دورية أكاديمية
أعرض في EDS

Endothelin receptor antagonism improves glucose tolerance and adipose tissue inflammation in an experimental model of systemic lupus erythematosus.

التفاصيل البيبلوغرافية
العنوان: Endothelin receptor antagonism improves glucose tolerance and adipose tissue inflammation in an experimental model of systemic lupus erythematosus.
المؤلفون: Rivera-Gonzalez O; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi., Case CT; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi., Wilson NA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi., Speed JS; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi., Taylor EB; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi.
المصدر: American journal of physiology. Endocrinology and metabolism [Am J Physiol Endocrinol Metab] 2023 Jan 01; Vol. 324 (1), pp. E73-E84. Date of Electronic Publication: 2022 Dec 07.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Physiological Society Country of Publication: United States NLM ID: 100901226 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1555 (Electronic) Linking ISSN: 01931849 NLM ISO Abbreviation: Am J Physiol Endocrinol Metab Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Bethesda, MD. : American Physiological Society
مواضيع طبية MeSH: Insulin Resistance* , Lupus Erythematosus, Systemic*/complications , Lupus Erythematosus, Systemic*/drug therapy, Mice ; Humans ; Animals ; Endothelin Receptor Antagonists/pharmacology ; Endothelin Receptor Antagonists/therapeutic use ; Atrasentan ; Bosentan ; Endothelin-1 ; Adipose Tissue ; Obesity/drug therapy ; Obesity/complications ; Body Weight ; Inflammation/drug therapy ; Receptors, Endothelin ; Models, Theoretical ; Glucose ; Receptor, Endothelin A
مستخلص: Endothelin-1 (ET-1) is elevated in patients with systemic lupus erythematosus (SLE), an autoimmune disease characterized by high rates of hypertension, renal injury, and cardiovascular disease. SLE is also associated with an increased prevalence of obesity and insulin resistance compared to the general population. In the present study, we tested the hypothesis that elevated ET-1 in SLE contributes to obesity and insulin resistance. For these studies, we used the NZBWF1 mouse model of SLE, which develops obesity and insulin resistance on a normal chow diet. To test this hypothesis, we treated control (NZW) and SLE (NZBWF1) mice with vehicle, atrasentan (ET A receptor antagonist, 10 mg/kg/day), or bosentan (ET A /ET B receptor antagonist, 100 mg/kg/day) for 4 wk. Neither treatment impacted circulating immunoglobulin levels, but treatment with bosentan lowered anti-dsDNA IgG levels, a marker of SLE disease activity. Treatment with atrasentan and bosentan decreased glomerulosclerosis, and atrasentan lowered renal T-cell infiltration. Body weight was lower in SLE mice treated with atrasentan or bosentan. Endothelin receptor antagonism also improved hyperinsulinemia, homeostatic model assessment for insulin resistance, and glucose tolerance in SLE mice. Adipose tissue inflammation was also improved by endothelin receptor blockade. Taken together, these data suggest a potential therapeutic benefit for SLE patients with obesity and insulin resistance. NEW & NOTEWORTHY SLE is an autoimmune disease that is associated with obesity, insulin resistance, and elevated endothelin-1. The present study demonstrated that pharmacological inhibition of endothelin receptors decreased body weight, insulin resistance, and adipose tissue inflammation in a murine model of SLE. The therapeutic potential of endothelin receptor antagonists to treat obesity-related diseases and pathophysiological conditions, such as autoimmune diseases and insulin resistance, has become increasingly clear.
References: PLoS Pathog. 2020 Oct 19;16(10):e1008947. (PMID: 33075079)
Hypertension. 2008 Sep;52(3):452-9. (PMID: 18678788)
Autoimmun Rev. 2014 Sep;13(9):981-1000. (PMID: 25092612)
Nat Rev Rheumatol. 2021 Feb;17(2):98-108. (PMID: 33339987)
Br J Rheumatol. 1998 May;37(5):514-9. (PMID: 9651078)
Surg Obes Relat Dis. 2019 Jul;15(7):1044-1050. (PMID: 31147283)
Front Endocrinol (Lausanne). 2018 May 29;9:280. (PMID: 29896159)
Clin Sci (Lond). 2002 Aug;103 Suppl 48:430S-433S. (PMID: 12193138)
Diabetes. 2003 Aug;52(8):1904-9. (PMID: 12882904)
Best Pract Res Clin Rheumatol. 2002 Dec;16(5):847-58. (PMID: 12473278)
