Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus.

Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Research Abstract Details 

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Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Abstract Text:

Christine Guo,Diego Martinez-Vasquez,Gonzalo P Mendez,Maria F Toniolo,Tham M Yao,Eveline M Oestreicher,Taisuke Kikuchi,Nathalie Lapointe,Luminita Pojoga,Gordon H Williams,Vincent Ricchiuti,Gail K Adler,

To determine whether mineralocorticoid receptor (MR) activation plays a role in diabetic renal injury and whether this role differs in types 1 and 2 diabetes mellitus, we examined the effect of a MR antagonist on renal injury in rodent models of type 1 (streptozotocin-treated rat) and type 2 (db/db mouse) diabetes. We studied three groups of 8-wk-old, uninephrectomized Wistar rats for 4 wk: diabetic streptozotocin- (55 mg/kg) treated rats (n = 11), diabetic streptozotocin-treated rats receiving the MR antagonist eplerenone (n = 15), and nondiabetic rats (n = 9). In addition, we studied three groups of 8-wk-old mice for 16 wk: diabetic db/db mice (n = 10), diabetic db/db mice treated with eplerenone (n = 8), and nondiabetic, db/+ littermates (n = 11). Diabetic rats and mice developed albuminuria and histopathological evidence of renal injury, including glomerular hypertrophy, mesangial expansion, and tubulointerstitial injury as well as increased renal cortical levels of MR protein, MR mRNA, TGFbeta mRNA, and osteopontin mRNA. All of these changes were significantly reduced by treatment with eplerenone except for the elevated MR levels. The beneficial effects of eplerenone were not attributable to changes in blood pressure or glycemia. In summary, MR expression was increased in kidneys of diabetic rodents, and MR antagonists effectively reduced diabetic renal injury irrespective of the species or specific cause of the diabetes. Thus, these data suggest that MR activation is a critical factor in the early pathogenesis of renal disease in both type 1 and type 2 diabetes mellitus.

Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Publishing Authors By Initials

C Guo,D Martinez-Vasquez,GP Mendez,MF Toniolo,TM Yao,EM Oestreicher,T Kikuchi,N Lapointe,L Pojoga,GH Williams,V Ricchiuti,GK Adler,

For similar circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: myocardial contraction: systole research abstracts see: circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: myocardial contraction: systole research

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Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Endocrinology

VOLUME: 147

Page Numbers: 5363-73

Journal Abbreviation: Endocrinology

ISSN: 0013-7227

DAY: 10

MONTH: 08

YEAR: 2006

Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375040

Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Keywords Mesh Terms:

KEYWORDS: Systole

MESH TERMS: therapeutic use

Chemical & Substance for Abstract: Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus. Information

Substance Name: Spironolactone

Registry Number: 52-01-7

Grant and Affiliation Information for Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus.

AFFILIATION: Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, Massachusetts 02115, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01HL069208

ACRONYM: HL

MEDLINETA: Endocrinology

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