AMP-activated protein kinase signaling in metabolic regulation
Yun Chau Long, Juleen R. Zierath
Yun Chau Long, Juleen R. Zierath
Published July 3, 2006
Citation Information: J Clin Invest. 2006;116(7):1776-1783. https://doi.org/10.1172/JCI29044.
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AMP-activated protein kinase signaling in metabolic regulation

Abstract

AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. When activated by a deficit in nutrient status, AMPK stimulates glucose uptake and lipid oxidation to produce energy, while turning off energy-consuming processes including glucose and lipid production to restore energy balance. AMPK controls whole-body glucose homeostasis by regulating metabolism in multiple peripheral tissues, such as skeletal muscle, liver, adipose tissues, and pancreatic β cells — key tissues in the pathogenesis of type 2 diabetes. By responding to diverse hormonal signals including leptin and adiponectin, AMPK serves as an intertissue signal integrator among peripheral tissues, as well as the hypothalamus, in the control of whole-body energy balance.

Authors

Yun Chau Long, Juleen R. Zierath

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Figure 3

Integration of intertissue signaling by AMPK.

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Integration of intertissue signaling by AMPK. Adipocyte-derived leptin r...
Adipocyte-derived leptin reduces food intake though inhibition of hypothalamic AMPK. Leptin increases skeletal muscle fatty acid oxidation via direct activation of AMPK and the hypothalamus–sympathetic nervous system axis. The involvement of hypothalamic AMPK in leptin-induced skeletal muscle lipid oxidation and glucose uptake is unknown. Adiponectin is secreted by adipose tissue and increases skeletal muscle lipid oxidation and glucose uptake, as well as suppressing liver glucose production by activating AMPK.