Feedback regulation between AMPK and HIF-1α contributes to color stability via energy metabolism and mitochondrial efficiency regulation of yak meat

文献类型： 外文期刊

第一作者： Zhu, Xijin

作者： Zhu, Xijin;Yang, Chao;Tan, Siyi;Han, Ling;Yu, Qunli;Zhu, Xijin;Wang, Linlin;Liu, Wenyu

作者机构：

关键词： HIF-1 alpha phosphorylation; AMPK; pH decline; Myoglobin; Mitochondria; Oxygen consumption

期刊名称：LWT-FOOD SCIENCE AND TECHNOLOGY （ 影响因子：6.0； 五年影响因子：6.0 ）

ISSN： 0023-6438

年卷期： 2024 年 199 卷

页码：

收录情况： SCI

摘要： Despite the well-established individual roles of AMP-activated protein kinase (AMPK) and hypoxia-inducible factor-1 alpha (HIF-1 alpha) in sensing energy stress and/or hypoxia in postmortem muscle, a knowledge gap persists regarding their interplay and the consequent impact on the yak meat color stability. This study aimed to elucidate the AMPK-HIF-1 alpha interaction and its consequential impact on mitochondrial functionality, energy metabolism, and ultimately, color attributes. Postmortem yak longissimus thoracis et lumborum (LTL) muscles were incubated with saline, AMPK inhibitor (Compound C), Compound C plus HIF-1 alpha activator (DMOG), and Compound C plus HIF-1 alpha inhibitor (YC-1) for 0, 6, 12, 24, 72, and 120 h, respectively. Results indicate that Compound C hindered the nuclear translocation of HIF-1 alpha (P < 0.001), in turn, DMOG upregulated AMPK protein levels (P < 0.05) by a yet unknown mechanism. Mass spectrometry analysis identified seven AMPK-induced phosphorylation sites (Ser58, Thr63, Ser65, Tyr66, Thr677, Ser14, and Ser15) mapped onto three phosphopeptides on HIF-1 alpha. Moreover, Compound C induced a significant reduction in energy metabolism levels, evidenced by decreased glycogen degradation, lactate accumulation, and pH decline (P < 0.05). Besides, Compound C promoted a consistently decreased mitochondrial protein yield, reduced NADH content, and OCR (P < 0.05). However, DMOG attenuated the effects of Compound C on mitochondrial efficiency, and interconversion of oxyto deoxymyoglobin. Collectively, these findings establish the collaborative influence of AMPK and HIF-1 alpha on postmortem energy metabolism, concurrently emphasizing their antagonistic effects on mitochondrial function.

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