Background And Objectives: Ethanol exposure during gestation induces marked aberrations in growth and development of offsprings collectively known as foetal alcohol syndrome (FAS);. However, its effects on the postnatal development of alcohol dehydrogenase (ADH) are not adequately investigated. Therefore, ADH activity in liver and intestine of rats exposed to ethanol during gestation was studied in relation to postnatal development.
View Article and Find Full Text PDFIndian J Biochem Biophys
October 2004
The activities of lactase, sucrase, alkaline phosphatase (AP) and y-glutamyl transpeptidase (gamma-GTP) were studied in the intestinal brush border membranes of pups born to rat mothers exposed to ethanol (1 ml of 30% ethanol daily during gestation) at different days of postnatal development. The activities of lactase (at day 4-20) and sucrase (at day 20-30) were considerably reduced in response to prenatal exposure to ethanol, while AP (at day 4-30) and gamma-GTP activities were significantly enhanced (p < 0.05) at day 4, 8, 14 and 20, but there was no significant difference by day 30 of postnatal development.
View Article and Find Full Text PDFPrevious studies show that feedback inhibition of bile acid production by bile acids is mediated by multiple mechanisms, including activation of pregnane X receptor (PXR). Consistent with these studies, the antibiotic rifampicin, a ligand for human PXR, reduces hepatic bile acid levels in cholestasis patients. To delineate the mechanisms underlying PXR-mediated suppression of bile acid biosynthesis, we examined the functional cross-talk between human PXR and HNF-4, a key hepatic activator of genes involved in bile acid biosynthesis including the cholesterol 7-alpha hydroxylase (CYP7A1) and sterol 12-alpha hydroxylase (CYP8B1) genes.
View Article and Find Full Text PDFThe orphan receptor SHP interacts with many nuclear receptors and inhibits their transcriptional activities. SHP is central to feedback repression of cholesterol 7alpha hydroxylase gene (CYP7A1) expression by bile acids, which is critical for maintaining cholesterol homeostasis. Using CYP7A1 as a model system, we studied the molecular mechanisms of SHP repression at the level of native chromatin.
View Article and Find Full Text PDFBackground: 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.
Indian J Biochem Biophys
September 2012
Effect of prenatal ethanol exposure has been studied on microvillus membrane glycosylation in developing rat intestine. In utero ethanol administration did not affect the gestation period but reduced litter size in ethanol-exposed group. Body weight, intestinal length and weight of pups born to ethanol-exposed rats during gestation, aged 4 to 30 days were significantly low compared to the respective controls.
View Article and Find Full Text PDFThe effect of feeding 1 ml of 30% ethanol to pregnant female rats during gestation on the IgG absorption has been studied in the developing intestine. Pups born to dams fed ethanol during gestation exhibited a significant decline in body weight (p < 0.01), intestinal weight (p < 0.
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