Premium
Thyroid Hormone Ameliorates Diabetic Nephropathy in Type II Diabetes
Author(s) -
Lin Yi,
Sun Zhongjie
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.812.4
Subject(s) - endocrinology , diabetic nephropathy , medicine , albuminuria , ly294002 , diabetes mellitus , nephropathy , renal function , creatinine , kinase , chemistry , phosphatidylinositol , biochemistry
Our recent study showed that the T3 level was decreased in db/db mice, a model of type II diabetes. The purpose of this study was to test our hypothesis that treatments with T3 would improve diabetic nephropathy. We treated 16 week‐old male db/db mice with T3 for 4 weeks. T3 decreased albuminuria and plasma creatinine and increased creatinine clearance, suggesting improved renal function. T3 significantly decreased accumulation of collagenous components in cortical interstitium and expansion of mesangial matrix in glomeruli and prevented the loss of glomeruli in db/db mice. Therefore, T3 improved the renal structural damage in type II diabetes. Notably, diabetic nephropathy was accompanied by a decrease in phosphatidylinosital 3‐kinase (PI3‐kinase) activity and an increase of transforming growth factor‐β (TGF‐β) expression in kidneys. Interestingly, T3 restored PI3 kinase activity and decreased TGF‐β expression in db/db mice. Simultaneous treatments with PI3 kinase inhibitor (LY294002) abolished the beneficial effects of T3 on diabetic nephropathy and the attenuating effect of T3 on increased TGF‐β expression. These data revealed, for the first time, that T3 can prevent progressive renal insufficiency and overt diabetic nephropathy in db/db mice and that this protective effect may be mediated by up‐regulation of PI3‐kinase activity.