Introduction: Hyperprolactinaemia has been implicated in the pathogenesis of obesity and glucose intolerance and is reportedly associated with impaired metabolic profile and metabolic syndrome in approximately one third of patients.
Areas covered: Suppression of dopaminergic tone has been proposed as a potential mechanism responsible for weight gain and metabolic abnormalities in such patients. Dopamine receptor type 2 (D2R) is abundantly expressed on human pancreatic β-cell and adipocytes, suggesting a regulatory role for peripheral dopamine in insulin and adipose functions. Medical treatment with the dopamine-agonists bromocriptine and cabergoline has been shown to significantly improve gluco-insulinemic and lipid profile, also reducing the prevalence of metabolic syndrome. In patients with concomitant hypogonadism, simultaneous correction of both PRL excess and testosterone deficiency is mandatory to improve insulin resistance and metabolic abnormalities.
Expert commentary: Hyperprolactinemia promotes metabolic alterations. Control of PRL excess by dopamine agonists is mandatory to induce weight loss and to improve metabolic profile, and replacement treatment for concomitant hypogonadism effectively ameliorates insulin resistance and metabolic syndrome.
Keywords: Hyperprolactinemia; body weight; bromocriptine; cabergoline; dopamine agonists; glucose metabolism; insulin metabolism; lipid metabolism; metabolic syndrome; obesity; pituitary tumor.