Efek Suplementasi Virgin Coconut Oil Terhadap Parameter Metabolik Dan Antropometrik Tikus Wistar Jantan Obesitas

There are several lifestyle modifications protocols to overcome global obesity epidemic, through dieting and excercising. Two diet protocols recognized by many people are low-fat diet and low-carbohydrate diet. Several researchs showed that positive effects exerted by the low-carbohydrate diet are mediated by ketone bodies in blood. In addition to alternative energy source, ketone also acts as signal molecule that can affect cell metabolism and behavior. Virgin coconut oil is a natural source of medium chain fatty acids which high in quantity and quality that could be absorbed through the small intestine and metabolized by the liver directly and easily to produce ketone bodies. Objectives: This research was conducted to investigate the effect of virgin coconut oil supplementation on blood ketone level, blood glucose level, food intake, visceral mass and body weight. in high-fat sucrose diet induced obesity model. Methods: A total of 32 male wistar rats which had been induced to become obesity (Lee’s index > 0,300) through high-fat sucrose diet induced for 20 weeks divided into four groups. Group (A) for distilled water, Group (S) for sucrose solution, group (VCO) for virgin coconut oil, and Group (CO) for corn oil. All of those treatment was provided orally for four weeks before every meal in the dark cycle. Results: The results indicated that there was no significant difference observed in blood glucose, food intake, visceral mass and body weight between groups. However, this research indicated that giving virgin coconut oil orally preprandially increased ketone level and decreased food intake significantly (p=0,023 and p=0,000, respectively). These results showed that virgin coconut oil supplementation could decrease food intake in subsequent mea compared to other substances. Conclusion: Virgin coconut oil supplementation could increase blood ketone level and suppress food intake in high-fat sucrose induced obese rats. But it’s effect in suppressing food intake was unlikely mediated by ketone levels