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NDUFAB1作为牛脂肪细胞中NEFA诱导的代谢功能障碍的新型调节因子。

NDUFAB1 as a Novel Regulator of NEFA-Induced Metabolic Dysfunction in Bovine Adipocytes.

作者信息

Zhou Jing, Tang Tao, Sun Wenqiang, Jia Xianbo, Wang Jie, Yu Hengwei, Lai Songjia

机构信息

College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, China.

出版信息

Animals (Basel). 2025 May 30;15(11):1618. doi: 10.3390/ani15111618.

DOI:10.3390/ani15111618
PMID:40509084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12153833/
Abstract

Elevated non-esterified fatty acid (NEFA) levels are closely associated with metabolic disorders in dairy cattle, yet their direct effects on adipocyte physiology remain poorly understood. In this study, we demonstrate that high NEFA concentrations significantly impair bovine adipocyte function by simultaneously inhibiting proliferation/differentiation ( < 0.01) and promoting pathological lipid deposition. Through integrated transcriptomic and functional analyses, we identified NDUFAB1 as a central metabolic regulator that counteracts NEFA-induced adipocyte dysfunction. Mechanistically, NDUFAB1 activation attenuates the cytotoxic effects of excessive NEFA exposure. These findings provide both fundamental insights into energy metabolism regulation and a potential therapeutic target (NDUFAB1) for preventing bovine metabolic diseases.

摘要

非酯化脂肪酸(NEFA)水平升高与奶牛的代谢紊乱密切相关,但其对脂肪细胞生理的直接影响仍知之甚少。在本研究中,我们证明高NEFA浓度通过同时抑制增殖/分化(<0.01)和促进病理性脂质沉积,显著损害牛脂肪细胞功能。通过综合转录组学和功能分析,我们确定NDUFAB1是一种对抗NEFA诱导的脂肪细胞功能障碍的核心代谢调节因子。从机制上讲,NDUFAB1的激活减弱了过量NEFA暴露的细胞毒性作用。这些发现为能量代谢调节提供了基本见解,并为预防牛代谢疾病提供了一个潜在的治疗靶点(NDUFAB1)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/3f3e08d98b85/animals-15-01618-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/fff77d238ec6/animals-15-01618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/7e8fca50faec/animals-15-01618-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/8c1567684b83/animals-15-01618-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/e0bd3956002e/animals-15-01618-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/1782b98a7a4c/animals-15-01618-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/b8b87724f1a2/animals-15-01618-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/8ce8d4227886/animals-15-01618-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/3f3e08d98b85/animals-15-01618-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/fff77d238ec6/animals-15-01618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/7e8fca50faec/animals-15-01618-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/8c1567684b83/animals-15-01618-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/e0bd3956002e/animals-15-01618-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/1782b98a7a4c/animals-15-01618-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/b8b87724f1a2/animals-15-01618-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/8ce8d4227886/animals-15-01618-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0579/12153833/3f3e08d98b85/animals-15-01618-g008.jpg

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Cellular ATP demand creates metabolically distinct subpopulations of mitochondria.
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