title: The role of somatostatin (octreotide) in the regulation of melatonin secretion in healthy volunteers and in patients with primary hypothyroidism.
abstract: Somatostatin has been found in the pineal gland of several animal species, which suggests that it may be involved in the regulation of melatonin secretion. Whether somatostatin has regulatory influence on melatonin secretion in man has never been unequivocally shown. We studied the nocturnal melatonin secretion in 8 healthy volunteers, and 6 women with untreated primary hypothyroidism, a disease state that is associated with increased nocturnal secretion of melatonin. The participants were given subcutaneous injections at 18:00 h and 23:00 h of either saline or octreotide (Sandostatin; each injection 50 microg). During the nights when the healthy volunteers were given octreotide, melatonin secretion was similar to that recorded during administration of saline. Also the urinary excretion of melatonin was of similar magnitude at these two occasions. By contrast, the GH secretion was significantly lower the nights the healthy controls were given octreotide (GH AUC 22.6+/-5.4 mU/l x h during octreotide and 126.6+/-21.9 mU/l x h during saline; p<0.01). The patients with hypothyroidism also showed similar nocturnal melatonin secretion during octreotide and saline. Urinary excretion of melatonin also remained unchanged, as did GH secretion. The total nocturnal secretion of TSH was, however, significantly reduced by octreotide (TSH AUC 562+/-136 mU/l x h during octreotide and 851+/-185 mU/l x h during saline; p<0.05), thus suggesting that 100 microg of octreotide should be sufficient to inhibit also the pinealocytes if their function were regulated by somatostatin. Since exogenous somatostatin--in the form of octreotide--fails to influence nocturnal secretion and urinary excretion of melatonin in normal subjects and in patients with primary hypothyroidism, it is reasonable to assume that endogenous somatostatin may not be an important regulator of melatonin secretion in man.
authors.affiliation: Karolinska Institute, Department of Internal Medicine, Stockholm Söder Hospital, Sweden. johan.wikner@medklin.sos.sll.se
authors.forename: J
authors.initials: J
authors.lastname: Wikner
authors.forename: L
authors.initials: L
authors.lastname: Wetterberg
authors.forename: S
authors.initials: S
authors.lastname: Röjdmark
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004311:Double-Blind Method; D005260:Female; D006728:Hormones; D019382:Human Growth Hormone / Q000097:blood / Q000378:metabolism; D006801:Humans; D007037:Hypothyroidism / Q000503:physiopathology*; D008297:Male; D008550:Melatonin / Q000097:blood / Q000378:metabolism* / Q000652:urine; D015282:Octreotide; D013004:Somatostatin / Q000502:physiology*; D013972:Thyrotropin / Q000097:blood
chemical_list: D001786:Blood Glucose; D006728:Hormones; D019382:Human Growth Hormone; D013004:Somatostatin; D013972:Thyrotropin; D008550:Melatonin; D015282:Octreotide