Insulin resistence and oxidative stress induced by a fructose-rich diet in adipose tissue.

OSCAR REBOLLEDO; CARLOS ALBERTO MARRA; AGUSTINA RASCHIA; SEBASTÍÁN RODRÍGUEZ; JUAN JOSÉ GAGLIARDINO

Chicago, USA

Congreso; 67th Scientific Sessions of the American Diabetes Association.; 2006

American Diabetes Association

Abstract Submission System American Association Diabetes 67th Scientific session  22-26, 2007 .CHlCAGO, IL (USA) Controlffracking Number: 2007-A-1054-Diabetes Activity: Abstract Current Daterrime: 12/27/20069:54:54 AM Insulin Resistance And Oxidative Stress Induced by A Fructose-Rich Diet In Rat Adipose Tissue Author Block: OSCAR R. REBOLLEDO, CARLOS A. MARRA, AGUSTINA RASCHIA, SEBASTIAN RODRIGUEZ, JUAN J. GAGLIARDINO, La Plata. Abstract: 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. Author Disclosure Block: O.R. Rebolledo, None; C.A. Marra, None; A. Raschia, None; S. Rodriguez, None; J.J. Gagliardino, None. Category (Complete): 17-A Integrated Physiology -Adipocyte Biology Keyword (Complete): Adipose Tissue Metabolism ; Oxidative Stress; Insulin Resistance Presentation Preference oral Sponsor (Complete): -- * I am a member of the ADA 's Professional Section and do not require a sponsor. : Yes Copyright & Support (Complete): 27/12/20 -'-