Abstract

Activation of the adrenergic system has a profound effects on metabolism. Increased circulating catecholamine and activation of the different adrenergic receptors deployed in the various organs produce important metabolic responses which include: (1) increased lipolysis and elevated levels of fatty acids in plasma, (2) increased gluconeogenesis by the liver to provide substrate for the brain, and (3) moderate inhibition of insulin release by the pancreas to conserve glucose and to shift fuel metabolism of muscle in the direction of fatty acid oxidation. These physiological responses, typical of the stress conditions, are demonstrated to be detrimental for the functioning of different organs like the cardiac muscle when they become chronic. Indeed, a common feature of many pathological conditions involving over-activation of the adrenergic system is the development of metabolic alterations which can include insulin resistance, altered glucose and lipid metabolism and mitochondrial dysfunction. These patterns are involved with a variably extent among the different pathologies, however, they are in general strictly correlated to the level of activation of the adrenergic system. Here we will review the effects of the different adrenergic receptors subtypes on the metabolic variation observed in important disease like Heart Failure.

Highlights

  • Heart function relies to a great extent on cardiac muscle oxidative metabolism

  • Insulin receptor signaling is critically involved in increasing glucose uptake in the myocardium and cardiac insulin resistance contributes to the development of left ventricular (LV) dysfunction by reducing cardiac efficiency through metabolic shift toward fatty acids utilization (Peterson et al, 2004b)

  • Several hypotheses have been proposed to explain the association between altered cardiac metabolism, insulin resistance, and HF, and among these there is a strong correlation with neurohormonal activation (Kostis and Sanders, 2005; Zucker, 2006), which increases plasma free fatty acid (FFA) levels, inhibits insulin receptor signaling and causes the loss of myocyte glucose uptake (Opie and Sack, 2002)

Read more

Summary

Introduction

Heart function relies to a great extent on cardiac muscle oxidative metabolism. Given the high mitochondrial content of this tissue, cardiac muscle generates ATP almost exclusively (about 90%) through oxidative phosphorylation (Stanley et al, 2005) by using different metabolic substrates. This metabolic remodeling is characterized by a lower oxidative capacity, contractile dysfunction and cardiac muscle insulin resistance (Stanley et al, 2005; Neubauer, 2007).

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.