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Morphofunctional renal alterations in rats induced by intrauterine hyperglycemic environment
Nathane França-Silva1, Natácia Dreyce Gonçalves Oliveira1, Ana Paula Coelho Balbi1
1Department of Physiological Sciences, Federal University of Uberlândia, Uberlândia, Brazil.
Insights
Maternal diabetes in rats leads to kidney damage in offspring, evidenced by altered cell growth and protein expression. Adult offspring exhibit impaired kidney function and elevated blood pressure.
Area of Science:
- Developmental Biology
- Nephrology
- Endocrinology
Background:
- Renal development in rats concludes shortly after birth.
- Maternal diabetes and other pregnancy complications can induce lasting systemic changes in offspring.
- Prenatal exposure to maternal diabetes can impact fetal development and long-term health outcomes.
Purpose of the Study:
- To investigate the structural and functional renal alterations in offspring born to diabetic mothers.
- To assess the impact of maternal diabetes on kidney development and function in rat pups.
- To evaluate the potential long-term renal consequences of prenatal exposure to hyperglycemia.
Main Methods:
- Pregnant rats were divided into control, untreated diabetic, and insulin-treated diabetic groups.
- Offspring kidneys were analyzed histologically and immunohistochemically at 1, 7, and 30 days old.
- Glomerular filtration rate (GFR) and blood pressure were measured in adult offspring.
Main Results:
- Increased PCNA(+) glomerular cells were observed at 7 days old, with a reduction by 30 days old in offspring of diabetic mothers.
- Elevated α-smooth muscle actin (α-SMA) tubulointerstitial expression was noted at 1 and 7 days old.
- Adult offspring from untreated diabetic mothers showed reduced GFR and increased blood pressure.
Conclusions:
- Maternal diabetes can induce developmental programming of renal damage in offspring.
- Prenatal exposure to hyperglycemia may contribute to impaired renal function in offspring.
- These findings highlight the critical role of maternal metabolic health in fetal kidney development.
Introduction:
The renal development of rats begins in intrauterine life, finishing by 15 days after birth. Diabetes and other diseases during pregnancy can cause systemic changes in the offspring. We evaluated the structural and functional renal alterations of the offspring from diabetic mothers.
Material And Methods:
Pregnant rats were separated and 1, 7, 30 and 90 days-old (DO) pups were divided into groups according to the treatment that the mothers received: G1: control, G2: untreated diabetic and G3: insulin-treated diabetic. The kidneys from offspring at 1, 7 and 30 DO were removed for immunohistochemical and histological studies. Furthermore, blood and urine samples were collected from animals at 30 DO to determine the glomerular filtration rate (GFR) by creatinine clearance, and the animals at 90 DO were subjected to blood pressure measurement by plethysmography.
Results:
Our results show an increase of PCNA(+) glomerular cells at 7 DO and a reduction in 30 DO animals as well as increased α-smooth muscle actin (α-SMA) tubulointerstitial expression at 1 and 7 DO in animals from G2, when compared with controls. The adult offspring from G2 showed reduced GFR and increased blood pressure.
Conclusions:
Maternal diabetes may have induced programming of renal damage in offspring of hyperglycemic mothers, which may have contributed to the impairment of renal function.
