RESUMO
Several reports have demonstrated that pharmacological concentrations of biotin reduce hyperglycemia, hypertriglyceridemia, and hypertension. We hypothesized that biotin could exert a protective effect on some illness-associated metabolic syndrome. To test this hypothesis, male Wistar rats were fed a diet containing 30% fructose in drinking water and classified into four groups: C, the control group; B, the group receiving biotin (intraperitoneal injection, 2 mg/kg); F, the group receiving fructose (30% w/v); and FB, the group receiving fructose-biotin. The administration of biotin began after the rats had been on a high-fructose diet for 12 weeks and continued for 4 weeks. Our results showed that food and fluid intake were diminished in the F and FB groups. However, the final body weights were similar between the groups. A significant increase in hepatic triglyceride and cholesterol content, plasma cholesterol, triglycerides, transaminases, low-density lipoprotein cholesterol (LDL-c), systolic blood pressure, and vasocontraction, as well as a decrease in high-density lipoprotein cholesterol (HDL-c) were observed in the F group. Glucose tolerance and insulin tolerance were also impaired in the F group. The administration of biotin ameliorated all these changes. Hepatic oxidative stress as well as macrovesicular fatty changes in hepatocytes caused by a high-fructose diet were also improved by biotin. Our findings demonstrate that biotin has a protective role against metabolic syndrome by improving insulin resistance associated with normal hepatic and serum levels of triglyceride and cholesterol, blood pressure, and the prevention of steatosis and hepatic oxidative damage. Therefore, biotin could be used as a therapeutic strategy in the pharmacological treatment of metabolic syndrome.