دورية أكاديمية
أعرض في EDS

Adipocyte β-arrestin-2 is essential for maintaining whole body glucose and energy homeostasis.

التفاصيل البيبلوغرافية
العنوان: Adipocyte β-arrestin-2 is essential for maintaining whole body glucose and energy homeostasis.
المؤلفون: Pydi SP; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Jain S; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Tung W; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Cui Y; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Zhu L; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Sakamoto W; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA., Jain S; Mouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 20892, USA., Abel BS; Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 20892, USA., Skarulis MC; Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 20892, USA., Liu J; Center for Molecular Medicine, National Heart, Lung, and Blood Institute, Bethesda, MD, 20892, USA., Huynh T; Section on Medical Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, 20892, USA., Pacak K; Section on Medical Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, 20892, USA., Caron MG; Department of Cell Biology, Duke University Medical Center, Durham, NC, 27710, USA., Gavrilova O; Mouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 20892, USA., Finkel T; Center for Molecular Medicine, National Heart, Lung, and Blood Institute, Bethesda, MD, 20892, USA., Wess J; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, NIH-20892, USA. jurgenw@niddk.nih.gov.
المصدر: Nature communications [Nat Commun] 2019 Jul 03; Vol. 10 (1), pp. 2936. Date of Electronic Publication: 2019 Jul 03.
نوع المنشور: Journal Article; Research Support, N.I.H., Intramural
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Energy Metabolism*, Adipocytes/*metabolism , Glucose/*metabolism , beta-Arrestin 2/*metabolism, Animals ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Adrenergic, beta-3/genetics ; Receptors, Adrenergic, beta-3/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; beta-Arrestin 2/genetics
مستخلص: β-Arrestins are major regulators of G protein-coupled receptor-mediated signaling processes. Their potential roles in regulating adipocyte function in vivo remain unexplored. Here we report the novel finding that mice lacking β-arrestin-2 (barr2) selectively in adipocytes show significantly reduced adiposity and striking metabolic improvements when consuming excess calories. We demonstrate that these beneficial metabolic effects are due to enhanced signaling through adipocyte β3-adrenergic receptors (β3-ARs), indicating that barr2 represents a potent negative regulator of adipocyte β3-AR activity in vivo. Interestingly, essentially all beneficial metabolic effects caused by adipocyte barr2 deficiency are absent in adipocyte barr2-PRDM16 double KO mice, indicating that the metabolic improvements caused by the lack of barr2 in adipocytes are mediated by the browning/beiging of white adipose tissue. Our data support the novel concept that 'G protein-biased' β3-AR agonists that do not promote β3-AR/barr2 interactions may prove useful for the treatment of obesity and related metabolic disorders.
References: J Clin Invest. 2000 Mar;105(5):615-23. (PMID: 10712433)
Dev Cell. 2006 Jun;10(6):839-50. (PMID: 16740485)
Proc Natl Acad Sci U S A. 2016 Dec 13;113(50):E8178-E8186. (PMID: 27911814)
J Clin Invest. 2016 Nov 1;126(11):4273-4288. (PMID: 27701146)
Cell Metab. 2016 Jun 14;23(6):1167-1184. (PMID: 27238639)
J Biol Chem. 2004 Jul 2;279(27):28756-65. (PMID: 15123695)
J Clin Invest. 1993 Jan;91(1):344-9. (PMID: 8380813)
Nat Rev Drug Discov. 2016 Mar;15(3):161-72. (PMID: 26822831)
BMB Rep. 2014 Sep;47(9):506-11. (PMID: 24393528)
Cell Metab. 2017 Oct 3;26(4):660-671.e3. (PMID: 28844881)
