Male gonadal function, prolactin secretion and lactotroph population in an experimental model of cirrhosis

Abstract

Liver cirrhosis, a highly prevalent chronic disease, is frequently associated with endocrine dysfunctions, notably in the gonadal axis. We evaluated lactotroph population by immunohistochemistry, gonadotropins and prolactin by immunoradiometric assay and testosterone and estradiol by radioimmunoassay in adult male Wistar rats with cirrhosis induced by carbon tetrachloride. No significant difference in mean ± SEM percentages of lactotrophs was found between cirrhotic animals and controls (N = 12, mean 18.95 ± 1.29%). Although there was no significant difference between groups in mean serum levels of prolactin (control: 19.2 ± 4 ng/mL), luteinizing hormone (control: 1.58 ± 0.43 ng/mL), follicle-stimulating hormone (control: 19.11 ± 2.28 ng/mL), estradiol (control: 14.65 ± 3.22 pg/mL), and total testosterone (control: 138.41 ± 20.07 ng/dL), 5 of the cirrhotic animals presented a hormonal profile consistent with hypogonadism, all of them pointing to a central origin of this dysfunction. Four of these animals presented high levels of estradiol and/or prolactin, with a significant correlation between these two hormones in both groups (r = 0.54; P = 0.013). It was possible to detect the presence of central hypogonadism in this model of cirrhotic animals. The hyperestrogenemia and hyperprolactinemia found in some hypogonadal animals suggest a role in the genesis of hypogonadism, and in the present study they were not associated with lactotroph hyperplasia.

Hypothalamic-pituitary-gonadal function in men with liver cirrhosis before and after liver transplantation

“…Portal hypertension can lead to a diversion of blood flow from the liver to peripheral tissues, resulting in a further increase in the conversion of steroids into estrogens 8 . Although some studies 2,19,20 have established a correlation between increased PRL in cirrhosis and hyperestrogenemia, the mechanism that leads to hyperprolactinemia is not yet clear.…”

“…It is speculated that liver cirrhosis alone can cause a malfunction of the hypothalamicpituitary-gonadal axis 1,3,10 . Furthermore, high circulating levels of estradiol and prolactin also contribute to hypogonadism 2,3 , either by regulatory suppression or by direct inhibition of the testicular function 10 . The results also showed that both the PRL and E2 were at levels above normal in patients with end-stage liver disease, with normalization after OLT, in line with previous studies 1,17,18 .…”

“…Hypothalamic-pituitary-gonadal function in men with liver Hypothalamic-pituitary-gonadal function in men with liver Hypothalamic-pituitary-gonadal function in men with liver Hypothalamic-pituitary-gonadal function in men with liver Hypothalamic-pituitary-gonadal function in men with liver cirrhosis before and after liver transplantation cirrhosis before and after liver transplantation cirrhosis before and after liver transplantation cirrhosis before and after liver transplantation cirrhosis before and after liver transplantation atients with end-stage liver disease have several endocrine dysfunctions, which include alterations in the functioning of the hypothalamic-pituitary-gonadal axis and the serum levels of sex hormones [1][2][3][4] . Testicular atrophy, decrease in libido, impotence, oligospermia, infertility, loss of body hair, reduction of prostate size, gynecomastia, vascular spiders, gynecoid distribution of fat and palm erythema are often found in cirrhotic men [5][6][7][8][9][10] .…”

Follicle-stimulating hormone increases cholangiocyte proliferation by an autocrine mechanism via cAMP-dependent phosphorylation of ERK1/2 and Elk-1

“…cirrhosis is associated with endocrine dysfunction, notably in the gonadal axis (28). Patients with liver failure have low levels of LH and FSH (11).…”

Recent advances in pathophysiology of biliary tree: influence of sex hormones in cholangiocyte growth

“…FSH, also called gonadotropin because it stimulates the gonads, is produced in the anterior pituitary gland of the brain (74). Several studies demonstrated that liver cirrhosis is associated with endocrine dysfunction, notably in the gonadal axis (75). Patients with liver damage have low levels of LH and FSH (76).…”