دورية أكاديمية
أعرض في EDS

Fibroblast growth factor 21 is not required for the antidiabetic actions of the thiazoladinediones.

التفاصيل البيبلوغرافية
العنوان: Fibroblast growth factor 21 is not required for the antidiabetic actions of the thiazoladinediones.
المؤلفون: Adams AC; Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN 46285, USA., Coskun T, Cheng CC, O Farrell LS, Dubois SL, Kharitonenkov A
المصدر: Molecular metabolism [Mol Metab] 2013 May 29; Vol. 2 (3), pp. 205-14. Date of Electronic Publication: 2013 May 29 (Print Publication: 2013).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier GmbH Country of Publication: Germany NLM ID: 101605730 Publication Model: eCollection Cited Medium: Print ISSN: 2212-8778 (Print) Linking ISSN: 22128778 NLM ISO Abbreviation: Mol Metab Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [München] : Elsevier GmbH, 2012-
مستخلص: Fibroblast growth factor 21 is an emerging metabolic regulator that was recently proposed to be a fed-state inducible factor in adipose tissue. As mice lacking FGF21 were refractory to treatment with rosiglitazone, FGF21 was suggested to underlie PPARγ-driven pharmacology and side effect profile (Dutchak et al., 2012 [12]). To evaluate FGF21/PPARγ cross-talk we conducted experiments in control and FGF21 null animals and found that rosiglitazone was equally efficacious in both strains. Specifically, diverse endpoints ranging from enhanced glycemic control, improved lipid homeostasis and side effects such as adipose accumulation were evident in both genotypes. Furthermore, the transcriptional signature and cytokine secretion profile of rosiglitazone action were maintained in our FGF21KO animals. Finally, we found that FGF21 in adipose was expressed at comparable levels in fasted and fed states. Thus, our data present a new viewpoint on the FGF21/PPARγ interplay whereby FGF21 is not necessary for the metabolic events downstream of PPARγ.
References: Eur J Endocrinol. 2009 Sep;161(3):391-5. (PMID: 19528204)
Mol Med. 2011;17(7-8):736-40. (PMID: 21373720)
Endocrinology. 2012 Jan;153(1):69-80. (PMID: 22067317)
Trends Endocrinol Metab. 2011 Mar;22(3):81-6. (PMID: 21194964)
Proc Natl Acad Sci U S A. 2007 May 1;104(18):7432-7. (PMID: 17452648)
Endocrinology. 2011 Aug;152(8):2996-3004. (PMID: 21712364)
J Clin Endocrinol Metab. 2009 Sep;94(9):3594-601. (PMID: 19531592)
Mol Endocrinol. 2008 Apr;22(4):1006-14. (PMID: 18187602)
Cell Metab. 2013 May 7;17(5):779-89. (PMID: 23663741)
Biochem Biophys Res Commun. 2007 Aug 24;360(2):437-40. (PMID: 17601491)
Biochim Biophys Acta. 2000 Jun 21;1492(1):203-6. (PMID: 10858549)
PLoS One. 2012;7(7):e40164. (PMID: 22792234)
PLoS One. 2012;7(3):e33870. (PMID: 22442730)
Gastroenterology. 2010 Aug;139(2):456-63. (PMID: 20451522)
Mol Pharmacol. 2008 Aug;74(2):403-12. (PMID: 18467542)
J Biol Chem. 2007 Sep 14;282(37):26687-26695. (PMID: 17623664)
Endocrinology. 2007 Feb;148(2):774-81. (PMID: 17068132)
Nature. 2005 Sep 29;437(7059):759-63. (PMID: 16127449)
PLoS One. 2012;7(11):e49977. (PMID: 23209629)
Diabetes. 2012 Feb;61(2):505-12. (PMID: 22210323)
Cell Metab. 2013 May 7;17(5):790-7. (PMID: 23663742)
Cell Metab. 2007 Jun;5(6):415-25. (PMID: 17550777)
Curr Diabetes Rev. 2012 Jul 1;8(4):285-93. (PMID: 22587513)
Clin Pharmacol Ther. 2009 Dec;86(6):592-5. (PMID: 19915603)
Endocrinology. 2008 Dec;149(12):6018-27. (PMID: 18687777)
J Biol Chem. 2004 Jul 9;279(28):29551-7. (PMID: 15123625)
Eur J Pharmacol. 2008 Feb 2;580(1-2):277-83. (PMID: 18048028)
Cell Metab. 2008 Aug;8(2):169-74. (PMID: 18680716)
FEBS Lett. 2008 Oct 29;582(25-26):3639-42. (PMID: 18840432)
J Cell Physiol. 2008 Apr;215(1):1-7. (PMID: 18064602)
Endocrinology. 2009 Oct;150(10):4625-33. (PMID: 19589869)
Elife. 2012 Oct 15;1:e00065. (PMID: 23066506)
Mol Metab. 2012 Aug 28;2(1):31-7. (PMID: 24024127)
Cell Metab. 2007 Jun;5(6):426-37. (PMID: 17550778)
Cell Metab. 2010 Mar 3;11(3):206-12. (PMID: 20197053)
PLoS One. 2012;7(5):e38438. (PMID: 22675463)
Genome Res. 2010 Jan;20(1):28-35. (PMID: 19923254)
J Clin Invest. 2005 Jun;115(6):1627-35. (PMID: 15902306)
Endocrinology. 2009 Nov;150(11):4931-40. (PMID: 19819944)
J Cell Physiol. 2007 Jan;210(1):1-6. (PMID: 17063460)
Cell Metab. 2012 Sep 5;16(3):387-93. (PMID: 22958921)
Diabetes. 2010 Nov;59(11):2781-9. (PMID: 20682689)
Biol Pharm Bull. 2011;34(7):1120-1. (PMID: 21720023)
Cell. 2012 Feb 3;148(3):556-67. (PMID: 22304921)
Mol Cell Biol. 2008 Jan;28(1):188-200. (PMID: 17954559)
Genes Dev. 2012 Feb 1;26(3):271-81. (PMID: 22302939)
فهرسة مساهمة: Keywords: Adiponectin; FGF21; Metabolism; PPARγ; Rosiglitazone
تواريخ الأحداث: Date Created: 20130920 Date Completed: 20130919 Latest Revision: 20211021
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3773835
DOI: 10.1016/j.molmet.2013.05.005
PMID: 24049735
قاعدة البيانات: MEDLINE
الوصف
تدمد:2212-8778
DOI:10.1016/j.molmet.2013.05.005