MacPherson 2016 Am J Physiol Cell Physiol: Difference between revisions
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Copyright ยฉ 2016 the American Physiological Society. | Copyright ยฉ 2016 the American Physiological Society. | ||
|keywords=5โฒ-AMP-activated protein kinase, Adipose tissue triglyceride lipase, Lipolysis, Mitochondria, Mouse, White adipose tissue | |keywords=5โฒ-AMP-activated protein kinase, Adipose tissue triglyceride lipase, Lipolysis, Mitochondria, Mouse, White adipose tissue | ||
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|tissues=Fat | |tissues=Fat | ||
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|pathways=N | |pathways=N | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
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Latest revision as of 14:45, 31 July 2017
| MacPherson RE, Dragos SM, Ramos S, Sutton C, Frendo-Cumbo S, Castellani L, Watt MJ, Perry CG, Mutch DM, Wright DC (2016) Reduced ATGL-mediated lipolysis attenuates ฮฒ-adrenergic-induced AMPK signaling, but not the induction of PKA-targeted genes, in adipocytes and adipose tissue. Am J Physiol Cell Physiol 311:C269-76. |
MacPherson RE, Dragos SM, Ramos S, Sutton C, Frendo-Cumbo S, Castellani L, Watt MJ, Perry CG, Mutch DM, Wright DC (2016) Am J Physiol Cell Physiol
Abstract: 5'-AMP-activated protein kinase (AMPK) is activated as a consequence of lipolysis and has been shown to play a role in regulation of adipose tissue mitochondrial content. Conversely, the inhibition of lipolysis has been reported to potentiate the induction of protein kinase A (PKA)-targeted genes involved in the regulation of oxidative metabolism. The purpose of the current study was to address these apparent discrepancies and to more fully examine the relationship between lipolysis, AMPK, and the ฮฒ-adrenergic-mediated regulation of gene expression. In 3T3-L1 adipocytes, the adipose tissue triglyceride lipase (ATGL) inhibitor ATGListatin attenuated the Thr(172) phosphorylation of AMPK by a ฮฒ3-adrenergic agonist (CL 316,243) independent of changes in PKA signaling. Similarly, CL 316,243-induced increases in the Thr(172) phosphorylation of AMPK were reduced in adipose tissue from whole body ATGL-deficient mice. Despite reductions in the activation of AMPK, the induction of PKA-targeted genes was intact or, in some cases, increased. Similarly, markers of mitochondrial content and respiration were increased in adipose tissue from ATGL knockout mice independent of changes in the Thr(172) phosphorylation of AMPK. Taken together, our data provide evidence that AMPK is not required for the regulation of adipose tissue oxidative capacity in conditions of reduced fatty acid release.
Copyright ยฉ 2016 the American Physiological Society. โข Keywords: 5โฒ-AMP-activated protein kinase, Adipose tissue triglyceride lipase, Lipolysis, Mitochondria, Mouse, White adipose tissue
โข O2k-Network Lab: CA Toronto Perry CG
Labels: MiParea: Respiration, nDNA;cell genetics, Genetic knockout;overexpression
Organism: Mouse
Tissue;cell: Fat
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS
Pathway: N
HRR: Oxygraph-2k
