Endocrinol Metab.  2016 Dec;31(4):519-524. 10.3803/EnM.2016.31.4.519.

Brain Regulation of Energy Metabolism

• Roh E
• Kim MS

• KMID: 2373070
• DOI: http://doi.org/10.3803/EnM.2016.31.4.519

Abstract

In healthy individuals, energy intake is in balance with energy expenditure, which helps to maintain a normal body weight. The brain's inability to control energy homeostasis underlies the pathology of hyperphagia and obesity. The brain detects body energy excess and deficit by sensing the levels of circulating metabolic hormones and nutrients and by receiving metabolic information from the periphery via the autonomic nervous system. A specialized neuronal network coordinates energy intake behavior and the metabolic processes affecting energy expenditure. Here, we briefly review neuronal mechanisms by which our body maintains energy balance.

Keyword

Hypothalamus; Brain stem; Energy metabolism; Obesity

MeSH Terms

Autonomic Nervous System
Brain Stem
Brain*
Energy Intake
Energy Metabolism*
Homeostasis
Hyperphagia
Hypothalamus
Ideal Body Weight
Metabolism
Neurons
Obesity
Pathology

Figure

• 

  Fig. 1 Model of brain regulation of energy metabolism. The brain integrates multiple, peripheral metabolic inputs, such as nutrients, gut-derived hormones (glucagon-like peptide-1 [GLP-1], cholecystokinin [CCK], and peptide YY), and adiposity-related signals (leptin and insulin) to regulate food intake and energy expenditure. Proopiomelanocortin (POMC)-producing and neuropeptide Y/agouti-related peptide (AgRP)-producing neurons in the hypothalamic arcuate nucleus (ARC) primarily sense the body's energy state and project to other hypothalamic nuclei, including the paraventricular nucleus (PVN) and lateral hypothalamus (not shown), which, in turn, project to the nucleus of the solitary tract (NTS) in the brainstem. The NTS responds to satiety signals via direct inputs to the NTS and indirect inputs to the hypothalamus and activates vagal afferents to reduce food intake. The preoptic area (POA) in the hypothalamus receives thermal sensory signals from cold exposure and activates the POA-dorsomedial hypothalamus (DMN)-rostral raphe pallidus (rRPa) pathway to promote brown adipose tissue (BAT) thermogenesis. The rRPa contains sympathetic premotor neurons that convey thermal signals from the POA and DMN to influence sympathetic outflow to the BAT in order to produce heat. The hypothalamic melanocortin system is also involved in thermoregulation. WAT, white adipose tissue; GI, gastrointestinal.

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