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.