scholarly journals Functional and Molecular Aspects of Glucocorticoids in the Endocrine Pancreas and Glucose Homeostasis

10.5772/50233 ◽  
2012 ◽  
Author(s):  
Alex Rafacho ◽  
Antonio C. ◽  
Henrik Ortsater
Keyword(s):  
Glucose Homeostasis ◽  
Endocrine Pancreas ◽  
Molecular Aspects

The role of ghrelin in the regulation of glucose homeostasis

2016 ◽  
Vol 26 (1) ◽  
Author(s):  
Bader N. Alamri ◽  
Kyungsoo Shin ◽  
Valerie Chappe ◽  
Younes Anini
Keyword(s):  
Insulin Resistance ◽  
Insulin Release ◽  
Glucose Homeostasis ◽  
Energy Homeostasis ◽  
Endocrine Pancreas ◽  
Distinct Group ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Ghrelin Receptor ◽  
Glucose Plasma

AbstractGhrelin is a 28-amino acid (aa) stomach-derived peptide discovered in 1999 as the endogenous ligand for growth hormone secretagogue-receptor (GHS-R). Ghrelin-producing cells constitute a distinct group of endocrine cells dispersed throughout the gastric mucosa and to a lesser extent in the small intestine and the endocrine pancreas. Ghrelin plasma levels rise during fasting and chronic caloric restriction to stimulate food intake and fat storage and to prevent life-threatening falls in blood glucose. Plasma ghrelin levels decrease after a meal is consumed and in conditions of energy surplus (such as obesity). Ghrelin has emerged as a key player in the regulation of appetite and energy homeostasis. Ghrelin achieves these functions through binding the ghrelin receptor GHS-R in appetite-regulating neurons and in peripheral metabolic organs including the endocrine pancreas. Ghrelin levels are negatively correlated with body mass index (BMI) and insulin resistance. In addition, ghrelin secretion is impaired in obesity and insulin resistance. Several studies highlight an important role for ghrelin in glucose homeostasis. Genetic, immunological, and pharmacological blockade of ghrelin signaling resulted in improved glucose tolerance and insulin sensitivity. Furthermore, exogenous ghrelin administration was shown to decrease glucose-induced insulin release and increase glucose level in both humans and rodents. GHS-R was shown to be expressed in pancreatic β-cells and ghrelin suppressed insulin release via a Ca

scholarly journals ERO1-β, a pancreas-specific disulfide oxidase, promotes insulin biogenesis and glucose homeostasis

2010 ◽  
Vol 188 (6) ◽  
pp. 821-832 ◽  
Author(s):  
Ester Zito ◽  
King-Tung Chin ◽  
Jaime Blais ◽  
Heather P. Harding ◽  
David Ron
Keyword(s):  
Glucose Homeostasis ◽  
Double Mutant ◽  
Endocrine Pancreas ◽  
Bond Formation ◽  
Mutant Mice ◽  
Oxidative Protein Folding ◽  
Insulin Producing Cells ◽  
Genes Encoding ◽  
Reducing Environment

Mammals have two genes encoding homologues of the endoplasmic reticulum (ER) disulfide oxidase ERO1 (ER oxidoreductin 1). ERO1-β is greatly enriched in the endocrine pancreas. We report in this study that homozygosity for a disrupting allele of Ero1lb selectively compromises oxidative folding of proinsulin and promotes glucose intolerance in mutant mice. Surprisingly, concomitant disruption of Ero1l, encoding the other ERO1 isoform, ERO1-α, does not exacerbate the ERO1-β deficiency phenotype. Although immunoglobulin-producing cells normally express both isoforms of ERO1, disulfide bond formation and immunoglobulin secretion proceed at nearly normal pace in the double mutant. Moreover, although the more reducing environment of their ER protects cultured ERO1-β knockdown Min6 cells from the toxicity of a misfolding-prone mutant Ins2Akita, the diabetic phenotype and islet destruction promoted by Ins2Akita are enhanced in ERO1-β compound mutant mice. These findings point to an unexpectedly selective function for ERO1-β in oxidative protein folding in insulin-producing cells that is required for glucose homeostasis in vivo.

scholarly journals Role of leptin in the pancreatic β-cell: effects and signaling pathways

