Insulin Resistance and Oxidative Stress Induced by a Fructose-Rich Diet in Rat Adipose Tissue.

Rebolledo, Oscar R.; Marra, Carlos A.; Raschia, Agustina; Rodriguez, Sebastian; Gagliardino, Juan J.

We have already shown that the administration of a fructose-rich diet (FRD) to normal rots 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 simultaneons impairment of AT oxidative state and the development of IR. Normal Wistar ram 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), liposuluble antioxidants α-tocoferol (α-TC), β-carotene (β-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 370° 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±20.17; 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) αTC: 331±6 vs. 288±2; βCT: 0.89±0.02 vs. 0.56±0.03; GSH (nmol/g): 88.7±3.43 vs. 63.9±1.87; (mol %) Σ PUFAs: 38.1±0.9 vs. 35.0±0.8; ΣSat/ΣPUFA: 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 β-cell failure. Consequently, its early control might represent an appropriate strategy to prevent the development of type 2 diabetes.

INSULIN resistance; OXIDATIVE stress; ADIPOSE tissues; FRUCTOSE; DIABETES; FATTY acids; LABORATORY rats; PHYSIOLOGY

Diabetes, 2007, Vol 56, pA353

0012-1797

Academic Journal