Basic and Genetic Aspects of Food Intake Control and Obesity: Role of Dopamin Receptor D2 TaqIA Polymorphism.
Homeostatic control of food intake, hunger and satiety involves adipose and gastrointestinal hormones, such as leptin, insulin and ghrelin, which eventually affect neuronal signaling in the hypothalamus arcuate nucleus. On the other hand, hedonic control of food intake relates to substances such as opioids, endocannabinoids, gamma-aminobutyric acid, serotonin and dopamine, which act on the motivation and reward mechanisms. Dopamine is a precursor of noradrenaline and adrenaline and modulates a number of physiological functions, such as appetite, depending on the brain area and the type of receptor stimulated.
Obesity is a multifactorial condition influenced by genetic, endocrine-metabolic, environmental and psychological factors. A delicate balance between three main biochemical and behavioral processes maintains body weight: food intake, energy expenditure control and energy storage control.
Homeostatic control of intake depends on the hormonal peripheral signaling produced in response to changes in nutrient concentrations. Leptin and insulin are the main hormonal adiposity signals, and by reaching the CNS trigger mechanisms that promote inhibition of food intake and increased energy expenditure. During prolonged fasting, the stomach produces ghrelin that
acts on the hypothalamus as an orexigenic signal. After food intake, ghrelin concentration falls, giving rise to the secretion of anorectic hormones, such as cholecystokinin (CCK), peptide YY
(PYY) and glucagon-like peptide-1 (GLP1). Regarding appetite, DA has varying effects depending on the brain area and the type of receptor stimulated. It has anorectic effect when it operates in the ARC, LHA and NAc, but acts as orexigenic in the ventromedial hypothalamic nucleus (VMH).
Obes Res Open J. 2016; 2(4): 119-127. doi: 10.17140/OROJ-2-119
