ＧＰＲ１２０

高脂肪の食事を取った場合に、脂肪を蓄積したり、肥満リスクを高めたりする遺伝子の働きを、京都大大学院薬学研究科の辻本教授（ゲノム創薬）の研究グループなどが突き止め、２０日付の英科学誌「ネイチャー」電子版に発表した。肥満の治療薬への応用が期待されるという。
　辻本教授らは、体内に入ってきた脂肪をセンサーのように感知する受容体「ＧＰＲ１２０」に着目。遺伝子異常でＧＰＲ１２０を持たないマウスを、低脂肪食と高脂肪食を与えるグループに分けて飼育し、体重や脂肪量の変化を正常なマウスと比較した。
　高脂肪食グループのＧＰＲ１２０がないマウスは、正常のマウスよりも体重や脂肪量が１０～１５％程度増え、内臓の脂肪細胞も肥大化。ＧＰＲ１２０の機能低下が、肥満や脂肪蓄積に大きく関わっていると結論づけた。低脂肪食グループは、ＧＰＲ１２０の有無による差は、ほぼなかったという。
　また、欧州の約１万５千人の遺伝子を調査したところ、約３％の人にＧＰＲ１２０の配列の一部に変異がみられ、正常な人に比べて肥満になるリスクが１・６倍高くなっているという。
　辻本教授は「肥満に関するより詳細なメカニズムを解明できれば、新たな治療薬の創出が期待できるのでは」と話している。太り気味の方にとっては朗報になるかもしれませんね。

If you took a high-fat meal, such as research groups (drug discovery) is located, dated 20 Tsujimoto, Professor of Kyoto University Graduate School of Pharmaceutical Sciences, the workings of the gene or the fat accumulation, or increase the risk of obesity electronic version was released in "Nature" of British science journal. That is expected to be applied to the treatment of obesity.

Prof. Tsujimoto, the focus on "GPR120" receptor of the sensor to be perceived as coming into the body fat. Reared in groups to give a high-fat diet and low-fat diet, the mice without the gene abnormality GPR120, were compared with normal mice changes in the amount of body weight and fat.

Mouse GPR120 do not have a high-fat diet group, body weight and fat mass increased from about 10 to 15% of normal mice, visceral fat cells are also bloated. Was concluded that decreased function of GPR120, and heavily involved in obesity and fat accumulation. Low-fat diet group, the difference is due to the presence or absence of GPR120, that almost did not.

, While studying the gene of approximately 15,000 people in Europe, the mutation was observed to human GPR120 part of an array of about 3%, 1.6 times risk of becoming obese compared to normal human that is higher.

That said, "If you can clarify the mechanism for more details about obesity, they can be expected that the creation of a new treatment," Professor and Tsujimoto. Of overweight for people who might actually be good news become.