Supplementation of SK1 from Platycodi Radix Ameliorates Obesity and Glucose Intolerance in Mice Fed a High-Fat Diet

Jul 25, 2009Journal of medicinal food

SK1 from Platycodi radix reduces obesity and improves blood sugar in high-fat diet mice

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Abstract

Supplementation with SK1 significantly decreased body weight and fat accumulation in mice fed a high-fat diet.

SK1 supplementation reduced visceral fat mass and adipocyte area in a dose-dependent manner.
Plasma triglycerides, total cholesterol, and free fatty acid levels were significantly lowered with SK1 treatment.
Fecal lipid excretion increased with SK1 supplementation in the diet-induced obese mice.
SK1 improved postprandial glucose levels and insulin resistance index compared to the high-fat control group.
SK1 normalized hepatic activities related to fatty acid synthesis and oxidation that were elevated due to a high-fat diet.

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This study investigated the beneficial effects of SK1 on obesity and insulin resistance in C57BL/6 mice, which were fed a high-fat diet (37% calories from fat). SK1 is an edible saponin-rich compound from Platycodi radix. The mice were supplemented with two doses of SK1 (0.5% and 1.0%, wt/wt) for 9 weeks. The body weight, visceral fat mass, and adipocyte area were significantly decreased in the SK1 supplemented-groups in a dose-dependent manner compared to the high-fat group. The SK1 supplement significantly lowered plasma triglycerides, total cholesterol, and free fatty acid levels, whereas it significantly elevated the fecal excretion of lipids in the diet-induced obese mice. Supplementation of SK1 decreased the triglyceride and cholesterol levels and the accumulation of lipid droplets in the liver compared to the high-fat control group. High-fat diet induced glucose intolerance and insulin resistance with the elevation of blood glucose levels compared to the normal group; however, the SK1 supplement significantly improved postprandial glucose levels and insulin resistance index. After 9 weeks of being fed a high-fat diet, the mice presented with significantly increased activities of hepatic fatty acid synthase, fatty acid beta-oxidation, and glucokinase; however, both 0.5% and 1.0% SK1 supplementation normalized these activities. Notably, SK1 supplementation effectively diminished the ratio of fatty acid biosynthesis to fatty acid oxidation compared to the high-fat group. These results indicate that SK1 exhibits a potential anti-obesity effect and may prevent glucose intolerance by reducing body weight and fat accumulation, increasing fecal lipid excretions, and regulating hepatic lipid and glucose metabolism in high-fat fed mice.

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Supplementation of SK1 from Platycodi Radix Ameliorates Obesity and Glucose Intolerance in Mice Fed a High-Fat Diet

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