한빛사논문
- 조회447
서울대학교 수의과대학
Gi-Sue Kang 1, Hye-Ju Jo 1, Ye-Rim Lee 1, Taerim Oh 1, Hye-Joon Park 2 and G-One Ahn 1,2,*
1College of Veterinary Medicine, Seoul National University, 1 Gwanak-Ro, Gwanak-Gu, Seoul 08826, Korea.
2College of Medicine, Seoul National University, 1 Gwanak-Ro, GwanakGu, Seoul 08826, Korea.
*Corresponding author: correspondence to G-One Ahn
Abstract
Adipose tissues, composed of various cell types, including adipocytes, endothelial cells, neurons, and immune cells, are organs that are exposed to dynamic environmental challenges. During diet-induced obesity, white adipose tissues experience hypoxia due to adipocyte hypertrophy and dysfunctional vasculature. Under these conditions, cells in white adipose tissues activate hypoxia-inducible factor (HIF), a transcription factor that activates signaling pathways involved in metabolism, angiogenesis, and survival/apoptosis to adapt to such an environment. Exposure to cold or activation of the β-adrenergic receptor (through catecholamines or chemicals) leads to heat generation, mainly in brown adipose tissues through activating uncoupling protein 1 (UCP1), a proton uncoupler in the inner membrane of the mitochondria. White adipose tissues can undergo a similar process under this condition, a phenomenon known as ‘browning’ of white adipose tissues or ‘beige adipocytes’. While UCP1 expression has largely been confined to adipocytes, HIF can be expressed in many types of cells. To dissect the role of HIF in specific types of cells during diet-induced obesity, researchers have generated tissue-specific knockout (KO) mice targeting HIF pathways, and many studies have commonly revealed that intact HIF-1 signaling in adipocytes and adipose tissue macrophages exacerbates tissue inflammation and insulin resistance. In this review, we highlight some of the key findings obtained from these transgenic mice, including Ucp1 KO mice and other models targeting the HIF pathway in adipocytes, macrophages, or endothelial cells, to decipher their roles in diet-induced obesity.
논문정보
- Review Paper
- 2023년 11월 (BRIC 등록일 2023-11-02)
- 국내 연구진
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