Molecular and cell biological studies on the regulation of UCP1 gene expression aiming to prevent obesity in dogs

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K05963
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 42020:Veterinary medical science-related
• Research Institution: Azabu University
• Principal Investigator: Murakami Masaru 麻布大学, 獣医学部, 教授 (80271360)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: イヌ / UCP1 / 脂肪細胞 / 肥満 / 遺伝子発現制御 / エネルギー消費

Outline of Final Research Achievements

Obesity is a serious problem in canine veterinary medicine that must be resolved. One of the trump cards to eliminate obesity is the activation of brown and beige adipocytes, and UCP1 is the key gene responsible for this. In this study, we showed that canine UCP1 was expressed in a variety of tissues, and we also isolated a new variant of the UCP1 gene. We also explored candidate regulators that modulate UCP1 transcription. Using subcutaneous or visceral adipose tissues from 129 dogs hospitalized at veterinary clinics, we examined the expression levels of a total of 23 genes including obesity-related genes, and analyzed in detail the relationships between the expression of these genes and canine health conditions such as BCS, age, and tumor. Primary adipose progenitor cell lines were also cultured from normal canine adipose stem cells.

Free Research Field

基礎獣医学、分子・細胞生物学

Academic Significance and Societal Importance of the Research Achievements

肥満はペット犬が健康を維持する上で最大の関心事である。肥満は様々な疾病の誘発因子であり、その制御は重要な獣医学的課題である。ヒトの肥満解消の切り札として、褐色・ベージュ脂肪細胞の活性化が注目され、脱共役タンパク質1(UCP1)がそのカギを握っている。我々は、イヌのUCP1発現パターンは実験動物やヒトとは異なり、ユニークであることを見つけ、イヌのUCP1を介したエネルギー代謝調節は独特である可能性を示した。本研究でのイヌ個体及び細胞培養系の解析から得られた、イヌの脂肪組織でのUCP1を含む脂肪関連遺伝子の発現と制御に関する成果は、イヌの肥満やその関連疾患の予防や治療に向けた基礎的知見を提供する。