Insulinoresistencia y estrés oxidativo en tejido adiposo inducido por dieta rica en fructosa.

OSCAR REBOLLEDO; CARLOS ALBERTO MARRA; AGUSTINA RSCHIA; SEBASTÍAN RODRÍGUEZ; JUAN JOSÉ GAGLIARDINO

Mendoza

Congreso; XV Congreso Argentino de Diabetes.; 2006

Sociedad Argentina de Diabetes

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 (A T) would contribute to IR and OS deve1opment 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 A T the activity of superoxide dismutase (SOD), catalase (CT), glutathion peroxidase, reductase and ; transferase (GSH-Px, GSH-R, GSH- Tr), total glutathione (GSH), liposoluble antioxidants a- .Alpha-tocoferol (a-TC), p-carotene (P-CT), lipid peroxidation as TBARS, the major fatty acid composition,(FA) of A T -TG and lipolysis (L) as NEF A released by pieces of A T incubated for 2 h at 370 C :J (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:i:0.27 vs. 8.3:i:0.23; TG: 0.76:i:0.08 vs. 1.30:1:0.07; I (ng/ml): 2.7:i:0.5 vs. 4.7:i:0.6; TBARS (nmol/mg): 243.4:i:12.2 vs. 378.9:i:31.9; (U/mg) SOD: 5.68:i:0.29 vs. 3.44:i:0.17; CT: 0.09:i:0.01 vs. 0.13:i:0.01; GSH-Px: 2.87:i:0.08 vs. 1.62:1:0.06; GSH-R: 6.70:i:0.36 vs 9.62:i:0.69; GSH- Tr: 12.8:i:0.24 vs 17.0:1:0.13; (~g/g) a- TC: 331:i:6 vs. 288:i:2; B-CT: 0.89:i:0.02 vs. 0.56:i:0.03; GSH (nmoVg): 88.7:i:3.43 vs. 63.9:i:1.87; (mol %) L PUFAs:38.1:i:0.9 vs. 35.0:1:0.8; LSat/LPUF A: 1.19:i:0.05 vs. 1.49:i:0.04; total L (mg/g A T): 0.70:i:0.03 vs. FRD 1.30:1: 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 wou1d contribute to the development of IR favoring the ulterior development of p-cel1 fai1ure. Consequently, its early I control might represent an appropriate strategy to prevent the development of type 2 diabetes.