The effects of hyperprolactinemia and its control on metabolic diseases

ABSTRACT

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.

Area 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
• pituitary tumor
• dopamine agonists
• bromocriptine
• cabergoline
• body weight
• obesity
• glucose metabolism
• insulin metabolism
• lipid metabolism
• metabolic syndrome

Declaration of interest

A.C. has been principal investigator of research studies from Novartis, Ipsen, Pfizer and Lilly, has received research grants from Ferring, Lilly, Ipsen, Merck-Serono, Novartis, Novo-Nordisk and Pfizer, has been occasional consultant for Novartis, Ipsen and Pfizer, and has received fees and honoraria from Ipsen, Novartis, and Pfizer. R.P. has been principal investigator of research studies from Novartis and HRA Pharma, has received research grants from Novartis, Ipsen, Pfizer, Viropharma and IBSA, has been occasional consultant for Novartis, Ipsen, Pfizer, Viropharma, Ferring and Italfarmaco, and received lecture fees and honoraria from Novartis, Pfizer and Shire. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This manuscript was not funded.