Abstract
Background The rise in consumption of refined sugars high in fructose appears to be an important factor contributing to epidemic of obesity and metabolic syndrome [1]. Fructose is involved in the genesis and progression of the syndrome through deregulation of metabolic pathways in the liver and adipose tissue, as sites of insulin-modulated metabolism [2]. Enhanced regeneration of glucocorticoids within the liver and adipose tissue, mediated by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11bHSD1), may contribute to adiposity and metabolic disease [3]. 11bHSD1 reductase activity is crucially dependent on NADPH, a cofactor generated by the enzyme hexose-6phosphate dehydrogenase (H6PDH) [4]. We hypothesized that harmful effects of high fructose consumption are mediated by alterations in prereceptor metabolism of glucocorticoids and in the level of glucocorticoid receptor (GR) expression and compartmental redistribution in the liver and adipose tissue. We also assume that high fructose intake differently affects glucocorticoid signaling in the liver and adipose tissue of male and female rats.
Highlights
The rise in consumption of refined sugars high in fructose appears to be an important factor contributing to epidemic of obesity and metabolic syndrome [1]
In male rats, insulin sensitivity was impaired, while blood pressure, non-esterified fatty acid (NEFA) release and plasma triglycerides level were increased by fructose diet
The fructose-provoked increase in corticosterone level was accompanied by enhanced 11bHSD1 and hexose-6phosphate dehydrogenase (H6PDH) expression, as well as by stimulated glucocorticoid receptor (GR) translocation to the nucleus
Summary
The rise in consumption of refined sugars high in fructose appears to be an important factor contributing to epidemic of obesity and metabolic syndrome [1]. Fructose is involved in the genesis and progression of the syndrome through deregulation of metabolic pathways in the liver and adipose tissue, as sites of insulin-modulated metabolism [2]. Enhanced regeneration of glucocorticoids within the liver and adipose tissue, mediated by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11bHSD1), may contribute to adiposity and metabolic disease [3]. We hypothesized that harmful effects of high fructose consumption are mediated by alterations in prereceptor metabolism of glucocorticoids and in the level of glucocorticoid receptor (GR) expression and compartmental redistribution in the liver and adipose tissue. We assume that high fructose intake differently affects glucocorticoid signaling in the liver and adipose tissue of male and female rats
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