Nature. 2014 Dec 18;516(7531):395-9. (PMID: 25317558)
Curr Pharm Des. 2001 Sep;7(14):1433-49. (PMID: 11472270)
Recent Prog Horm Res. 2001;56:309-28. (PMID: 11237219)
Endocrinology. 1992 Sep;131(3):1369-76. (PMID: 1505468)
Diabetes. 1997 Dec;46(12):2044-8. (PMID: 9392494)
Nat Rev Mol Cell Biol. 2002 Sep;3(9):639-50. (PMID: 12209124)
J Biol Chem. 2005 Feb 11;280(6):4880-7. (PMID: 15561704)
Nat Med. 2013 May;19(5):631-4. (PMID: 23603813)
Nat Rev Drug Discov. 2013 Mar;12(3):205-16. (PMID: 23411724)
Curr Opin Cell Biol. 2014 Apr;27:18-24. (PMID: 24680426)
Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5677-81. (PMID: 8202547)
BMB Rep. 2014 Oct;47(10):587-92. (PMID: 25248563)
Clin Chem. 1986 Nov;32(11):2030-3. (PMID: 3096593)
PLoS Biol. 2009 Aug;7(8):e1000172. (PMID: 19688034)
Med Res Rev. 2014 Nov;34(6):1286-330. (PMID: 24796277)
Methods Enzymol. 2014;538:233-47. (PMID: 24529442)
Cell. 2012 Jul 20;150(2):366-76. (PMID: 22796012)
Life Sci. 1994;54(7):491-8. (PMID: 8309351)
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3665-9. (PMID: 8386380)
Nat Rev Dis Primers. 2017 Jun 15;3:17034. (PMID: 28617414)
Mol Cell Endocrinol. 1984 Oct;37(3):245-56. (PMID: 6094283)
Nat Rev Drug Discov. 2010 May;9(5):373-86. (PMID: 20431569)
J Biol Chem. 2009 May 22;284(21):14087-95. (PMID: 19336408)
Bioorg Med Chem Lett. 2016 Jan 15;26(2):241-250. (PMID: 26707396)
Physiol Rep. 2016 May;4(10):. (PMID: 27230905)
Cell Metab. 2015 Oct 6;22(4):546-59. (PMID: 26445512)
J Biol Chem. 2000 Dec 8;275(49):38131-4. (PMID: 11013230)
J Biol Chem. 2004 Mar 12;279(11):10020-31. (PMID: 14699102)
Cardiol Rev. 2013 Nov-Dec;21(6):265-9. (PMID: 23707990)
Physiol Rev. 2004 Jan;84(1):277-359. (PMID: 14715917)
Nat Commun. 2017 Apr 18;8:15054. (PMID: 28416805)
Nat Med. 2013 Oct;19(10):1252-63. (PMID: 24100998)
J Mol Endocrinol. 1993 Apr;10(2):193-7. (PMID: 8387311)
Br J Pharmacol. 2004 Sep;143(2):235-45. (PMID: 15289291)
Proc Natl Acad Sci U S A. 2017 Apr 4;114(14):3756-3761. (PMID: 28325873)
Mol Pharmacol. 2012 Oct;82(4):575-82. (PMID: 22821234)
Pharmacol Ther. 2015 Feb;146:61-93. (PMID: 25242198)
J Endocrinol. 2015 May;225(2):R35-47. (PMID: 25804606)
N Engl J Med. 2009 Apr 9;360(15):1500-8. (PMID: 19357405)
Anal Biochem. 1979 Jul 1;96(1):236-45. (PMID: 495987)
Methods Mol Biol. 2000;126:329-43. (PMID: 10685421)
Mol Pharmacol. 2015 Sep;88(3):579-88. (PMID: 26134495)
Mol Pharmacol. 1993 Apr;43(4):548-55. (PMID: 8386307)
Nat Rev Mol Cell Biol. 2016 Nov;17(11):691-702. (PMID: 27552974)
Cell. 2015 Oct 22;163(3):643-55. (PMID: 26496606)
Am J Physiol. 1994 Apr;266(4 Pt 2):R1371-82. (PMID: 7910436)
Cell Metab. 2015 Jan 6;21(1):33-8. (PMID: 25565203)
J Lipid Res. 2012 Dec;53(12):2791-6. (PMID: 22993232)
N Engl J Med. 2009 Apr 9;360(15):1509-17. (PMID: 19357406)
Cell Metab. 2011 Mar 2;13(3):249-59. (PMID: 21356515)
Diabetes. 2015 Jul;64(7):2346-51. (PMID: 26050670)
Cell. 2014 Jan 16;156(1-2):304-16. (PMID: 24439384)
Nat Rev Drug Discov. 2016 Sep;15(9):639-660. (PMID: 27256476)
Cell Metab. 2017 Apr 4;25(4):811-822.e4. (PMID: 28380374)
J Biol Chem. 2002 Jan 4;277(1):702-10. (PMID: 11696538)
Cell. 2014 Jan 16;156(1-2):20-44. (PMID: 24439368)
Curr Protoc Pharmacol. 2014 Dec 01;67:Unit 2.10.1-9. (PMID: 25446289)
Prog Mol Biol Transl Sci. 2013;118:413-27. (PMID: 23764063)
N Engl J Med. 2009 Apr 9;360(15):1518-25. (PMID: 19357407)
المشرفين على المادة: 0 (DNA-Binding Proteins)
0 (Prdm16 protein, mouse)
0 (Receptors, Adrenergic, beta-3)
0 (Transcription Factors)
0 (beta-Arrestin 2)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20190705 Date Completed: 20190925 Latest Revision: 20210110
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC6610117
DOI: 10.1038/s41467-019-11003-4
PMID: 31270323
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-019-11003-4