Excess fructose intake-induced hypertrophic visceral adipose tissue results from unbalanced precursor cell adipogenic signals

ZUBIRÍA GUILLERMINA; FARIÑA JUAN; MORENO GRISELDA; GAGLIARDINO JUAN; SPINEDI EDUARDO; GIOVAMBATTISTA ANDRÉS

FEBS JOURNAL

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2013 vol. 280 p. 5864 - 5874

1742-464X

We studied the effect of feeding normal adult male rats with a commercial diet (CD)supplemented with fructose added to the drinking water (10% wt/vol; fructose-rich diet, FRD)on the adipogenic capacity of stromal-vascular fraction (SVF) cells isolated from visceraladipose tissue (VAT) pads. Animals received either the CD or FRD ad libitum for 3 weeks;thereafter, we evaluated the in vitro proliferative and adipogenic capacities of their VAT SVFcells. FRD significantly increased plasma insulin, triglyceride and leptin levels, VATmass/cell size, and the in vitro adipogenic capacity of SVF cells. Flow cytometry studiesindicated that VAT precursor cell population number did not differ between groups;however, the accelerated adipogenic process could result from an imbalance betweenendogenous pro- and anti-adipogenic SVF cell signals, clearly shifted towards the former. Theincreased insulin milieu and its intracellular mediator (insulin receptor substrate-1) in VATpads, and the enhanced SVF cell expression of Zpf423 and PPAR-γ2 (all pro-adipogenicmodulators), together with a decreased SVF cell concentration of anti-adipogenic factors(preadipocyte factor-1 and wingless-type MMTV-10b) strongly support this assumption. Wehypothesize that the VAT mass expansion recorded in FRD rats results from the combinationof initial accelerated adipogenesis and final cell hypertrophy. It remains to be determinedwhether FRD administration over longer periods of time could perpetuate both processes, orwhether cell hypertrophy itself remains responsible for a further VAT mass expansion, asobserved in advanced/morbid obesity.