Hyperprolactinemia following chronic alcohol administration

Research output: Chapter in Book/Report/Conference proceedingChapter

12 Scopus citations

Abstract

There are several reports showing evidence for the existence of high levels of prolactin (PRL) in alcoholic men and women. Alcohol-induced hyperprolactinemia has also been demonstrated in nonhuman primates and laboratory animals. Therefore, the clinical data as well as animal data suggest that ethanol consumption is a positive risk factor for hyperprolactinemia. In animal studies, it was found that chronic ethanol administration not only elevates plasma levels of PRL but also increases proliferation of pituitary lactotropes. Ethanol action on lactotropes involves crosstalk with estradiol-responsive signaling cascade or estradiol-regulated cell-cell communication. Additionally, it involves suppression of dopamine D2 receptors inhibition of G proteins and intracellular cyclic adenosine monophosphate (cAMP), modulation of transforming growth factor-beta (TGF-β) isoforms and their receptors (TβRII), as well as factors secondary to TGF-β actions, including production of beta-fibroblast growth factor (bFGF) from follicular-stellate cells. The downstream signaling that governs b-FGF production and secretion involves activation of the MAP kinase p44/42-dependent pathway. A coordinated suppression of D2 receptor-and TβRII receptor-mediated signaling as well as enhancement of bFGF activity might be critical for ethanol action on PRL production and cell proliferation in lactotropes.

Original languageEnglish (US)
Title of host publicationPituitary Today II
Subtitle of host publicationNew Molecular, Physiological and Clinical Aspects
EditorsEduardo Artz, Marcello Bronstein, Mirtha Guitelman
Pages32-41
Number of pages10
DOIs
StatePublished - Aug 20 2010

Publication series

NameFrontiers of Hormone Research
Volume38
ISSN (Print)0301-3073

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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