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Open AccessArticle

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

1
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, 05508-000 SP, Brazil
2
Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas, Campinas, 13083-887 SP, Brazil
*
Author to whom correspondence should be addressed.
Nutrients 2020, 12(10), 3062; https://doi.org/10.3390/nu12103062
Received: 3 September 2020 / Revised: 30 September 2020 / Accepted: 2 October 2020 / Published: 7 October 2020
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. View Full-Text
Keywords: intrauterine growth restriction (IUGR); fructose; dexamethasone; intestinal gluconeogenesis intrauterine growth restriction (IUGR); fructose; dexamethasone; intestinal gluconeogenesis
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Pereira, G.A.; Sodré, F.S.; Murata, G.M.; Amaral, A.G.; Payolla, T.B.; Campos, C.V.; Sato, F.T.; Anhê, G.F.; Bordin, S. Fructose Consumption by Adult Rats Exposed to Dexamethasone In Utero Changes the Phenotype of Intestinal Epithelial Cells and Exacerbates Intestinal Gluconeogenesis. Nutrients 2020, 12, 3062.

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