Fructose increases corticosterone production in association with NADPH metabolism alterations in rat epididymal white adipose tissue.

PRINCE PD; SANTANDER Y; GEREZ E; HOCHT C; POLIZIO AH; MAYER M; TAIRA CA; FRAGA CG; GALLEANO M (COMPARTEN ULTIMA AUTORIA); CARRANZA A (COMPARTEN ULTIMA AUTORIA)

JOURNAL OF NUTRITIONAL BIOCHEMISTRY

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2017 p. 109 - 116

0955-2863

Metabolic syndrome is an array of closely metabolic disorders that includes glucose intolerance/insulin resistance, central obesity, dyslipidemia, and hypertension. Fructose, a highly lipogenic sugar, has profound metabolic effects in adipose tissue, and has been associated with the etiopathology of many components of the metabolic syndrome. The adipocyte enzyme 11 β-HSD1 amplifies local glucocorticoid action and is a key player in the pathogenesis of central obesity and metabolic syndrome. 11 β-HSD1 reductase activity is dependent on NADPH, a cofactor generated by H6PD.Our focus was to explore the effect of fructose overload on epididymal white adipose tissue (EWAT) machinery involved in glucocorticoid production and NADPH and oxidants metabolism.Male Sprague Dawley rats fed with a fructose solution (10% (w/v) in tap water) during 9 weeks developed some characteristic features of metabolic syndrome, such as hypertriglyceridemia, and hypertension. In addition, high levels of plasma and EWAT corticosterone were detected. Activities and expressions of H6PD and 11 β-HSD1, NAPDH content, superoxide anion production, expression of NADPH oxidase 2 subunits, and indicators of oxidative metabolism were measured. Fructose overload rats showed an increased potential in oxidant production respect to control rats. In parallel, in EWAT from fructose overload rats we found higher expression/activity of H6PD and 11 β-HSD1, and NADPH/NADP+ ratio.Our in vivo results support that fructose overload installs in EWAT conditions favoring glucocorticoid production through higher H6PD expression/activity supplying NADPH for enhanced 11 β-HSD1 expression/activity, becoming this tissue a potential extra-adrenal source of corticosterone under these experimental conditions.