Shikonin protects against obesity through the modulation of adipogenesis, lipogenesis, and β-oxidation in vivo

• Shikonin resulted in amelioration of body weight in high-fat diet induced-obese mice.
• Shikonin inhibited hepatic lipids accumulation in HFD induced mice.
• The mRNA levels of adipogenic and lipogenic genes were decreased by shikonin.
• Fatty acid oxidation was alleviated by shikonin supplementation.
• Shikonin may have potential use as a therapy for treatment of obesity.

Shikonin, a napthoquinone pigment in the L. erythrorhizon (Lithospermum erythrorhizon) plant, is used as a functional food to promote blood circulation and detoxification in Asia. We investigated the effect and molecular mechanisms of shikonin on high-fat diet-induced obesity in mice. C57BL/6J mice were fed a normal diet, a high-fat diet, or a high-fat diet supplemented with shikonin for 8 weeks. We measured body weight change, adipose tissue weights, and biochemical markers. To elucidate the molecular mechanism of shikonin on diet-induced obesity, western blotting and quantitative real time PCR were performed. Shikonin reduced high-fat diet-induced increases in body weight, white adipose tissue mass, serum triglyceride, and total cholesterol levels. Blood insulin and leptin levels were significantly decreased by shikonin supplementation. Shikonin supplementation reduced protein content and mRNA expression of adipogenesis-related genes in white adipose tissue and lipogenesis-related genes in the liver, along with hepatic lipid content. Moreover, shikonin increased mRNA expression of the β-oxidation genes PPAR-α, PGC-1α, and ACOX1 in liver and skeletal muscle. Shikonin prevents high-fat diet-induced obesity in mice and may be a novel therapeutic approach for obesity prevention by modulating adipogenesis, lipogenesis, and fatty acid oxidation.