Cell Signaling Within Endocrine Glands: Thyroid, Parathyroids and Adrenal Glands

Abstract

Despite the fact that there can be argued that no single cell in the human body can be devoid of molecular tools that fit into the broad definition of an endocrine function, some organs are primarily dedicated to hormone secretion and are therefore designated endocrine glands. Under regulation by pituitary gland (reviewed on the previous chapter), three peripheral organs are exclusively devoted to endocrine functions: the thyroid, the parathyroid and the adrenal glands. This Chapter on endocrine system will cover the signaling pathways implied in these three organs, with identification of their particular and shared features.

Case Report: A Paternal 20q13.2-q13.32 Deletion Patient With Growth Retardation Improved by Growth Hormone

“…For example, adenylyl cyclase facilitates the production of cAMP, which can bind to the protein kinase A (PKA) and further lead to the activation of its catalytic subunit. Catalytic-active PKA is involved in the iodine uptake and the expression of genes associated with thyroid hormone production ( Pereira et al, 2020 ). As a result, mutation of GNAS can cause different types of endocrine-related diseases, such as McCune-Albright syndrome (OMIM#174800), progressive osseous heteroplasia (OMIM#166350) and pseudohypoparathyroidism (PHP).…”

Vasoactive Intestinal Peptide Indirectly Elicits Pituitary LH Secretion Independent of GnRH in Female Zebrafish

“…We have shown before that even the double KO line (gnrh2 -/-; gnrh3 -/-) is fertile (6), ruling out GnRH2 as a potential compensator for GnRH3 in gnrh3 -/zebrafish. It is well known that the pituitary gonadotropes are tightly controlled by multiple molecular regulators, which cooperate towards a single aim, possibly through redundant pathways (7,8). Several brain neurohormones and neurotransmitters, such as kisspeptin, GnRH, gonadotropin inhibitory hormone, dopamine, gamma aminobutyric acid, pituitary adenylate cyclase-activating polypeptide (PACAP), neuropeptide Y, secretoneurin, among others, are known to affect LH cells and release in teleosts (8,48).…”

“…The lack of a mutant phenotype, e.g., normal fertility in gnrh3 -/zebrafish (4,5), may be explained by functional redundancy, in which the hypophysiotropic GnRH, GnRH3, is not a sole or a central controller of reproduction in zebrafish, particularly pertaining to regulating LH release from the pituitary. Multiple molecules have recently been implicated in the regulation of pituitary gland coordination of the perfectly timed and accurate secretion of pituitary hormones (7). Hence, unlike GnRH1-dependent mechanisms in other species, functional redundancy may exist along the HPG axis and support the successful LH secretion in zebrafish.…”