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Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,118
Online ISSN 1827-1634
OBESITY IN 2007
Laval Hospital Research Center and Merck Frosst/CIHR Research Chair in Obesity Chemin Sainte-FoyQuébec, Canada
Energy stores are regulated through complex neural controls exerted on both food intake and energy expenditure. These controls are insured by interconnected neurons that produce different peptides or classic neurotransmitters, which have been regrouped into ‘anabolic’ and ‘catabolic’ systems. While the control of energy intake has been addressed in numerous investigations, that of energy expenditure has, as yet, only received a moderate interest, even though energy expenditure represents a key determinant of energy balance. In laboratory rodents, in particular, a strong regulatory control is exerted on brown adipose tissue (BAT), which represent an efficient thermogenic effector. BAT thermogenesis is governed by the sympathetic nervous system (SNS), whose activity is controlled by neurons comprised in various brain regions, which include the paraventricular hypothalamic nucleus (PVH), the arcuate nucleus (ARC) and the lateral hypothalamus (LH). Proopiomelanocortin neurons from the ARC project to the PVH and terminate in the vicinity of the melanocortin-4 receptors, which are concentrated in the descending division of the PVH, which comprise neurons controlling the SNS outflow to BAT. The LH contains neurons producing melanin-concentrating hormone or orexins, which also are important peptides in the control of energy expenditure. These neurons are not only polysynaptically connected to BAT, but also linked to brains regions controlling motivated behaviors and locomotor activity and, consequently, their role in the control of energy expenditure could go beyond BAT thermogenesis.