Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome.
Balázs Legeza, Paola Marcolongo, Alessandra Gamberucci, Viola Varga, Gábor Bánhegyi, Angiolo Benedetti, Alex Odermatt
Author Information
Balázs Legeza: Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland. balazs.legeza@dkf.unibe.ch.
Paola Marcolongo: Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. paola.marcolongo@unisi.it.
Alessandra Gamberucci: Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. alessandra.gamberucci@unisi.it.
Viola Varga: Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest 1085, Hungary. varviola@gmail.com.
Gábor Bánhegyi: Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest 1085, Hungary. banhegyi.gabor@med.semmelweis-univ.hu.
Angiolo Benedetti: Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. benedetti@unisi.it.
Alex Odermatt: Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland. alex.odermatt@unibas.ch.
中文译文
English
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.
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11-beta-Hydroxysteroid Dehydrogenase Type 1
Adipose Tissue
Fructose
Gene Expression Regulation, Enzymologic
Glucocorticoids
Humans
Metabolic Syndrome
Glucocorticoids
Fructose
11-beta-Hydroxysteroid Dehydrogenase Type 1
HSD11B1 protein, human