期刊
PEDIATRIC RESEARCH
卷 61, 期 1, 页码 42-47出版社
INT PEDIATRIC RESEARCH FOUNDATION, INC
DOI: 10.1203/01.pdr.0000250208.09874.91
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- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD021350] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016474] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL065399] Funding Source: NIH RePORTER
- NCRR NIH HHS [1P20RR16474-01] Funding Source: Medline
- NHLBI NIH HHS [HL65399] Funding Source: Medline
- NICHD NIH HHS [HD21350, P01 HD021350] Funding Source: Medline
Inadequate nutrition compromises fetal development and poses long-term health risks for the offspring, even without decreased birth weight. The present study sought to 1) establish the ontogeny of fetal renal glomerulus number (GN) in sheep and 2) evaluate the effects of 50% global nutrient restriction (NR)during early to midgestation on GN and the renin-angiotensin system in the fetal kidney. GN increased from 78 dG (68,560 +/- 3802) to 135 dG (586,118 25,792). NR increased combined kidney weight (29 0.6 g versus 23 +/- 1.1 g), whereas decreased GN relative to right kidney weight approached significance in males (26,000 +/- 5300 versus 39,000 +/- 2800 GN/g) compared with control (C) males and females. NR decreased immunoreactive angiotensin II (Ang II) type I receptor (AT1) in the NR kidneys at 78 dG and increased renin at 135 dG. Immunoreactive renin decreased from 78 to 135 dG. Female fetuses had more immunoreactive Ang II type 2 receptor (AT2) than male fetuses at 78 dG and males had more AT1 at 135 dG. The present study demonstrates gender-specific differences in fetal growth and development and in fetal kidney development in pregnancies affected by NR.
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