Volume 7, Issue 4 (10-2003)
IBJ 2003, 7(4): 179-182 |
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Abstract:
Insulin resistance syndrome, also referred to as the metabolic syndrome or syndrome X, refers to a constellation of common metabolic and cardiovascular disorders (e.g. obesity, type 2 diabetes mellitus, hypertension, and dyslipidemia), which are all cardiovascular risk factors. Insulin resistance can be induced by fructose-rich diet in rats. We investigated the effect of vanadyl sulfate (0.2 mg/ml in drinking water for 7 days) on glucose, triglyceride, and plasma insulin levels in male Wistar rats that were fed with fructose-rich diets. Control rats were fed with standard chow for 7 days. The animals were divided into three groups: fructose-fed rats, fructose fed-vanadyl sulfate treated rats, and control rats. Fasting plasma glucose levels of the three groups were comparable (p>0.05). Fasting plasma insulin increased in the fructose-fed rats (190 ± 6.3 pM vs. control rats 83.06 ± 3.3 pM, p<0.001), likewise, plasma triglyceride significantly increased in fructose-fed rats (394.0 ± 25.8 vs. control rats 98.63 ± 6.7, p<0001). Vanadyl sulfate treatment prevented the increase in plasma insulin levels in the fructose fed-vanadyl treated rats (78.9 ± 5.1 pM vs. fructose fed-groups, p<0.001). Also vanadyl sulfate treatment significantly decreased plasma triglyceride levels (116.43 ± 6.7 vs. fructose-fed rats, p<0.001). Furthermore, fructose-fed groups had higher fasting insulin resistance index (FIRI: p<0.001) than control rats. In contrast, vanadyl sulfate significantly decreased FIRI in the fructose fed- vanadyl treated groups (p<0.001) compared with fructose- fed animals. These results indicate that administration of low doses of vanadyl sulfate may be advantageous for preservation of the functional characteristics of pancreatic beta cells, probably by improving insulin action and thereby insulin resistance prevention
Keywords: Insulin resistance, Vanadyl sulfate, Diabetes mellitus, Fasting insulin resistance index (FIRI), Triglyceride
Type of Study: Full Length/Original Article |
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