Melatonin, N-acetyl-5-methoxytryptamine, is an indole mainly synthesized from tryptophan in the pineal gland and secreted exclusively during the night in all the animals reported to date. While the pineal gland is the major source responsible for this night rise, it is not at all the exclusive production site and many other tissues and organs produce melatonin as well. Likewise, melatonin is not restricted to vertebrates, as its presence has been reported in almost all the phyla from protozoa to mammals. Melatonin displays a large set of functions including adaptation to light: dark cycles, free radical scavenging ability, antioxidant enzyme modulation, immunomodulatory actions or differentiation–proliferation regulatory effects, among others. However, in addition to those important functions, this evolutionary ‘ancient’ molecule still hides further tools with important cellular implications. The major goal of the present review is to discuss the data and experiments that have addressed the relationship between the indole and glucose. Classically, the pineal gland and a pinealectomy were associated with glucose homeostasis even before melatonin was chemically isolated. Numerous reports have provided the molecular components underlying the regulatory actions of melatonin on insulin secretion in pancreatic beta-cells, mainly involving membrane receptors MTNR1A/B, which would be partially responsible for the circadian rhythmicity of insulin in the organism. More recently, a new line of evidence has shown that glucose transporters GLUT/SLC2A are linked to melatonin uptake and its cellular internalization. Beside its binding to membrane receptors, melatonin transportation into the cytoplasm, required for its free radical scavenging abilities, still generates a great deal of debate. Thus, GLUT transporters might constitute at least one of the keys to explain the relationship between glucose and melatonin. These and other potential mechanisms responsible for such interaction are also discussed here.

IntroductionGalactorrhea wiht antidepressants SSRIs or SNRI is a rarely adverse effect. Some authors believe that the risk of galactorrhea in women who use SSRIs is 8 times higher than in patients treated with other types of drugs. Serotonin is believed to be a potent physiological stimulator of prolactin release.Prolactin stimulates the growth of the mammary glands and the galactorrhea. The SSRIs would activate the serotonergic pathways, these in turn would stimulate the release of prolactin directly in the pituitary and in the hypothalamus, inhibiting the release of dopamine and increasing the release of stimulating factors. The main inhibitor of prolactin secretion is dopamine.ObjectivesThe objective is to reveal this rare complication through the report of a clinical caseMethodsA 45-year-old woman with a diagnosis of mixed anxiety-depressive disorder. Treatment with 20 mg of escitalopram was started, with a good therapeutic response, but with breast pain and swelling. She was switched to duloxetine 60 mg, with a good response and adequate tolerance. At 6 months of treatment, she begins to present breast pain and yellow-green breast discharge, with elevated prolactin levels and normal cranial MRI.ResultsShe was diagnosed with functional hyperprolactinemia, and treatment with vortioxetine was started. Finally, the Prolactin levels normalize.ConclusionsGalactorrhea is a very rare and annoying side effect that can lead to discontinuation of treatment and requires a change in the therapeutic strategy.DisclosureNo significant relationships.