scholarly journals Role and Cytotoxicity of Amylin and Protection of Pancreatic Islet β-Cells from Amylin Cytotoxicity

Cells ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 95 ◽  
Author(s):  
Yoshimitsu Kiriyama ◽  
Hiromi Nochi
Keyword(s):  
Blood Glucose ◽  
Small Molecules ◽  
Pancreatic Islet ◽  
Peptide Hormone ◽  
Β Cells ◽  
Islet Amyloid ◽  
Amino Acid Peptide ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Human Amylin

Amylin, (or islet amyloid polypeptide; IAPP), a 37-amino acid peptide hormone, is released in response to nutrients, including glucose, lipids or amino acids. Amylin is co-stored and co-secreted with insulin by pancreatic islet β-cells. Amylin inhibits food intake, delays gastric emptying, and decreases blood glucose levels, leading to the reduction of body weight. Therefore, amylin as well as insulin play important roles in controlling the level of blood glucose. However, human amylin aggregates and human amylin oligomers cause membrane disruption, endoplasmic reticulum (ER) stress and mitochondrial damage. Since cytotoxicity of human amylin oligomers to pancreatic islet β-cells can lead to diabetes, the protection of pancreatic islet β cells from cytotoxic amylin is crucial. Human amylin oligomers also inhibit autophagy, although autophagy can function to remove amylin aggregates and damaged organelles. Small molecules, including β-sheet breaker peptides, chemical chaperones, and foldamers, inhibit and disaggregate amyloid formed by human amylin, suggesting the possible use of these small molecules in the treatment of diabetes. In this review, we summarize recent findings regarding the role and cytotoxicity of amylin and the protection of pancreatic islet β-cells from cytotoxicity of amylin.

scholarly journals Development and Characteristics of Pancreatic Epsilon Cells

2019 ◽  
Vol 20 (8) ◽  
pp. 1867 ◽  
Author(s):  
Naoaki Sakata ◽  
Gumpei Yoshimatsu ◽  
Shohta Kodama
Keyword(s):  
Transcription Factors ◽  
Blood Glucose ◽  
Endocrine Cells ◽  
Current Evidence ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Ghrelin Gene ◽  
Pancreatic Endocrine Cells

Pancreatic endocrine cells expressing the ghrelin gene and producing the ghrelin hormone were first identified in 2002. These cells, named ε cells, were recognized as the fifth type of endocrine cells. Differentiation of ε cells is induced by various transcription factors, including Nk2 homeobox 2, paired box proteins Pax-4 and Pax6, and the aristaless-related homeobox. Ghrelin is generally considered to be a “hunger hormone” that stimulates the appetite and is produced mainly by the stomach. Although the population of ε cells is small in adults, they play important roles in regulating other endocrine cells, especially β cells, by releasing ghrelin. However, the roles of ghrelin in β cells are complex. Ghrelin contributes to increased blood glucose levels by suppressing insulin release from β cells and is also involved in the growth and proliferation of β cells and the prevention of β cell apoptosis. Despite increasing evidence and clarification of the mechanisms of ε cells over the last 20 years, many questions remain to be answered. In this review, we present the current evidence for the participation of ε cells in differentiation and clarify their characteristics by focusing on the roles of ghrelin.

Compensatory Recovery of Blood Glucose Levels in KKAy Mice Fed a High-Fat Diet: Insulin-Sparing Effects of PACAP Overexpression in β Cells

2012 ◽  
Vol 48 (3) ◽  
pp. 647-653 ◽  
Author(s):  
Yusuke Sakurai ◽  
Hiroaki Inoue ◽  
Norihito Shintani ◽  
Akihiro Arimori ◽  
Ken-ichi Hamagami ◽  
...  
Keyword(s):  
Blood Glucose ◽  
High Fat Diet ◽  
High Fat ◽  
Β Cells ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Kkay Mice

Molecular regulation of insulin granule biogenesis and exocytosis

2016 ◽  
Vol 473 (18) ◽  
pp. 2737-2756 ◽  
Author(s):  
Pia V. Röder ◽  
Xiuming Wong ◽  
Wanjin Hong ◽  
Weiping Han
Keyword(s):  
Peptide Hormone ◽  
Signaling Cascades ◽  
Β Cells ◽  
Glucose Levels ◽  
Exogenous Glucose ◽  
Blood Glucose Levels ◽  
Insulin Dependent ◽  
Underlying Mechanisms ◽  
Disease Stages

Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by hyperglycemia, insulin resistance and hyperinsulinemia in early disease stages but a relative insulin insufficiency in later stages. Insulin, a peptide hormone, is produced in and secreted from pancreatic β-cells following elevated blood glucose levels. Upon its release, insulin induces the removal of excessive exogenous glucose from the bloodstream primarily by stimulating glucose uptake into insulin-dependent tissues as well as promoting hepatic glycogenesis. Given the increasing prevalence of T2DM worldwide, elucidating the underlying mechanisms and identifying the various players involved in the synthesis and exocytosis of insulin from β-cells is of utmost importance. This review summarizes our current understanding of the route insulin takes through the cell after its synthesis in the endoplasmic reticulum as well as our knowledge of the highly elaborate network that controls insulin release from the β-cell. This network harbors potential targets for anti-diabetic drugs and is regulated by signaling cascades from several endocrine systems.

