Oxytocin and Food Intake

Oxytocin is a mammalian hormone that also behaves as a neurotransmitter in the brain. This neurohypophysial hormone was the first peptide hormone to have its structure identified and the first to be chemically synthesized in its biologically active form. Oxytocin has several functions in the body. It plays an important role in the expression of central functions, such as maternal behavior, sexual behavior, yawning, memory and learning, tolerance and dependence mechanisms, feeding patterns, grooming, trust formation, bonding, cardiovascular regulation, and thermoregulation. However, its roles in postpartum uterine contractions and feeding behaviors are the most relevant when discussing the hormone's relationship to obesity.

Oxytocin is a nine-amino acid peptide that is synthesized in neurons in the hypothalamus and is transported down axons to the posterior pituitary for secretion into the blood. In the pituitary gland, oxytocin is packaged in large, dense-core vesicles, where it is bound to neurophysin I. Neurophysin I is a large peptide fragment of the precursor molecule from which oxytocin is derived. Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to not act at a distance from its point of origin.

In pregnant women, oxytocin is released mainly after dilation of the cervix and the vagina during labor to facilitate birth, and after stimulation of the nipples to facilitate breastfeeding. Studies have shown that during pregnancy, body weight, and particularly adiposity, increase, due to increased food intake as opposed to decreased energy metabolism. This adaptation provides the growing fetus with adequate nutrition and prepares the mother for the metabolically demanding lactation period after birth. During feeding in nonpregnant rats, oxytocin neurons become strongly activated indicating their role in meal termination. However, in mid-pregnancy the excitability of these neurons is decreased, oxytocin release is inhibited, and patterns of oxytocin receptor binding in the brain alter. Thus, an increase in food intake occurs.

Oxytocin release during breastfeeding causes mild but painful uterine contractions during the first few weeks of lactation. These contractions facilitate in maternal postpartum weight loss. Studies have shown that the longer mothers breastfeed, the greater weight loss they experience and they are more likely to return to their prepregnancy weight. The findings from these studies and many others have been used to encourage women to practice optimum breastfeeding, not only to ensure adequate nutrition for their infants, but also to decrease postpartum weight retention. If adequate breastfeeding practices are maintained as well as physical activity levels, risk of obesity in later adulthood dramatically decreases.

[Page 578]Oxytocin has been studied in nonpregnant animals as well. It is considered to be a “satiety” hormone because it has been shown to reduce food consumption when administered peripherally and centrally in rats. Also, the inhibition of food intake is not directly associated with circulating oxytocin. When rats were administered with anorexigenic treatments such as cholecystokinin, hypertonic saline, and lithium chloride, pituitary secretion of oxytocin resulted and caused a greater increase in inhibition of food intake occurred. These data suggest that nausea and satiety induce a common hypothalamic oxytocin pathway that results in the inhibition of digestion. Another study showed that oxytocin reduced food consumption and the time spent consuming food, and it also increased the time before first meal in fasted rats. Conversely, when treating the rats with an oxytocin antagonist, their food intake increased.

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