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Fructose, glucocorticoids and adipose tissue: Implications for the metabolic syndrome

Type of publication Peer-reviewed
Publikationsform Review article (peer-reviewed)
Author Legeza Balázs, Marcolongo Paola, Gamberucci Alessandra, Varga Viola, Bánhegyi Gábor, Benedetti Angiolo, Odermatt Alex,
Project Impact of the NADPH pool in the endoplasmic reticulum on metabolic and hormonal regulation
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Review article (peer-reviewed)

Journal Nutrients
Volume (Issue) 9(5)
Page(s) 426
Title of proceedings Nutrients
DOI 10.3390/nu9050426

Open Access

Type of Open Access Publisher (Gold Open Access)


© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. The modern Western society lifestyle is characterized by a hyperenergetic, high sugar containing food intake. Sugar intake increased dramatically during the last few decades, due to the excessive consumption of high-sugar drinks and high-fructose corn syrup. Current evidence suggests that high fructose intake when combined with overeating and adiposity promotes adverse metabolic health effects including dyslipidemia, insulin resistance, type II diabetes, and inflammation. Similarly, elevated glucocorticoid levels, especially the enhanced generation of active glucocorticoids in the adipose tissue due to increased 11β-hydroxysteroid dehydrogenase 1 (11β -HSD1) activity, have been associated with metabolic diseases. Moreover, recent evidence suggests that fructose stimulates the 11β -HSD1-mediated glucocorticoid activation by enhancing the availability of its cofactor NADPH. In adipocytes, fructose was found to stimulate 11β -HSD1 expression and activity, thereby promoting the adipogenic effects of glucocorticoids. This article aims to highlight the interconnections between overwhelmed fructose metabolism, intracellular glucocorticoid activation in adipose tissue, and their metabolic effects on the progression of the metabolic syndrome.