| Summary: | 博士 === 國立成功大學 === 基礎醫學研究所 === 101 === Obesity is a well-known metabolic disease in which appetite plays an important role. Imidazoline receptors have a profound influence on metabolic diseases. Thus, the aim of the present study is to investigate the effects of imidazoline receptors on the association between obesity and appetite. We have found that rilmenidine can attenuate hyperphagia in a streptozotocin (STZ)-induced diabetic animal model and that the effect was mediated through the activation of the central imidazoline I1-receptor (I1R) to decrease neuropeptide Y (NPY) expression. Additionally, we investigated how rilmenidine attenuated obesity in high fat diet (HFD)-fed mice and found that rilmenidine decreased body weight, energy intake and epididymal white adipose tissue (eWAT) accumulation via the activation of I1R. However, rilmenidine did not reduce appetite in leptin receptor-deficient db/db mice, which suggests that rilmenidine regulates hyperphagia via leptin. We tested allantoin as an alternative therapy to determine if it could decrease obesity. Allantoin reduced body weight, energy intake and NPY expression in HFD-fed mice. Allantoin also decreased eWAT weight and accumulation. The above effects of allantoin resulted from the activation of I1R. In contrast, allantoin significantly reduced hyperleptinemia in HFD-fed mice, but it could not decrease energy intake in db/db mice. The results suggested that the I1R-mediated obesity-reducing activity of allantoin was associated with the modulation of leptin. Taken together, the activation of I1R has beneficial effects in preventing obesity via the regulation of appetite and the reduction of fat accumulation.
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