在十大死亡原因中，就有惡性腫瘤、心臟疾病、腦血管疾病、糖尿病、慢性肝病及肝硬化和高血壓性疾病等六項與肥胖有關，肥胖是其危險因子。Hedgehog（Hh）信號調節非脊椎動物和脊椎動物的發育，但是未明確定義其在脂肪發展之機制。因此，本篇論文在於探討Hh對於脂肪生成之影響。我們利用3T3-L1前脂肪細胞分化成脂肪細胞之方法，分析其Hh信號途徑之mRNA表現量。分化前的前脂肪細胞與分化後的脂肪細胞，比較其Hh信號途徑之mRNA表現量，發現分化後的脂肪細胞Hh信號之mRNA表現量減少。比較分化成功與否之細胞其Hh信號途徑之mRNA表現差異，發現分化成功的脂肪細胞其Hh信號之mRNA表現量減少。進一步地研究，在小鼠體內脂肪分解時，Hh對脂肪細胞的影響，因此，更了解Hh對於脂肪生成之影響。換言之，Hh對於脂肪生成具有抑制作用，而且Hh途徑成為治療肥胖，甚至因肥胖所引起的慢性疾病的可能潛在性角色。
Obesity is implicated as a risk factor in 6 out of the 10 major causes of death, namely malignant tumour , heart disease , brain blood vessel disease , diabetes , chronic liver diseases, cirrhosis and hypertension. Hedgehog (Hh) signaling is known as a pivotal regulator during invertebrate and vertebrate embryonic development, and is known to cause various tumors if it is hyperactivated beyond normal status. However, whether Hedgehog signaling is involved in fat formation is not defined clearly . Hence, this project aimed to elucidate the effect of Hh in adipogenesis. 3T3-L1 cell and mouse adipogenesis models are used to assay the Hh signaling during the entire process. Our data showed that Hh signaling was decreased during adipogenesis. Hh signaling was also compared between failed adipogenesis and successful adipogenesis. The results showed that only in successfully differentiated adipocytes that Hh _expression was downregulated. Furthermore, comparable effects of Hh in fat formation was seen in mice. We conclude that Hh signaling inhibits fat formation under both in vivo and in vitro conditions. Results of this study potentiate the use of Hh pathway in developing therapeutic targets for obesity and in prevention of diseases caused by obesity.
