Thounaojam Menaka C, Jadeja Ravirajsinh N, Ramani Umed V, Devkar Ranjitsinh V, Ramachandran A V
Division of Phytothrapeutics and Metabolic Endocrinology, Department of Zoology, The M. S. University of Baroda, Gujarat 390002, India; E-Mails:
Int J Mol Sci. 2011;12(7):4661-77. doi: 10.3390/ijms12074661. Epub 2011 Jul 19.
Sida rhomboidea. Roxb leaf extract (SRLE) is being used by the populace of North-East India to alleviate symptoms of diabetes and obesity. We have previously reported its hypolipidemic and anti-diabetic properties. In this study, we report the effect of SRLE on (i) in vivo modulation of genes controlling high fat diet (HFD) induced obesity and (ii) in vitro 3T3L1 pre-adipocyte differentiation and leptin release. Supplementation with SRLE significantly prevented HFD induced increment in bodyweight, plasma lipids and leptin, visceral adiposity and adipocyte hypertrophy. Also, SRLE supplementation reduced food intake, down regulated PPARγ2, SREBP1c, FAS and LEP expressions and up-regulated CPT-1 in epididymal adipose tissue compared to obese mice. In vitro adipogenesis of 3T3L1 pre-adipocytes was significantly retarded in the presence of SRLE extract. Also decreased triglyceride accumulation, leptin release and glyceraldehyde-3-Phosphate dehydrogenase activity along with higher glycerol release without significant alteration of viability of 3T3L1 pre-adipocytes, was recorded. Our findings suggest that prevention of HFD induced visceral adiposity is primarily by down regulation of PPARγ2 and leptin gene expression coupled with attenuation of food intake in C57BL/6J mice. SRLE induced prevention of pre-adipocytes differentiation, and leptin release further substantiated these findings and scientifically validates the potential application of SRLE as a therapeutic agent against obesity.
菱叶金午时花。罗克斯伯里叶提取物(SRLE)被印度东北部民众用于缓解糖尿病和肥胖症状。我们之前报道过它的降血脂和抗糖尿病特性。在本研究中,我们报告了SRLE对(i)控制高脂饮食(HFD)诱导肥胖的基因的体内调节作用,以及(ii)体外3T3L1前脂肪细胞分化和瘦素释放的影响。与肥胖小鼠相比,补充SRLE可显著预防HFD诱导的体重、血脂和瘦素增加、内脏脂肪增多和脂肪细胞肥大。此外,补充SRLE还可减少食物摄入量,下调附睾脂肪组织中PPARγ2、SREBP1c、FAS和LEP的表达,并上调CPT-1。在SRLE提取物存在的情况下,3T3L1前脂肪细胞的体外脂肪生成明显受阻。还记录到甘油三酯积累、瘦素释放和甘油醛-3-磷酸脱氢酶活性降低,同时甘油释放增加,而3T3L1前脂肪细胞的活力没有明显改变。我们的研究结果表明,在C57BL/6J小鼠中,预防HFD诱导的内脏脂肪增多主要是通过下调PPARγ2和瘦素基因表达以及减少食物摄入量来实现的。SRLE诱导的前脂肪细胞分化预防和瘦素释放进一步证实了这些发现,并从科学上验证了SRLE作为抗肥胖治疗剂的潜在应用价值。