Research press release


Nature Medicine

Shutting the door on obesity


ヒトは、効率よく食物中の脂肪を吸収し、エネルギー貯蔵のために脂肪組織へと取り込む。この能力はカロリー欠乏のときには有利だが、食餌中の脂肪が多いときには肥満の一因となる。R Farese, Jr.たちは、脂肪の蓄積に腸の酵素MGAT2が不可欠なことをマウスで明らかにした。



Knocking out an enzyme responsible for the metabolism of fat in the intestine protects mice from obesity, reports research published online in Nature Medicine this week. The findings suggest a possible new target for reducing obesity.

Humans are efficient in absorbing fat within their diet and assimilating it into adipose tissue for the storage of energy. Although this ability suggests an advantage in times of calorie deprivation, it contributes to obesity when dietary fat is abundant. Robert Farese, Jr., and his colleagues show that the intestinal enzyme MGAT2 is crucial for the buildup of fat in mice.

They find that the absence of MGAT2 protects mice on a high-fat diet against developing obesity, high cholesterol and fatty liver. Although food intake and fat absorption are normal in MGAT2-deficient mice, entry of dietary fat into the circulation is reduced, favoring the partitioning of fat toward energy dissipation instead of towards storage in the adipose tissue.

As MGAT2 is an intestinal enzyme that can, in principle, be readily accessible to pharmacological inhibition, these results point to a new target in the fight against obesity that may have medical potential before long.

doi: 10.1038/nm.1937


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