相关实验视频

Updated: Jun 6, 2025

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice

Published on: May 16, 2021

较高的AMPK激活在小鼠氧化与糖溶性肌肉相比,与LKB1或CaMKKβ表达不相关

Romain Bernasconi¹, Kärol Soodla¹, Alex Sirp²

¹Laboratory of Systems Biology, Department of Cybernetics, Tallinn University of Technology, Tallinn, Estonia.

American journal of physiology. Endocrinology and metabolism

|November 28, 2024

概括

与培养细胞相反,AMP激活蛋白激酶 (AMPK) 的激活在氧化肌肉中高于糖溶性肌肉,与培养细胞相反. 这种差异不能由LKB1或CaMKKβ解释,这表明复杂的肌肉调节.

科学领域:

肌肉生理学肌肉生理学
细胞代谢的细胞代谢.
生物化学生化学

背景情况:

AMP激活蛋白激酶 (AMPK) 是细胞能量代谢的关键调节剂.
AMPK激活受上游激酶的影响,例如肝激酶B1 (LKB1) 和CaMKKβ.
在培养细胞中,AMPK激活通常与LKB1活性相关.

研究的目的:

为了比较基底AMPK激活水平在糖溶性肌肉和氧化肌肉.
在不同肌肉类型中研究AMPK激活与LKB1或CaMKKβ之间的关系.
为了阐明AMPK在肌肉组织中的复杂调节.

主要方法:

西方涂抹被用来评估AMPK,LKB1和CaMKKβ的表达和酸化.
测量AMPK激活和CaMKKβ活性是在小鼠单体,胃半体,EDL和心脏组织中进行的.
分析包括雄性和雌性C57BL6J小鼠.

主要成果:

在氧化肌肉 (脚底,心脏) 中,AMPK的激活显著高于在糖溶性肌肉 (胃腹肌,EDL) 中.
这种更高的激活与AMPKα1-异型表达相关,但与LKB1或CaMKKβ表达或活性无关.
LKB1表达显示性二态,在男性较低,而CaMKKβ表达在骨肌肉中是最小的.

结论:

在氧化肌肉中AMPK激活率较高,与其在维持氧化表型中的作用保持一致.
肌肉中AMPK的调节比培养细胞更复杂,不仅仅依赖于LKB1或CaMKKβ.
未来的研究应该探索AMPK的异型,局部化和能量细分,以治疗向.

关键词:

这就是AMPKK.这就是为什么CaMKKββ.一个LKB1一个LKB1 糖溶性肌肉是一种肌肉.氧化肌肉是一种氧化肌肉.

更多相关视频

Activating Autophagy by Aerobic Exercise in Mice

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

相关概念视频

cAMP-dependent Protein Kinase Pathways

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...