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

• Published in: Nutrients 2020-10, Vol.12 (10), p.3062
• Main Authors: Pereira, Gizela A, Sodré, Frhancielly S, Murata, Gilson M, Amaral, Andressa G, Payolla, Tanyara B, Campos, Carolina V, Sato, Fabio T, Anhê, Gabriel F, Bordin, Silvana
• Format: Article
• Language: English
• Subjects: Animal Nutritional Physiological Phenomena - physiology; Animals; Birth weight; Cytotoxicity; Dexamethasone; Dexamethasone - adverse effects; Dietary Carbohydrates - adverse effects; Drinking water; Enzymes; Epithelial cells; Epithelial Cells - pathology; Epithelium; Euthanasia; Fasting; Fatty liver; Female; Fructose; Fructose - adverse effects; Gluconeogenesis; Glucose; Glucose transporter; Glucose Transporter Type 2 - metabolism; Glucose transporter type 5; intestinal gluconeogenesis; Intestinal Mucosa - cytology; Intestinal Mucosa - metabolism; Intestine; Intracellular Signaling Peptides and Proteins - metabolism; Intrauterine exposure; intrauterine growth restriction (IUGR); Jejunum; Jejunum - metabolism; Lactic acid; Lipid Metabolism; Lipids; Lymphocytes T; Maternal Exposure - adverse effects; Maternal Nutritional Physiological Phenomena - physiology; Maternal-Fetal Exchange - physiology; Metabolism; Neonates; Offspring; Phenotypes; Phosphoenolpyruvate Carboxykinase (GTP) - metabolism; Pregnancy; Prenatal Exposure Delayed Effects; Proliferating cell nuclear antigen; Proteins; Rats, Wistar; Small intestine; Steatosis; Steroids
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu12103062

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.