J Am Soc Nephrol. 2017 Aug;28(8):2443-2458. (PMID: 28348063)
J Biol Chem. 2009 Nov 13;284(46):31936-44. (PMID: 19776010)
Can J Physiol Pharmacol. 2020 Sep;98(9):604-610. (PMID: 32083942)
Lupus. 2018 May;27(6):1001-1006. (PMID: 29451068)
Am J Kidney Dis. 1996 Mar;27(3):416-23. (PMID: 8604712)
Clin Rheumatol. 2019 Nov;38(11):3117-3127. (PMID: 31363873)
Clin Exp Rheumatol. 2017 Nov-Dec;35(6):885-892. (PMID: 28281456)
Front Immunol. 2018 Oct 30;9:2509. (PMID: 30459770)
Clin Immunol. 2017 Dec;185:59-73. (PMID: 27519955)
Environ Sci Pollut Res Int. 2021 Feb;28(6):7180-7190. (PMID: 33026618)
Immunology. 2015 Dec;146(4):497-507. (PMID: 26173489)
Clin Sci (Lond). 2021 Jul 30;135(14):1773-1789. (PMID: 34278410)
Kidney Int. 1995 Feb;47(2):481-9. (PMID: 7723234)
J Immunol Res. 2015;2015:147616. (PMID: 26090478)
Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1323-32. (PMID: 18812462)
Front Immunol. 2019 Jul 17;10:1667. (PMID: 31379858)
Kidney Int. 2014 Nov;86(5):896-904. (PMID: 24805108)
Metabolism. 2005 Jun;54(6):735-40. (PMID: 15931607)
Biomed Res Int. 2014;2014:658913. (PMID: 25110685)
Eur J Immunol. 2009 Sep;39(9):2629-35. (PMID: 19662632)
Exp Mol Med. 2012 Jul 31;44(7):424-31. (PMID: 22513335)
J Clin Immunol. 2000 Sep;20(5):354-61. (PMID: 11051277)
Exp Biol Med (Maywood). 2005 Oct;230(9):652-8. (PMID: 16179733)
J Neuroimmune Pharmacol. 2014 Mar;9(2):209-17. (PMID: 24068577)
Am J Physiol Renal Physiol. 2009 Jun;296(6):F1477-83. (PMID: 19279127)
Int J Mol Sci. 2021 Apr 15;22(8):. (PMID: 33920997)
Arthritis Care Res (Hoboken). 2011 Feb;63(2):261-8. (PMID: 20824801)
Ann Rheum Dis. 1995 May;54(5):361-5. (PMID: 7794041)
Curr Obes Rep. 2020 Sep;9(3):245-254. (PMID: 32632847)
Rev Endocr Metab Disord. 2013 Mar;14(1):29-38. (PMID: 23299657)
Am J Physiol Endocrinol Metab. 2022 Jun 1;322(6):E508-E516. (PMID: 35373585)
Am J Hypertens. 2001 Jun;14(6 Pt 2):83S-89S. (PMID: 11411770)
Diabetologia. 1990 May;33(5):306-10. (PMID: 2198188)
J Biomed Biotechnol. 2011;2011:271694. (PMID: 21403825)
Diabetes. 1995 Apr;44(4):431-6. (PMID: 7698512)
J Am Soc Nephrol. 2015 May;26(5):1071-80. (PMID: 25377076)
Clin Rheumatol. 2004 Oct;23(5):416-20. (PMID: 15459813)
Atherosclerosis. 2014 Apr;233(2):419-428. (PMID: 24530773)
Obes Rev. 2020 Dec;21(12):e13086. (PMID: 32627269)
J Immunol. 2015 Oct 15;195(8):3866-79. (PMID: 26342031)
Ren Physiol Biochem. 1993 Sep-Oct;16(5):233-43. (PMID: 7694336)
Front Immunol. 2019 Sep 04;10:2015. (PMID: 31552019)
Proc Natl Acad Sci U S A. 1976 Apr;73(4):1279-83. (PMID: 1063408)
Ann Rheum Dis. 1991 Jul;50(7):526-7. (PMID: 1877866)
Br J Clin Pharmacol. 2013 Oct;76(4):573-9. (PMID: 23228194)
Metabolism. 2004 May;53(5):550-5. (PMID: 15131756)
J Rheumatol. 2002 Dec;29(12):2551-4. (PMID: 12465150)
Hypertension. 2014 Oct;64(4):792-800. (PMID: 25024282)
Proc Natl Acad Sci U S A. 1978 Mar;75(3):1500-4. (PMID: 306627)
Am J Physiol Endocrinol Metab. 2012 Dec 1;303(11):E1313-24. (PMID: 23032686)
Am J Physiol Regul Integr Comp Physiol. 2007 Feb;292(2):R736-42. (PMID: 16971374)
Diabetes. 2008 Feb;57(2):378-86. (PMID: 18025413)
Blood. 2004 Oct 1;104(7):2107-15. (PMID: 15213100)
Clin Rheumatol. 2021 Oct;40(10):4253-4258. (PMID: 33839992)
Autoimmun Rev. 2007 Jun;6(6):366-72. (PMID: 17537382)
Expert Rev Cardiovasc Ther. 2008 Mar;6(3):343-68. (PMID: 18327995)
Gend Med. 2011 Apr;8(2):150-5. (PMID: 21536233)
Sci Rep. 2018 May 22;8(1):8001. (PMID: 29789608)
Hypertension. 2006 Nov;48(5):988-93. (PMID: 16982954)
Clin Sci (Lond). 2021 Mar 26;135(6):731-752. (PMID: 33729498)
Pharmacol Res. 2005 Feb;51(2):107-15. (PMID: 15629255)
Lupus. 2018 Mar;27(3):428-435. (PMID: 28795654)
معلومات مُعتمدة: P20 GM104357 United States GM NIGMS NIH HHS; R00 HL146888 United States HL NHLBI NIH HHS; R01 DK124327 United States DK NIDDK NIH HHS; R25 HL121042 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: adipose; autoimmunity; endothelin-1; insulin resistance; lupus; obesity
المشرفين على المادة: 0 (Endothelin Receptor Antagonists)
V6D7VK2215 (Atrasentan)
Q326023R30 (Bosentan)
0 (Endothelin-1)
0 (Receptors, Endothelin)
IY9XDZ35W2 (Glucose)
0 (Receptor, Endothelin A)
تواريخ الأحداث: Date Created: 20221208 Date Completed: 20230120 Latest Revision: 20240102
رمز التحديث: 20240102
مُعرف محوري في PubMed: PMC9870584
DOI: 10.1152/ajpendo.00274.2022
PMID: 36476039
قاعدة البيانات: MEDLINE
الوصف
تدمد:1522-1555
DOI:10.1152/ajpendo.00274.2022