Fructose Consumption by Adult Rats Exposed to Dexamethasone In Utero Changes the Phenotype of Intestinal Epithelial Cells and Exacerbates Intestinal Gluconeogenesis

Abstract

Fructose consumption by rodents modulates both hepatic and intestinal lipid metabolism and gluconeogenesis. We have previously demonstrated that in utero exposure to dexamethasone (DEX) interacts with fructose consumption during adult life to exacerbate hepatic steatosis in rats. The aim of this study was to clarify if adult rats born to DEX-treated mothers would display differences in intestinal gluconeogenesis after excessive fructose intake. To address this issue, female Wistar rats were treated with DEX during pregnancy and control (CTL) mothers were kept untreated. Adult offspring born to CTL and DEX-treated mothers were assigned to receive either tap water (Control-Standard Chow (CTL-SC) and Dexamethasone-Standard Chow (DEX-SC)) or 10% fructose in the drinking water (CTL-fructose and DEX-fructose). Fructose consumption lasted for 80 days. All rats were subjected to a 40 h fasting before sample collection. We found that DEX-fructose rats have increased glucose and reduced lactate in the portal blood. Jejunum samples of DEX-fructose rats have enhanced phosphoenolpyruvate carboxykinase (PEPCK) expression and activity, higher facilitated glucose transporter member 2 (GLUT2) and facilitated glucose transporter member 5 (GLUT5) content, and increased villous height, crypt depth, and proliferating cell nuclear antigen (PCNA) staining. The current data reveal that rats born to DEX-treated mothers that consume fructose during adult life have increased intestinal gluconeogenesis while recapitulating metabolic and morphological features of the neonatal jejunum phenotype.

Low Birth Weight Intensifies Changes in Markers of Hepatocarcinogenesis Induced by Fructose Consumption in Rats

“…Both Cyclin D1 and PCNA expression as well as the number of Ki-67 positive cells, were increased in the liver of rats exposed to DEX in utero and treated with fructose during adulthood. Of note, we previously demonstrated that the small intestine of DEX+fructose rats also shows a high proliferative epithelium, resembling the metabolic and morphological features of the neonatal jejunum phenotype [ 39 ].…”

Dietary Plant-Origin Bio-Active Compounds, Intestinal Functionality, and Microbiome

“…The presentation of how soluble extracts from chia seed (Salvia hispanica L.) affect brush border membrane functionality, morphology and intestinal bacterial populations in vivo (Gallus gallus) [21]. The fructose consumption by adult rats exposed to dexamethasone in utero changes the phenotype of intestinal epithelial cells and exacerbates intestinal gluconeogenesis [22]. Alterations in the intestinal morphology, gut microbiota, and trace mineral status following intra-amniotic administration (Gallus gallus) of teff (Eragrostis tef) seed extracts [23].…”