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Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance
Journal article   Open access   Peer reviewed

Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance

Miguel López, Luis Varela, María J Vázquez, Sergio Rodríguez-Cuenca, Carmen R González, Vidya R Velagapudi, Donald A Morgan, Erik Schoenmakers, Khristofor Agassandian, Ricardo Lage, …
Nature medicine, Vol.16(9), pp.1001-1008
09/2010
DOI: 10.1038/nm.2207
PMCID: PMC2935934
PMID: 20802499
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2935934View
Open Access

Abstract

Thyroid hormones have widespread cellular effects; however it is unclear whether their effects on the central nervous system (CNS) contribute to global energy balance. Here, we demonstrate that either whole body hyperthyroidism or central administration of triiodothyronine (T3) decreases the activity of hypothalamic AMP-activated protein kinase (AMPK), increases sympathetic nervous system (SNS) activity and upregulates thermogenic markers in brown adipose tissue (BAT). Inhibition of the lipogenic pathway in the ventromedial nucleus of the hypothalamus (VMH) prevents CNS-mediated activation of BAT by thyroid hormone and reverses the weight loss associated with hyperthyroidism. Similarly inhibition of thyroid hormone receptors (TRs) in the VMH reverses the weight loss associated with hyperthyroidism. This regulatory mechanism depends on AMPK inactivation as genetic ablation of this enzyme in the VMH of euthyroid rats induces feeding-independent weight loss and increases expression of thermogenic markers in BAT. These effects are reversed by pharmacological blockade of the SNS. Thus, thyroid-hormone-induced modulation of AMPK activity and lipid metabolism in the hypothalamus is an important regulator of energy homeostasis.

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