Several studies have linked dysregulation of prolactin-mediated signalling  with an imbalance in metabolic parameters. Ratner et al. explored the effects of prolonged hyperprolactinaemia in female mice and dysregulation of the hypothalamic-pituitary-gonadal (HPG) axis, achieved by transgenic overexpression of the β-subunit of human chorionic gonadotrophin (hCGβ)  on an array of metabolic parameters, including lipid profile, insulin and  glucose tolerance tests and pancreatic gene expression.

Transgenic animals with dysregulation of the HPG axis and hypersecretion of prolactin had higher circulating insulin, showing reduced insulin sensitivity with an elevated HOMA-IR (homeostatic model assessment of insulin resistance). Lipid and pancreatic markers were also significantly altered in females with elevated hCGβ. These effects were reversible using the dopamine agonist cabergoline, showing the direct effects of prolactin, and suggesting a link between prolactin and gonadotrophin hormone functionality and metabolic status.

Read the full article in Journal of Endocrinology 230 157–169