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Updated: Aug 23, 2026

Analysis of Chromosome Segregation, Histone Acetylation, and Spindle Morphology in Horse Oocytes
Published on: May 11, 2017
UCP1 maintains lipid homeostasis and developmental competence through MCU-mediated mitochondrial calcium uptake in
Yuwen Luo1, Jun Li2, Yun Wang3
1State Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, 100193, China; College of Biological Sciences, China Agricultural University, Beijing, 100193, China.
Abstract:
Lipid homeostasis is essential for oocyte quality and developmental competence, and uncoupling protein 1 (UCP1) has been identified as a critical regulator of lipid metabolism in oocytes. However, the downstream molecular mechanism by which UCP1 regulates lipid homeostasis remains unexplored. In this study, we demonstrate that UCP1 inhibition impairs oocyte developmental competence, accompanied by increased lipid accumulation, elevated oxidative stress, and disrupted mitochondrial function. Further investigation revealed that UCP1 inhibition markedly elevated mitochondrial calcium levels, which were associated with upregulation of the mitochondrial calcium uniporter (MCU). Functional inhibition of MCU with Ru360 reduced mitochondrial calcium accumulation and alleviated mitochondrial function, redox homeostasis, and lipid metabolic balance, ultimately improving oocyte developmental competence. These findings suggest that UCP1 regulates oocyte lipid homeostasis and developmental competence through MCU-dependent mitochondrial calcium uptake, establishing a mechanistic link between mitochondrial uncoupling, calcium homeostasis, and oocyte quality.
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