1288-95. (PMID: 12368907)
Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):436-41. (PMID: 16778573)
J Pharmacol Exp Ther. 2008 Mar;324(3):883-93. (PMID: 18165311)
Eur J Biochem. 1986 Jun 2;157(2):415-20. (PMID: 3709541)
معلومات مُعتمدة: T32 DK007044 United States DK NIDDK NIH HHS; K01 DK060484 United States DK NIDDK NIH HHS; DK-060484 United States DK NIDDK NIH HHS; T32 DK-007044 United States DK NIDDK NIH HHS; R21 DK073227 United States DK NIDDK NIH HHS; DK-073227 United States DK NIDDK NIH HHS
المشرفين على المادة: 0 (Fatty Acids)
0 (Insulin)
0 (Leptin)
EC 2.4.2.30 (Tankyrases)
تواريخ الأحداث: Date Created: 20090805 Date Completed: 20100106 Latest Revision: 20211020
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC2768175
DOI: 10.2337/db08-1781
PMID: 19651815
قاعدة البيانات: MEDLINE
الوصف
تدمد:1939-327X
DOI:10.2337/db08-1781