The regulation of food intake by hypothalamic malonyl-coenzyme A: the MaloA hypothesis.
In animals, food intake and therefore energy balance is regulated by a center in the hypothalamus of the brain. Neurons there release appetite-inhibiting (anorexigenic) or appetite-stimulating (orexigenic) peptide hormones according to whether energy intake exceeds or is less than expenditure, respectively. Recent evidence for the "malonyl coenzyme A hypothesis" showed that the level of malonyl coenzyme A (MalCoA) in the arcuate nucleus of the hypothalamus determines the stimulation or inhibition of food intake. A high level of MalCoA, indicative of energy surplus, signals the release of anorexigenic neuropeptides, resulting in decreased food intake; a low level of MalCoA, due to an energy deficit such as during fasting, signals the release of orexigenic neuropeptides, stimulating food intake.
Wolf
George
G
Department of Nutritional Sciences and Toxicology, University of California, Berkeley, USA. ilsipress@ilsi.org
D000818:Animals; D002149:Energy Intake / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology; D005247:Feeding Behavior / Q000502:physiology*; D006801:Humans; D007031:Hypothalamus / Q000502:physiology*; D008316:Malonyl Coenzyme A / Q000502:physiology*; D051379:Mice; D023421:Models, Animal
D008316:Malonyl Coenzyme A