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Effect of postnatal high-protein diet on kidney function of rats exposed to intrauterine protein restriction
Jing Chen1, Hong Xu, Qian Shen
1Department of Nephrology, Children's Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Insights
A postnatal high-protein diet worsens kidney damage in offspring with poor fetal growth, leading to higher blood pressure and protein in urine. This suggests fetal nutrition impacts long-term kidney health.
Area of Science:
- Nephrology
- Developmental Biology
- Nutritional Science
Background:
- Poor fetal growth is associated with long-term health issues, including hypertension and reduced kidney function in adulthood.
- Maternal protein restriction during pregnancy has been shown to cause hypertension and fewer glomeruli in offspring.
Purpose of the Study:
- To investigate the impact of a postnatal high-protein (HP) diet on renal development and function in rats previously exposed to a low-protein (LP) diet during fetal life.
- To determine if postnatal nutrition can exacerbate kidney damage initiated by fetal undernutrition.
Main Methods:
- Sprague-Dawley rats were fed a low-protein (LP) diet during pregnancy.
- Male offspring received either a normal-protein (NP) diet (LP/NP) or a high-protein (HP) diet (LP/HP) postnatally; a control group received NP diet throughout (NP/NP).
- Renal function, blood pressure, and histological markers were assessed at 12 weeks.
Main Results:
- Offspring fed a postnatal HP diet (LP/HP) showed elevated blood pressure and proteinuria compared to the LP/NP group.
- The LP/HP group exhibited moderate fusion of podocyte foot processes and mesangial cell hyperplasia, unlike the LP/NP group.
- Renal desmin mRNA levels were significantly elevated in the LP/HP group, indicating amplified renal damage.
Conclusions:
- A postnatal high-protein diet exacerbates kidney damage caused by fetal undernutrition.
- Podocyte injury is a potential mechanism contributing to proteinuria in offspring with fetal protein restriction.
- Early life nutrition plays a critical role in long-term renal health outcomes.
Abstract:
Poor fetal growth is linked with long-term detrimental effects on health in late life. We have previously shown that maternal protein restriction leads to hypertension and a reduced number of glomeruli in adult offspring. The aim of this study was to investigate the influence of a postnatal high-protein (HP) diet on renal development and renal function in rats subjected to a low-protein (LP) diet in fetal life. Sprague-Dawley rats were fed an LP diet throughout pregnancy. Male pups were given either a normal-protein (NP) diet (LP/NP) or HP diet (LP/HP), and normal male pups as control (NP/NP). At 12 wk, LP/HP offspring displayed no increase in glomerular number but showed elevated blood pressure and proteinuria compared with the LP/NP group. There was minimal fusion of foot processes in LP/NP rats compared with a moderate fusion of foot processes and hyperplasia of mesangial cells in LP/HP rats. Renal desmin mRNA levels were elevated in both LP/NP and LP/HP groups but more significantly in the LP/HP group. This study suggests that postnatal HP diet amplifies the renal damage induced by fetal under-nutrition. Podocyte injury may be one of the mechanisms by which fetal protein restriction leads to proteinuria.
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