Physiological factors determining cardiac energy expenditure

Author(s):  
Colin L. Gibbs
2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Kedryn K Baskin ◽  
Chad E Grueter ◽  
Christine M Kusminski ◽  
William L Holland ◽  
Santhosh Satapati ◽  
...  

The heart requires a continuous supply of energy but has little capacity for energy storage and thus relies on exogenous metabolic sources. We previously demonstrated that cardiac MED13 modulates systemic energy homeostasis in mice. In the present study, we sought to define the extra-cardiac tissue(s) that respond to cardiac MED13 signaling. Cardiac over-expression of MED13 in mice (MED13cTg) confers a lean phenotype that is associated with increased lipid uptake, beta-oxidation and mitochondrial content in white adipose tissue (WAT) and liver. Cardiac expression of MED13 decreases metabolic gene expression and metabolite levels in heart and liver but enhances them in WAT. Although exhibiting increased energy expenditure in the fed state, MED13cTg mice are metabolically flexible and adapt to fasting. These findings demonstrate that MED13 acts within the heart to promote systemic energy expenditure in extra-cardiac energy depots and point to an unexplored metabolic communication system between the heart and other tissues.


Author(s):  
Miyako Takaki ◽  
Taketoshi Namba ◽  
Junichi Araki ◽  
Kazunari Ishioka ◽  
Haruo Ito ◽  
...  

2020 ◽  
Vol 134 (5) ◽  
pp. 473-512 ◽  
Author(s):  
Ryan P. Ceddia ◽  
Sheila Collins

Abstract With the ever-increasing burden of obesity and Type 2 diabetes, it is generally acknowledged that there remains a need for developing new therapeutics. One potential mechanism to combat obesity is to raise energy expenditure via increasing the amount of uncoupled respiration from the mitochondria-rich brown and beige adipocytes. With the recent appreciation of thermogenic adipocytes in humans, much effort is being made to elucidate the signaling pathways that regulate the browning of adipose tissue. In this review, we focus on the ligand–receptor signaling pathways that influence the cyclic nucleotides, cAMP and cGMP, in adipocytes. We chose to focus on G-protein–coupled receptor (GPCR), guanylyl cyclase and phosphodiesterase regulation of adipocytes because they are the targets of a large proportion of all currently available therapeutics. Furthermore, there is a large overlap in their signaling pathways, as signaling events that raise cAMP or cGMP generally increase adipocyte lipolysis and cause changes that are commonly referred to as browning: increasing mitochondrial biogenesis, uncoupling protein 1 (UCP1) expression and respiration.


2003 ◽  
Author(s):  
Chung-Hee Chung ◽  
Kil-Dong Hong ◽  
Young-Sook Kim ◽  
Chung-Sik Her

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