Hypertension and impaired renal function accompany juvenile obesity: The effect of prenatal diet
Author(s) -
P.J. Williams,
Lesia O. Kurlak,
Alan C. Perkins,
Helen Budge,
Terence Stephenson,
D. H. Keisler,
Michael Symonds,
David S. Gardner
Publication year - 2007
Publication title -
kidney international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.499
H-Index - 276
eISSN - 1523-1755
pISSN - 0085-2538
DOI - 10.1038/sj.ki.5002276
Subject(s) - medicine , endocrinology , renal function , glomerulosclerosis , obesity , renal pathology , kidney , proteinuria
Obesity has been suggested to have a detrimental impact on kidney structure and function, leading to focal glomerulosclerosis and hypertension. It is also associated with hyperleptinemia and elevated renal sympathetic nerve activity. Prenatal undernutrition promotes postnatal obesity, hypertension, and an altered renal structure and function. In this study, we examined the effects of prenatal nutrient restriction and juvenile obesity in sheep. We found that juvenile obesity led to chronic hyperleptinemia and reduced renal function as assessed by nuclear scintigraphy. Additional factors include hypertension, glomerulosclerosis, and increased kidney apoptosis. Prenatal undernutrition, synchronous with early kidney development, coupled postnatally with juvenile obesity had no effect on systemic pathophysiological sequalae associated with obesity per se. Hypertension, hyperleptinemia, and poor renal function were all observed in this group. All indices of renal pathology such as increased expression of proinflammatory cytokines, angiotensin II, glucocorticoid receptors, and increased apoptosis and glomerulosclerosis were entirely absent in obese prenatally undernourished offspring. Our data indicate that juvenile obesity per se leads to systemic hypertension and renal structural and functional pathology. Prenatal undernutrition effectively abolishes any renal histopathology associated with juvenile obesity.
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