Hala Zaki

Increased fructose consumption is strongly associated with metabolic syndrome (MS). This study was performed to elucidate the role of co-enzyme Q10 (CoQ) and/or rosiglitazone (Rosi) in fructose induced MS. Four groups of rats (n=8–10) were fed on fructose-enriched diet (FED) for 16weeks. One served as FED-control while the remaining groups were treated with CoQ (10mg/kg/day), Rosi (4mg/kg/day) or their combination during the last 6weeks. Another group was fed on normal laboratory chow (normal control). At the end of the experiment, blood samples were collected for estimation of markers related to MS. In addition, histological examination of liver, kidney and pancreas samples was done. Induction of the MS was associated with increased body weight gain (34%) coupled with elevated levels of blood glucose (48%), insulin (86%), insulin resistance (270%), uric acid (69%), urea (155%), creatinine (129%) and blood lipids with different degrees. Fructose-induced MS also reduced plasma catalase (62%) and glutathione peroxidase (89%) activities parallel to increased serum leptin and tumor necrosis factor-alpha (TNF-α) levels. These changes were coupled by marked histological changes in the examined tissues. Treatment with CoQ or Rosi attenuated most of MS-induced changes. Besides, the combination of both agents further reduced blood glucose, total cholesterol, triglycerides and urea levels, as well as, normalized serum levels of leptin and TNF-α. In addition, combined therapy of both agents elevated HDL-cholesterol level and glutathione peroxidase activity. In conclusion, the present study proves the benefits of co-supplementation of CoQ and Rosi in a fructose-induced model of insulin resistance.

Objective: Incidence of Metabolic Syndrome (MS) is strongly associated with increased fructose consumption. This study aimed to elucidate the role of rosiglitazone, Chromium Picolinate (CP) and their combination on fructose-induced MS. Materials and methods: Four groups of rats (n = 10) were fed on Fructose-enriched Diet (FED) for 16 weeks. One served as FED-control while the remaining groups were treated with rosiglitazone (4 mg kg-1 day-1), CP (80 μg kg-1 day-1) or their combination during the last 6 weeks. A fifth group was fed on normal diet (normal group). At the end, blood samples were collected for estimation MS-related markers. Results: Histological examination of livers, kidneys and pancreases from all groups was done. Induction of MS was associated with increased weight gain and insulin resistance coupled with elevated levels of blood glucose, insulin, uric acid, urea, creatinine and lipids. FED also reduced plasma catalase and glutathione peroxidase activities parallel to increased serum leptin and TNF-α levels. This was coupled with marked histological changes in the livers, kidneys and pancreases. Treatment with rosiglitazone or CP attenuated most of the changes associated with MS. Besides, combination of both agents further improved disease markers and decreased hepatocytes fibrosis. Conclusion: The present results reveal the benefits of co-supplementation of rosiglitazone and CP in MS.