Format

Send to

Choose Destination
Nat Rev Endocrinol. 2016 Jul;12(7):421-32. doi: 10.1038/nrendo.2016.67. Epub 2016 May 20.

Hypothalamic AMPK: a canonical regulator of whole-body energy balance.

Author information

1
Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, 15782, Spain.
2
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, 15706, Spain.
3
Department of Cell Biology, Physiology and Immunology, University of Córdoba; Instituto Maimónides de Investigación Biomédica (IMIBIC)/Hospital Reina Sofía, 14004 Córdoba, Spain.
4
FiDiPro Program, Department of Physiology, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland.

Abstract

AMP-activated protein kinase (AMPK) has a major role in the modulation of energy balance. AMPK is activated in conditions of low energy, increasing energy production and reducing energy consumption. The AMPK pathway is a canonical route regulating energy homeostasis by integrating peripheral signals, such as hormones and metabolites, with neuronal networks. Current evidence has implicated AMPK in the hypothalamus and hindbrain with feeding, brown adipose tissue thermogenesis and browning of white adipose tissue, through modulation of the sympathetic nervous system, as well as glucose homeostasis. Interestingly, several potential antiobesity and/or antidiabetic agents, some of which are currently in clinical use such as metformin and liraglutide, exert some of their actions by acting on AMPK. Furthermore, the orexigenic and weight-gain effects of commonly used antipsychotic drugs are also mediated by hypothalamic AMPK. Overall, this evidence suggests that hypothalamic AMPK signalling is an interesting target for drug development, but is this approach feasible? In this Review we discuss the current understanding of hypothalamic AMPK and its role in the central regulation of energy balance and metabolism.

PMID:
27199291
DOI:
10.1038/nrendo.2016.67
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center