Basic and Genetic Aspects of Food Intake Control and Obesity: Role of Dopamin Receptor D2 TaqIA Polymorphism

Abstract

Regulation of food intake, energy expenditure and store are strikingly linked
to obesity. 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. It has been
established as the main neurotransmitter of the hypothalamic reward system. Beyond the
homeostatic and hedonic energy balance control, genetic aspects are also tightly involved in
obesity pathophysiology. In this context, some Single Nucleotide Polymorphism (SNP) has
been linked to common obesity. Here, we highlight the role of the dopamine receptor D2 gene
TaqAI polymorphism, which affects the D2 receptor availability and has been associated to
obesity. Therefore, the aim of this mini review is to cover basic aspects of food intake, energy
balance, dopamine-related aspects, including genetic ones, and the relation with obesity