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.
Highlights
The consumption of fructose-sweetened beverages has significantly increased during the last decades and a great number of observational studies have associated this nutritional habit with increased cardiometabolic risk [1]
The metabolic imprinting caused by excessive exposure to DEX during fetal life is hallmarked by glucose intolerance, increased whole-body gluconeogenesis, and upregulation of phosphoenolpyruvate carboxykinase (PEPCK) expression in the liver [17,33,34]
We have described that in utero exposure to DEX exacerbates hepatic steatosis caused by fructose consumption during adult life [16]
Summary
The consumption of fructose-sweetened beverages has significantly increased during the last decades and a great number of observational studies have associated this nutritional habit with increased cardiometabolic risk [1]. In accordance with this hypothesis, experimental studies have described that rats consuming high amounts of fructose or sucrose develop glucose intolerance and increased hepatic gluconeogenesis [2,3,4]. Intestinal fructose metabolism capacity is limited and when high amounts of fructose are consumed, a considerable fraction reaches the liver [7]. In turn, produces glyceraldehyde-3-phosphate that is driven to either gluconeogenesis or de novo lipogenesis (DNLG) [8]
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