We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Maternal diabetes programs hypertension and kidney injury in offspring.
- Authors
Chen, Yun-Wen; Chenier, Isabelle; Tran, Stella; Scotcher, Michael; Chang, Shiao-Ying; Zhang, Shao-Ling
- Abstract
We investigated whether maternal diabetes programs the offspring to develop hypertension and kidney injury in adulthood and examined potential underlying mechanisms. In a murine model we studied the offspring of three groups of dams (non-diabetic, diabetic, and diabetic treated with insulin). Mean systolic blood pressure in the offspring was monitored from 8 to 20 weeks. Body and kidney weights in the offspring of diabetic mothers were significantly lower than in offspring of non-diabetic mothers. Offspring of diabetic mothers developed hypertension, microalbuminuria, and glucose intolerance. Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-β1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers. By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers. These changes were prevented in the offspring of insulin-treated diabetic mothers. These data indicate that maternal diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin–angiotensin system and TGF-β1 gene expression in this process.
- Subjects
PREGNANCY complications; DIABETES in women; HYPERTENSION risk factors; ADULT children; KIDNEY disease risk factors; GENETIC regulation; DISEASES
- Publication
Pediatric Nephrology, 2010, Vol 25, Issue 7, p1319
- ISSN
0931-041X
- Publication type
Article
- DOI
10.1007/s00467-010-1506-1