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Galanin (GAL) plays an integral role in consummatory behavior. In particular, hypothalamic GAL has a positive, reciprocal relationship with dietary fat and alcohol. In this relationship, GAL increases the consumption of fat or alcohol which, in turn, stimulates the expression of GAL, ultimately leading to overconsumption. Through actions in the amygdala, this relationship may become especially important in stress-induced food or drug intake. These effects of GAL in promoting overconsumption may involve various neurotransmitters, with GAL facilitating intake by stimulating norepinephrine and dopamine and reducing satiety by decreasing serotonin and acetylcholine. In addition, GAL in the hypothalamus stimulates the opioid, enkephalin, throughout the brain, which also promotes overconsumption. The relationship between GAL, fat, and alcohol may involve triglycerides, circulating lipids that are released by fat or alcohol and that correlate positively with hypothalamic GAL expression. In females, levels of endogenous GAL also fluctuate across the reproductive cycle, driven by a rise in the ovarian steroids, estrogen, and progesterone. They peak during the proestrous phase and also at puberty, simultaneous to a sharp increase in preference for fat to meet energy demands. Prenatal exposure to a high-fat diet also enhances hypothalamic expression of GAL into adulthood because of an increase in neurogenesis and proliferation of GAL-expressing neurons in this region. This organizational change may reflect the role of GAL in neuronal development, including neurite growth in adulthood, cell survival in aging, and cell stability in the disease state. By responding positively to fat and alcohol and guiding further neuronal development, GAL potentiates a long-term propensity to overconsume fat and alcohol.

Galanin and Consummatory Behavior: Special Relationship with Dietary Fat, Alcohol and Circulating Lipids