Intra-uterine environment influences glomerular number and the acute renal adaptation to experimental diabetes

We sought to test the hypothesis of whether low birth weight rats would have reduced glomerular number, higher systolic blood pressure and an altered acute response to streptozotocin diabetes compared to normal birth weight rats. Female offspring of Wistar rats fed an isocaloric diet containing eith...

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Published inDiabetologia Vol. 44; no. 6; pp. 721 - 728
Main Authors Jones, S E, Bilous, R W, Flyvbjerg, A, Marshall, S M
Format Journal Article
LanguageEnglish
Published Germany Springer Nature B.V 01.06.2001
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Summary:We sought to test the hypothesis of whether low birth weight rats would have reduced glomerular number, higher systolic blood pressure and an altered acute response to streptozotocin diabetes compared to normal birth weight rats. Female offspring of Wistar rats fed an isocaloric diet containing either 6% casein (LPD) or 18% casein (NPD) in utero were studied. Birth weight, body weight, systolic blood pressure and urine albumin excretion were measured before and after streptozotocin diabetes. Glomerular number and volume were estimated after one week of diabetes. The LPD rats were of low birth weight (5.4 +/- 0.5 g vs 6.4 +/- 0.8 g, p < 0.0001) with higher systolic blood pressure (137 +/- 9mmHg vs 120 +/- 7 mmHg, p < 0.0001) and reduced glomerular number (17,435 +/- 2,074 vs 24,846 +/- 1,864, p < 0.0001). The LPD rats had smaller kidneys (0.925 +/- 0.009 g vs 1.200 +/- 0.173 g, p = 0.041) but similar glomerular volume to NPD control rats (1.11 +/- 0.15 x 10(6) microm3 vs 1.08 +/- 0.17 x 10(6) microm3). After 1 week of diabetes LPD rats had a greater proportional increase in renal size (diabetes 50 +/- 12 % vs control 20 +/- 4%, p = 0.003). Insulin suppressed renal hypertrophy in both LPD and NPD rats but failed to suppress glomerular hypertrophy in LPD rats (1.48 +/- 0.21 x 10(6) microm3 vs 1.03 +/- 0.23 x 10(6) microm3 p = 0.015). Abnormal intra-uterine environment reduces both renal size and glomerular number and influences the acute renal adaptation to experimental diabetes.
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ISSN:0012-186X
1432-0428
DOI:10.1007/s001250051681