Reduced lipid and glucose oxidation and reduced lipid synthesis in AMPKα2^-/- myotubes.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-01-09 DOI:10.1080/13813455.2024.2449409

Christine Skagen, Stanislava Stevanovic, Hege Gilbø Bakke, Tuula A Nyman, Maria Stensland, Eili Tranheim Kase, Olga Horakova, Arild C Rustan, G Hege Thoresen

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引用次数: 0

Abstract

Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) plays a crucial role in regulation of metabolic homeostasis. To understand the role of the catalytic α2 subunit of AMPK in skeletal muscle energy metabolism, myotube cultures were established from AMPKα2^+/+ and AMPKα2^-/- mice. Myotubes from AMPKα2^-/- mice had lower basal oleic acid and glucose oxidation compared to myotubes from AMPKα2^+/+ mice. However, the relative response to mitochondrial uncoupling was increased for oleic acid oxidation. Incorporation of acetate into lipids was also lower in myotubes from AMPKα2^-/- mice. Proteomics analysis revealed that AMPKα2^-/- myotubes had upregulated pathways related to mitochondrial function and fatty acid oxidation, and decreased pathways related to fatty acid biosynthesis. In conclusion, ablation of AMPKα2 catalytic subunit in skeletal muscle cells resulted in reduced basal oxidation of glucose and fatty acids, however upregulated pathways related to mitochondrial function and fatty acid oxidation and reduced lipid formation.

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减少AMPKα2-/-肌管中的脂质和葡萄糖氧化和脂质合成。

腺苷5′-单磷酸腺苷（AMP）活化蛋白激酶（AMPK）在调节代谢稳态中起着至关重要的作用。为了了解AMPK的催化α2亚基在骨骼肌能量代谢中的作用，我们建立了AMPKα2+/+和AMPKα2-/-小鼠的肌管培养。与AMPKα2+/+小鼠相比，AMPKα2-/-小鼠肌管的基础油酸和葡萄糖氧化水平较低。然而，油酸氧化对线粒体解偶联的相对响应增加。AMPKα2-/-小鼠肌管中脂质中乙酸的掺入也较低。蛋白质组学分析显示，AMPKα2-/-肌管中与线粒体功能和脂肪酸氧化相关的通路上调，与脂肪酸生物合成相关的通路下调。综上所述，骨骼肌细胞中AMPKα2催化亚基的消融导致葡萄糖和脂肪酸的基础氧化减少，但与线粒体功能和脂肪酸氧化相关的途径上调，脂质形成减少。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.