prolactini

I was surprised to find so many articles connecting the prolactinoma and PCOS dots. Here are a few excerpts-

1. Insulin Regulates Prolactin Secretion and Messenger Ribonucleic Acid Levels in Pituitary Cells^*

DIANE PRAGER, SHUNICHI YAMA****A and SHLOMO MELMED

Department of Medicine, Cedars-Sinai Medical Center, University of California School of Medicine Los Angeles, California 90048
Address all correspondence and requests for reprints to: Dr. Shlomo Melmed, Division of Endocrinology, Room 1735, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048.
Abstract The regulation of PRL production in GH₃ rat pituitary tumor cells and normal rat pituitary cells exposed to insulin was studied. Cells were treated with semisynthetic human insulin for up to 5 days. Insulin (0.7 nM) stimulated PRL production by 30%, and cortisol (100 nM) suppressed it by 80% in GH₃ cells. Insulin (3.5 nM) partially blocked the suppression of PRL secretion induced by up to 100 nM cortisol. Equimolar doses of insulin-like growth factor I failed to consistently stimulate either basal PRL secretion into the medium or cortisolsuppressed PRL in GH₃ cells. A 65 nM concentration of insulinlike growth factor I was required to stimulate basal PRL secretion in GH₃ cells. Relative levels of PRL mRNA sequences in both GH₃ cells and normal rat pituitary cells were stimulated by insulin. When cells were incubated with cortisol (10 nM), PRL mRNA levels were suppressed to 40% of control values. Simultaneous incubation of cells with insulin (3.5 nM) partially reversed the cortisol-induced suppression of PRL mRNA to 60% of control values. The results show that insulin antagonizes cortisol-induced suppression of PRL. Physiological doses of insulin stimulate PRL production and PRL mRNA levels, suggesting a direct effect of insulin on either PRL gene transcription or stabilization of PRL mRNA in these cells (Endocrinology 122: 2946–2952, 1988)


2. Prolactin: A diabetogenic hormone

R. Landgraf^{1, 2}, M. M. C. Landgraf-Leurs¹, A. Weissmann¹, R. Hörl¹, K. von Werder¹ and P. C. Scriba¹

(1)	Department of Internal Medicine Innenstadt, University of Munich, Munich, Federal Republic of Germany

(2)	II. Medizinische Klinik, Ziemssenstraße 1, D-8000 München 2, Federal Republic of Germany

Received: 24 May 1976 Revised: 26 November 1976
Summary During an oral glucose tolerance test (OGTT) glucose and insulin levels were measured in 26 patients with prolactin-producing pituitary tumours without growth hormone excess. Basal glucose and insulin levels did not differ from the values of an age-matched control group. After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia. Bromocriptine (CB 154), which suppressed PRL, improved glucose tolerance and decreased insulin towards normal in a second OGTT. — Human PRL or CB 154 had no significant influence on insulin release due to glucose in the perfused rat pancreas. — These findings suggest a diabetogenic effect of PRL. CB 154 might be a useful drug in improving glucose utilization in hormone-active pituitary tumours

3. Immunomodulatory role of prolactin in diabetes development

P. Cejkova

a

b

c Institute of Rheumatology, Na Slupi 4, Prague, Czech Republic


Pituitary hormone and cytokine prolactin (PRL) is one of the mediators of the bidirectional

communication between neuroendocrine and immune systems. It participates in many
immunomodulatory activities, affects differentiation and maturation of both, B and T lymphocytes and enhances in

cdebra72

I just posted a message about this, thanks for the information! My doctor is convinced they go hand in hand. I've been on Dostinex and fortamet and my insuln levels went from 11.2 in april to 2.4 in August, along with weight loss.