Identification of the causative gene and analysis of its role in glucose metabolism in antiobesity and high glucose tolerance mice.

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K09893
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: Kurume University
• Principal Investigator: Sato Takahiro 久留米大学, 付置研究所, 准教授 (50368883)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: CREBBP

Outline of Final Research Achievements

The anti-obesity high glucose tolerance mouse is a dwarf mutant mouse that emerged by mutation. From the analysis so far, it has been shown that this mouse has a low blood glucose level at rest, exhibits high glucose tolerance, and is resistant to obesity even when loaded with a high fat diet. In other words, since this mouse is characterized by high glucose tolerance and anti-obesity, it is considered that establishment of a new strain and advancement of functional analysis will lead to the understanding of the onset and pathological condition of lifestyle-related diseases. In the present study, we determined that the gene responsible for antiobesity and high glucose tolerance mice was the Crebbp gene on chromosome 16, and revealed that a single nucleotide deletion in this gene causes a frameshift.

Free Research Field

神経内分泌学

Academic Significance and Societal Importance of the Research Achievements

本研究で樹立に成功した抗肥満高耐糖能マウスは、糖負荷によって著しく血糖値が上昇したり、高脂肪食負荷によって過度の肥満を呈したりする従来の疾患モデルマウスとは異なり、これらの負荷条件下でも恒常性を維持できる高い適応力を持っている。このことから、糖尿病や肥満症の発症・進行の研究において、新しいタイプのモデル動物としての利用が期待される。さらに、本研究から抗肥満高耐糖能マウスの責任遺伝子を明らかにすることができたため、遺伝子レベルで基礎研究を進めることが可能となった。したがって、抗肥満高耐糖能マウスを用いた研究成果は、今後、新たな創薬ターゲットや治療戦略の創出にも繋がることが期待される。