(-)-Secoisolariciresinol attenuates high-fat diet-induced obesity in C57BL/6 mice

January 1, 2011 Human Health and Nutrition Data 0 Comments

(-)-Secoisolariciresinol attenuates high-fat diet-induced obesity in C57BL/6 mice

Year: 2011
Authors: Tominaga, S. Nishi, K. Nishimoto, S. Akiyama, K. Yamauchi, S.
Publication Name: Food and Function
Publication Details: DOI: 10.1039/c1fo10166h

Abstract:

Flaxseed lignan, secoisolariciresinol has been reported to possess health benefits. We previously synthesized each stereo isomer of secoisolariciresinol and found that (-)-secoisolariciresinol reduces lipid accumulation and induces adiponectin production in 3T3-L1 adipocytes. Here we show the effects of (-)-secoisolariciresinol on high-fat diet-induced obesity in C57BL/6 male mice. Oral administration of (-)-secoisolariciresinol for 28 consecutive days significantly suppressed the gain of body weight. Increased serum adiponectin level and decreased gene expression of fatty acids synthase and sterol regulatory element-binding protein-1c in liver, which are related to fatty acid synthesis, were observed in the mice orally administered with (-)-secoisolariciresinol. In addition, sub cutaneous injection of (-)- secoisolariciresinol also significantly suppressed the gain of body weight. Serum leptin levels were significantly increased by treating with (-)-secoisolariciresinol or (-)-enterolactone. Subcutaneous injection of (-)-secoisolariciresinol, (-)-enterolactone, or (-)-enterodio promoted gene expression of acyl-CoAoxidase, carnitine palmitoyltransferase-1, and peroxisome proliferator-activated receptor a, which are related to beta-oxidation. Overall results suggest that (-)-secoisolariciresinol exerts a suppressive effect on the gain of body weight of mice fed a high-fat diet by inducing gene expression of adiponectin, resulting in the altered expression of various genes related to the synthesis and b-oxidation of fatty acids. (Authors abstract)
Recent results from this lab showed that (-)-SECO, a synthetically prepared pure stereo isomer of SECO, has potent effects on suppressing triglyceride accumulation and stimulating adiponectin production in 3T3-L1 adipocytes, suggesting that (-)-SECO is useful to improve obesity by reducing fat accumulation. In the present study, the authors investigated the effects of sterically pure (-)-SECO on the suppression of fat accumulation in high-fat diet-induced obesity in C57BL/6 mice. The results showed that administration of (-)-SECO to obese mice suppresses body weight gain in a dose-dependent manner by regulating the expression of various genes related to fatty acid synthesis and beta-oxidation. Oral administration of (-)-SECO at 5.8 mg kg/day in mice fed a high-fat diet significantly decreases their body weight gain and reduced food intake and adiposity index with no statistical significance, indicating that (-)-SECO has an effect to regulate the body weight gain. Adiponectin levels were promoted by administering (-)-SECO in a dose-dependent manner which indicates that (-)-SECO might be useful for the prevention of lifestyle-related diseases for high-fat diet-induced obesity. The expression of SREBP-1c and FAS genes were significantly down regulated in liver from the group treated with (-)-SECO. The expression of beta-oxidation-related genes, such as PPARa, CPT-1, and ACOX, in liver were up-regulated in all groups treated with (-)-SECO, (-)-END, or (-)-END. Adiponectin induces the suppression of serum triglyceride levels through increasing the beta-oxidation-related genes in liver and skeletal muscle. Therefore, the overall results suggest that (-)-SECO reduces fatty acid synthesis by suppressing the expression of SREBP-1c and FAS genes in liver and promotes beta-oxidation of fatty acids in liver by inducing the expression of beta-oxidation-related genes, such as PPARa, CPT1, and ACOX. (Editors comments)



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