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Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
Published on: December 14, 2014
Effect of prenatal exposure to ethanol on postnatal development of intestinal transport functions in rats
Sonali Bhalla1, Safrun Mahmood, Akhtar Mahmood
1Department of Biochemistry, Panjab University, Chandigarh, India.
Insights
Prenatal ethanol exposure in rats impairs intestinal nutrient transporter development, leading to growth deficits. This study highlights delayed postnatal intestinal development in offspring exposed to alcohol in utero.
Area of Science:
- Developmental Biology
- Nutritional Science
- Toxicology
Background:
- Prenatal alcohol exposure causes Fetal Alcohol Syndrome, characterized by growth impairment and birth defects.
- Ethanol exposure in utero damages the developing intestinal epithelium, hindering nutrient assimilation and postnatal growth.
Purpose of the Study:
- To investigate the impact of prenatal ethanol exposure on rat intestinal D-glucose and amino acid transporters.
- To assess changes in Na(+)-dependent glucose transporter (SGLT1) mRNA expression during postnatal development.
Main Methods:
- Rats received ethanol (2 g/kg/day) during gestation; controls received glucose.
- Intestinal transport activity of glucose and amino acids was measured using tissue accumulation in everted intestines.
- SGLT1 mRNA levels were analyzed via Northern Blot at various postnatal ages.
Main Results:
- Ethanol-exposed pups exhibited reduced body weight, intestinal length, and weight.
- Uptake capacities for SGLT1, glycine, and L-leucine transporters were decreased compared to controls.
- SGLT1 mRNA levels remained unchanged across all postnatal ages in ethanol-exposed pups.
Conclusions:
- In utero ethanol exposure delays postnatal intestinal development in rat pups.
- The primary impact is on the development of energy-dependent D-glucose and amino acid transporters.
- This developmental delay contributes to impaired nutrient assimilation and growth retardation.
Background:
Alcohol consumption by pregnant animals and humans leads to general growth impairment in their offspring, delayed growth and multiple birth defects collectively called "Fetal Alcohol Syndrome". In utero exposure of ethanol to rat pups causes damage to their developing intestinal epithelium which leads to impairment of nutrient assimilation and growth retardation during postnatal development.
Aim:
To determine the effect of prenatal exposure of ethanol on the postnatal development of rat intestinal Na(+)-dependent and independent D-glucose transporter along with the amino acids (glycine and Lleucine) transporter activity at 4, 8, 14, 20 and 30 days of postnatal age. The changes in the expression levels of Na(+)-dependent glucose transporter (SGLT1) mRNA was assessed at different days of postnatal age in rat pups.
Methods:
Wistar strain albino female rats were fed ethanol at a dose of 2 g/kg body weight/day orally by Ryle's tube for one month before mating and during the entire period of gestation while the control females received isocaloric glucose. Transport studies were performed using the everted intestine of 4, 8, 14, 20 and 30 day-old control and ethanol-exposed pups employing the tissue accumulation method. The expression of SGLT1 mRNA at different days of postnatal age in control and ethanol-exposed rat pups was determined using a Northern Blot analysis.
Results:
Prenatal exposure of ethanol to rat pups leads to a decrease in their body weight, intestinal length and weight and reduces the uptake capacities of SGLT1 as well as energy dependent glycine and L-leucine transporters with respect to their age-matched controls. However, the mRNA levels of SGLT1 remained unaltered in the ethanol-exposed pups at all ages of postnatal development compared to their controls.
Conclusion:
These findings suggest that in utero exposure to ethanol leads to a general delay in the postnatal development of the intestine of ethanol-exposed rat pups affecting mainly the development of intestinal energy dependent D-glucose and amino acid (glycine and L-leucine) transporters.
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