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General Aspects of Endocrine Physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The peptide hormones are synthesized by mRNA transcription in the nucleus, leading to ribosomal translation with the production of the polypeptide within the endoplasmic reticulum. The polypeptide is concentrated in the Golgi apparatus and then stored in storage granules. Large protein hormones are usually retained in the storage granules, whereas small peptide hormones are bound to specific binding proteins within the granules (Figure 59.1). The hormones are released from the endocrine cell by exocytosis following a neural, chemical, hormonal or physical stimulus. Hormones not released are usually degraded to amino acids and recycled.
Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
During weeks 6–8 of human gestation, Rathke’s pouch constricts at its base and eventually separates from the oral epithelium. At the same time, a downward extension of the ventral diencephalon forms the posterior lobe, and the two nascent lobes connect to form the composite structure of the adult pituitary. Cells of the anterior wall of Rathke’s pouch undergo extensive proliferation to form the anterior lobe, while the posterior wall proliferates more slowly to form the vestigial IL. Cell patterning and terminal differentiation occurs within the anterior lobe, forming the five specialized endocrine cell types of the pituitary gland.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Pit cells (large granular lymphocytes) were first recognized as a distinct cell type by Wisse et al. (1976). Initially, they were presumed to have an endocrine function because they contain cytoplasmic granules which resemble those of endocrine cell types (Wisse et al., 1976). However, subsequent studies suggest that they are the perisinusoidal equivalent of large granular lymphocytes and natural killer lymphocytes (Bouwens and Wisse, 1988). Although their morphology has been well characterized (Wisse et al., 1976; Kaneda and Wake, 1983), pit cells remain the least investigated sinusoidal cell type, presumably because they are seen only infrequently.
GABA treatment does not induce neogenesis of new endocrine cells from pancreatic ductal cells
Published in Islets, 2023
Shihao Wang, Xin Dong, Mahan Maazi, Nan Chen, Amarpreet Mahil, Janel L. Kopp
To further address whether there were any changes in beta cell area with GABA treatment, we quantified the insulin+ cell area using insulin immunofluorescence staining (Figures 2A and 3A). We found that there were no significant differences in insulin+ area over total pancreatic area in mice treated with GABA compared to the respective saline-treated control groups in either founder lineages (Figure 3A). Additionally, the overall proliferation in the pancreas, as observed by immunofluorescence staining for EdU+ cells in the pancreas (Figure 3B), was not different. Altogether, these data are consistent with previously published studies where no increases in endocrine cell area were observed in response to long-term GABA treatment.18
Effect of feeding regimen on circadian activity rhythms of food anticipatory by ghrelin hormone in a pig model
Published in Nutritional Neuroscience, 2023
He Zhang, Xiaoxi Yan, Ailian Lin, Pengke Xia, Menglan Jia, Yong Su
Ghrelin is an acylated 28-amino acid peptide hormone secreted primarily from stomach tissue, which is regarded as an endogenous ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a) [12,13]. Most circulating ghrelin is produced from the stomach and duodenum, and the greatest number of ghrelin-secreting cells is found in the stomach appear as a closed-type endocrine cell lie but within close proximity to the gastric lumen known as X/A-like cells [13,14]. Plasma ghrelin level is rhythmic, manifested as a rise before expected meals and a rapid drop upon food intake [15], suggesting that meals or dietary nutrients help regulate ghrelin secretion [16]. Such ghrelin rhythms related to the fasting-feeding cycle, suggesting that ghrelin may drive food anticipatory activity (FAA), acting as an output of the food entrainable oscillators (FEOs). However, results about the effect of growth hormone secretagogues (GHSs) on the circadian rhythm and sleeping were inconsistent or even contradictory. Ghrelin decreases rapid eye movement sleep duration but promotes slow-wave sleep in humans, and induces phase advance in cultured suprachiasmatic nuclei (SCN) and mice under food deprivation [17–19]. However, both central administration and microinjection of ghrelin into the forebrain induce wakefulness in rodents [20,21].
Expression of Rasd1 in mouse endocrine pituitary cells and its response to dexamethasone
Published in Stress, 2021
Chad D. Foradori, Laci Mackay, Chen-Che J. Huang, Robert J. Kemppainen
Our results localized Rasd1 to all PD endocrine cell types and, with the exception of thyrotrophs, Dex treatment resulted in a rapid induction in the gene’s expression. There was however, a large difference in the intensity of Dex-induced increase in Rasd1 expression as measured using MFI. The gene was markedly responsive in corticotrophs as compared with all other cell types examined. The proportion and degree to which Dex-induces Rasd1 roughly correlates to the relative expression of glucocorticoid receptors (GR; NR3C1) in endocrine pituitary cell subtypes. Dex has a high avidity and affinity to bind to GR in the pituitary (De Kloet et al., 1975; McEwen, 1979). Prior co-localization studies have reported variable degrees of GR localization to different cells types in the PD (Kononen et al., 1993; Ozawa et al., 1999). GR was co-localized to corticotrophs and somatotrophs to a high extent (>70%) in both reports along with significant co-localization (>50%) to thyrotrophs. However, divergent results were found concerning GR in gonadotrophs and lactotrophs. It should also be noted that the single timepoint and dose of Dex used in the current work were specifically chosen to be consistent with our previous studies of Rasd1 and for maximum corticotroph activation. Further work is needed to determine Rasd1’s specific regulation in the other endocrine cells of the pituitary.