2012 ◽  
Vol 49 (1) ◽  
pp. R9-R17 ◽  
Author(s):  
Laura Marroquí ◽  
Alejandro Gonzalez ◽  
Patricia Ñeco ◽  
Ernesto Caballero-Garrido ◽  
Elaine Vieira ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Glucose Homeostasis ◽  
Endocrine Pancreas ◽  
Cell Function ◽  
Cell Mass ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Leptin Receptors ◽  
Β Cell Function ◽  
Insulin Gene Expression

Leptin plays an important role in the control of food intake, energy expenditure, metabolism, and body weight. This hormone also has a key function in the regulation of glucose homeostasis. Although leptin acts through central and peripheral mechanisms to modulate glucose metabolism, the pancreatic β-cell of the endocrine pancreas is a critical target of leptin actions. Leptin receptors are present in the β-cell, and their activation directly inhibits insulin secretion from these endocrine cells. The effects of leptin on insulin occur also in the long term, since this hormone inhibits insulin gene expression as well. Additionally, β-cell mass can be affected by leptin through changes in proliferation, apoptosis, or cell size. All these different functions in the β-cell are triggered by leptin as a result of the large diversity of signaling pathways that this hormone is able to activate in the endocrine pancreas. Therefore, leptin can participate in glucose homeostasis owing to different levels of modulation of the pancreatic β-cell population. Furthermore, it has been proposed that alterations in this level of regulation could contribute to the impairment of β-cell function in obesity states. In the present review, we will discuss all these issues with special emphasis on the effects and pathways of leptin signaling in the pancreatic β-cell.

Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis

2008 ◽  
Vol 31 (2) ◽  
pp. 194-200 ◽  
Author(s):  
A. B. Ropero ◽  
P. Alonso-Magdalena ◽  
E. García-García ◽  
C. Ripoll ◽  
E. Fuentes ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Bisphenol A ◽  
Glucose Homeostasis ◽  
Endocrine Pancreas ◽  
Blood Glucose Homeostasis

scholarly journals Effects of transplantation and resection of a radiation-induced rat insulinoma on glucose homeostasis and the endocrine pancreas

1987 ◽  
Vol 54 (4) ◽  
pp. 685-692 ◽  
Author(s):  
P R Flatt ◽  
K S Tan ◽  
C J Bailey ◽  
C J Powell ◽  
S K Swanston-Flatt ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
Endocrine Pancreas ◽  
Radiation Induced ◽  
Rat Insulinoma

scholarly journals Long-term increase of insulin secretion in mice subjected to pregnancy and lactation

2020 ◽  
Vol 9 (4) ◽  
pp. 299-308 ◽  
Author(s):  
Julia Modesto Vicente ◽  
Junia Carolina Santos-Silva ◽  
Caio Jordão Teixeira ◽  
Dailson Nogueira de Souza ◽  
Jean Franciesco Vettorazzi ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Endocrine Pancreas ◽  
Morphological Changes ◽  
Maternal Risk ◽  
Intracellular Ca ◽  
Pregnancy And Lactation ◽  
Molecular Aspects ◽  
Glucose Stimulated Insulin Secretion

Purpose Observational studies show that longer breastfeeding periods reduce maternal risk of type 2 diabetes mellitus. However, it is currently unknown if the long-term benefits of breastfeeding for maternal glucose homeostasis are linked to changes in the endocrine pancreas. Methods We presently evaluated functional, morphological and molecular aspects of the endocrine pancreas of mice subjected to two sequential cycles of pregnancy and lactation (L21). Age-matched mice not allowed to breastfeed (L0) and virgin mice were used as controls. Results L21 mice exhibited increased tolerance and increased glucose-stimulated insulin secretion (GSIS) by isolated islets. Pancreatic islets of L21 mice did not present evident morphological changes to justify the increased GSIS. On the other hand, islets of L21 mice exhibited a reduction in Cavb3 and Kir6.2 expression with concordant increased intracellular Ca2+ levels after challenge with glucose. Conclusion Altogether, the present findings show the breastfeeding exerts long-term benefits for maternal endocrine pancreas by increasing intracellular Ca2+ levels and GSIS.

scholarly journals Somatostatin blockade of acute and chronic stimuli of the endocrine pancreas and the consequences of this blockade on glucose homeostasis.

1975 ◽  
Vol 55 (4) ◽  
pp. 754-762 ◽  
Author(s):  
E W Chideckel ◽  
J Palmer ◽  
D J Koerker ◽  
J Ensinck ◽  
M B Davidson ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
Endocrine Pancreas
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