title: The effect of the ANKK1/DRD2 Taq1A polymorphism on weight changes of dopaminergic treatment in prolactinomas.
abstract: Treatment with dopamine agonists in patients with prolactinomas has been associated with weight loss in short term studies. However, long-term studies on weight changes are lacking. Taq1A is a restriction fragment length polymorphism considered as a gene marker for the DRD2 gene. The presence of at least one A1 allele is linked to reduced brain dopaminergic activity due to reduced receptor binding and lower density of the dopamine 2 receptor. We aimed at testing the hypothesis that the dopaminergic treatment in prolactinoma patients leads to sustained weight loss and that the presence of diminished weight loss response under dopamine agonists is associated with the minor A1 allele of Taq1A.We included n = 44 patients (17 male and 27 female, 26 macroadenomas and 18 microadenomas) with prolactinomas treated with dopamine agonists. Outcome measures were weight and body mass index (BMI) change under dopaminergic treatment after 2 years with regard to Taq1A status and sex. We observed that the dopaminergic treatment leads to a significant mean weight loss of 3.1 ± 6.25 kg after 2 years. Regarding Taq1A polymorphisms, 21 patients were carriers of at least one A1 allele and 23 patients had a genotype of A2/A2. However, the presence of the A1 allele was neither associated with the mean BMI at baseline nor with an altered weight loss response under dopamine agonist therapy. Our results implicate that the dopaminergic treatment leads to a sustained weight loss in patients with prolactinomas after 2 years. However, there was no association to the A1 allele of Taq1A, observation that needs to be analysed in larger cohorts.
authors.affiliation: Department of Internal Medicine, Endocrinology and Clinical Chemistry, Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804, Munich, Germany, athanasoulia@mpipsykl.mpg.de.
authors.forename: A P
authors.initials: AP
authors.lastname: Athanasoulia
authors.forename: C
authors.initials: C
authors.lastname: Sievers
authors.forename: M
authors.initials: M
authors.lastname: Uhr
authors.forename: M
authors.initials: M
authors.lastname: Ising
authors.forename: G K
authors.initials: GK
authors.lastname: Stalla
authors.forename: H J
authors.initials: HJ
authors.lastname: Schneider
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000627:therapeutic use*; D015992:Body Mass Index; D018491:Dopamine Agonists / Q000009:adverse effects* / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010911:Pituitary Neoplasms / Q000188:drug therapy* / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D015175:Prolactinoma / Q000188:drug therapy* / Q000235:genetics*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D015431:Weight Loss / Q000187:drug effects*; D055815:Young Adult
chemical_list: D000970:Antineoplastic Agents; C581293:DRD2 protein, human; D018491:Dopamine Agonists; D017448:Receptors, Dopamine D2; C489948:ANKK1 protein, human; D017346:Protein Serine-Threonine Kinases