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논문 기본 정보

자료유형
학술저널
저자정보
Zhang Yan (Tianjin Medical University China) Wu Zhaoxia (Tianjin Medical University China) Xi Pengjiao (Tianjin Medical University China) Wang Haomin (Tianjin Medical University China) Zhu Wenjuan (Tianjin Medical University China) Tian Derun (Tianjin Medical University China)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.44 No.4
발행연도
2022.4
수록면
467 - 475 (9page)
DOI
10.1007/s13258-021-01206-9

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Background Obesity is considered a major public health issue worldwide. Liver Kinase B1 (LKB1) is a serine/threonine kinase, peripheral LKB1 is involved in obesity by regulating adipogenesis, but the role of central LKB1 in the development of obesity remains unclear. Objective This study aims to explore the main role of LKB1 in POMC neurons on obesity, and reveal the underlying mechanism of central LKB1 affecting obesity through quantitative proteomics. Methods We constructed POMC neuron specific LKB1 knockout mice (PomcLkb1 KO) and exposed them to high fat diet intervention for three months. The effect of LKB1 knockout on obesity was evaluated by monitoring body weight, food intake and measuring fat content. The hypothalamus tissues were collected for proteomic analysis and validated by RT-PCR. Results The degree of obesity was aggravated in PomcLkb1 KO mice fed with high fat diet. Proteomic results showed that only Histone deacetylase 1 (HDAC1) was down-regulated in the hypothalamus of PomcLkb1 KO mice. Our research also found that LKB1 knockout on POMC neurons led to reduction of Peroxisome proliferator-activated receptor γ (PPARγ). Meanwhile, the software predicted that the transcription factor PPARγ binds to the HDAC1 promoter. Therefore, we speculated that central LKB1 may regulate diet-induced obesity development by influencing HDAC1/PPARγ expression. Conclusion We firstly found that central LKB1 may affect the development of obesity by regulating the expression of HDAC1, which provides a new idea for the central regulatory mechanism of obesity.

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