CENEXA   05419
CENTRO DE ENDOCRINOLOGIA EXPERIMENTAL Y APLICADA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Insulin resistance and oxidative stress induced by a fructose-rich diet in rat adipose tissue.
Autor/es:
REBOLLEDO OR; MARRA CA; RASCHIA A; RODRíGUEZ S; GAGLIARDINO JJ
Lugar:
Chicago, EEUU
Reunión:
Congreso; American Diabetes Association, 67th Scientific Sessions; 2007
Institución organizadora:
American Diabetes Association
Resumen:
We have already shown that the administration of a fructose-rich diet (FRD) to normal rats induces a state of insulin resistance (IR) and an increase of oxidative stress markers (OS) in different tissues. It was suggested that adipose tissue (AT) would contribute to IR and OS development by altering its production and release of adipocytokines. We tested whether FRD induces a simultaneous impairment of AT oxidative state and the development of IR. Normal Wistar rats were fed during 3 weeks with a commercial diet with (FRD) or without (CD) 10% fructose in the drinking water. In both groups we measured plasma glucose (G), triglyceride (TG) and insulin (I), and in abdominal AT the activity of superoxide dismutase (SOD), catalase (CT), glutathion peroxidase, reductase and transferase (GSH-Px, GSH-R, GSH-Tr), total glutathione (GSH), liposoluble antioxidants alpha-tocoferol (alpha-TC), B-carotene B-CT), lipid peroxidation as TBARS, the major fatty acid composition (FA) of AT-TG and lipolysis (L) as NEFA released by pieces of AT incubated for 2 h at 37°C (spectrophotometric, kinetic, HPLC and RIA techniques). Differences between CD vs. FRD in mmol/l (other units stated separately) and p<0.02 were: G:7.2±0.27 vs. 8.3±0.23; TG: 0.76±0.08 vs. 1.30±0.07; I (ng/ml): 2.7±0.5 vs. 4.7±0.6; TBARS (nmol/mg): 243.4±12.2 vs. 378.9±31.9; (U/mg) SOD: 5.68±0.29 vs. 3.44±0.17; CT: 0.09±0.01 vs. 0.13±0.01; GSH-Px: 2.87±0.08 vs. 1.62±0.06; GSH-R: 6.70±0.36 vs 9.62±0.69; GSH-Tr: 12.8±0.24 vs 17.0±0.13; µg/g) alpha-TC: 331±6 vs. 288±2; B-CT: 0.89±0.02 vs. 0.56±0.03; GSH (nmol/g): 88.7±3.43 vs. 63.9±1.87; (mol %) Ó PUFAs: 38.1±0.9 vs. 35.0±0.8; ÓSat/ÓPUFA: 1.19±0.05 vs. 1.49±0.04; total L (mg/g AT): 0.70±0.03 vs. FRD 1.30±0.11. FRD produced similar and significant modifications in TG composition in AD and NEFA released. We can conclude that FRD-induced pro-oxidative state in AT would contribute to the development of IR favoring the ulterior development of B-cell failure. Consequently, its early control might represent an appropriate strategy to prevent the development of type 2 diabetes.