scholarly journals AMP-activated protein kinase signalling pathways are down regulated and skeletal muscle development impaired in fetuses of obese, over-nourished sheep

2008 ◽  
Vol 586 (10) ◽  
pp. 2651-2664 ◽  
Author(s):  
Mei J. Zhu ◽  
Bin Han ◽  
Junfeng Tong ◽  
Changwei Ma ◽  
Jessica M. Kimzey ◽  
...  
2020 ◽  
Vol 134 (17) ◽  
pp. 2381-2398
Author(s):  
Miao Chen ◽  
Caoyu Ji ◽  
Qingchen Yang ◽  
Shuya Gao ◽  
Yue Peng ◽  
...  

Abstract Skeletal muscle is responsible for the majority of glucose disposal in the body. Insulin resistance in the skeletal muscle accounts for 85–90% of the impairment of total glucose disposal in patients with type 2 diabetes (T2D). However, the mechanism remains controversial. The present study aims to investigate whether AKT2 deficiency causes deficits in skeletal muscle development and metabolism, we analyzed the expression of molecules related to skeletal muscle development, glucose uptake and metabolism in mice of 3- and 8-months old. We found that AMP-activated protein kinase (AMPK) phosphorylation and myocyte enhancer factor 2 (MEF2) A (MEF2A) expression were down-regulated in AKT2 knockout (KO) mice, which can be inverted by AMPK activation. We also observed reduced mitochondrial DNA (mtDNA) abundance and reduced expression of genes involved in mitochondrial biogenesis in the skeletal muscle of AKT2 KO mice, which was prevented by AMPK activation. Moreover, AKT2 KO mice exhibited impaired AMPK signaling in response to insulin stimulation compared with WT mice. Our study establishes a new and important function of AKT2 in regulating skeletal muscle development and glucose metabolism via AMPK-dependent signaling.


Reproduction ◽  
2011 ◽  
Vol 141 (3) ◽  
pp. 301-312 ◽  
Author(s):  
Gi Fay Mok ◽  
Dylan Sweetman

The development and differentiation of vertebrate skeletal muscle provide an important paradigm to understand the inductive signals and molecular events controlling differentiation of specific cell types. Recent findings show that a core transcriptional network, initiated by the myogenic regulatory factors (MRFs; MYF5, MYOD, myogenin and MRF4), is activated by separate populations of cells in embryos in response to various signalling pathways. This review will highlight how cells from multiple distinct starting points can converge on a common set of regulators to generate skeletal muscle.


2017 ◽  
Vol 95 (8) ◽  
pp. 3552
Author(s):  
E. M. England ◽  
H. Shi ◽  
S. K. Matarneh ◽  
E. M. Oliver ◽  
E. T. Helm ◽  
...  

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