Glucose regulation of insulin gene expression in pancreatic β-cells

2008 ◽  
Vol 415 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Sreenath S. Andrali ◽  
Megan L. Sampley ◽  
Nathan L. Vanderford ◽  
Sabire Özcan
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Blood Glucose ◽  
Insulin Gene ◽  
Β Cells ◽  
Β Cell ◽  
Insulin Synthesis ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Insulin Gene Expression

Production and secretion of insulin from the β-cells of the pancreas is very crucial in maintaining normoglycaemia. This is achieved by tight regulation of insulin synthesis and exocytosis from the β-cells in response to changes in blood glucose levels. The synthesis of insulin is regulated by blood glucose levels at the transcriptional and post-transcriptional levels. Although many transcription factors have been implicated in the regulation of insulin gene transcription, three β-cell-specific transcriptional regulators, Pdx-1 (pancreatic and duodenal homeobox-1), NeuroD1 (neurogenic differentiation 1) and MafA (V-maf musculoaponeurotic fibrosarcoma oncogene homologue A), have been demonstrated to play a crucial role in glucose induction of insulin gene transcription and pancreatic β-cell function. These three transcription factors activate insulin gene expression in a co-ordinated and synergistic manner in response to increasing glucose levels. It has been shown that changes in glucose concentrations modulate the function of these β-cell transcription factors at multiple levels. These include changes in expression levels, subcellular localization, DNA-binding activity, transactivation capability and interaction with other proteins. Furthermore, all three transcription factors are able to induce insulin gene expression when expressed in non-β-cells, including liver and intestinal cells. The present review summarizes the recent findings on how glucose modulates the function of the β-cell transcription factors Pdx-1, NeuroD1 and MafA, and thereby tightly regulates insulin synthesis in accordance with blood glucose levels.

The Changes in Blood Glucose in Pleuronectes Platessa Following Capture From The Wild: A Stress Reaction

1972 ◽  
Vol 52 (3) ◽  
pp. 635-651 ◽  
Author(s):  
C. S. Wardle
Keyword(s):  
Blood Glucose ◽  
Carbohydrate Metabolism ◽  
Pancreatic Islet ◽  
Stress Reaction ◽  
Control Mechanisms ◽  
Physiological Changes ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Islet Tissue ◽  
Teleost Muscle

Changes in blood glucose levels in teleosts have been reviewed by a number of workers. Epple (1969) considered the regulation of glucose by the insulin of the fish pancreatic islet tissue, Nakano & Tomlinson (1967) examined the regulation of glucose by the catecholamines, Black, Robertson & Parker (1961) considered glucose in carbohydrate metabolism of teleost muscle, while knowledge of regulation of blood glucose in Chondrichthyans has recently been extended and reviewed by Patent (1968, 1970). The investigation of blood glucose levels and their control mechanisms dealt with in this paper forms part of a broader study of the changes that occur when fish are caught from the wild and placed in aquaria (Wardle, 1968, 1971, and unpublished). In this study, capture is considered as a stimulus imposed on the wild fish, which initiates a series of physiological changes that can be measured as the fish adapts to the aquarium.

scholarly journals THE EFFECT OF AMINO ACID COMPOUNDS IN FERMENTED SOYBEANS AGAINST FIBROBLAST GROWTH FACTOR IN MICE PANCREATIC β-CELLS FIGURES

2018 ◽  
Vol 11 (9) ◽  
pp. 157
Author(s):  
Surya Dharma ◽  
Dedy Almasdy ◽  
Dwisari Dillasamola ◽  
Roslinda Rasyid ◽  
Dianty Dwi Wahyuni ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Negative Control Group ◽  
Negative Control ◽  
Control Group ◽  
Fibroblast Growth ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Experimental Animals ◽  
Glucose Levels ◽  
Blood Glucose Levels

Objective: The aim of this study is to determine the effect of the amino acid compound in fermented soybeans against fibroblast growth factor (FGF) in mice’s pancreatic β-cell figures. This study was also done to know the effect of given combination of fertilized egg whites powder with tempe (Indonesian conventional food and the fermentation product of soybeans fermentation) in a dose of 7250 mg/kg.Methods: All of the experimental animals pancreases were designed to be damaged by given alloxan in a dose of 150 mg/kg, except for the negative control group without anything given. The experimental animals were divided into 7 groups which consist of the negative control group, positive control group, and the rests 5 group of FGF test preparation in dosages of 100; 140; 200; 300; and 425 mg/kg combined with fermented soybeans in a dose 7250 mg/kg. This experiment was conducted for 21 days, observed at 7th, 14th, and 21st day. The data analysis used is a statistical test of one-way analysis of variance (ANOVA) and two-way ANOVA.Results: The result showed a significant decrease in blood glucose levels (p<0.05) in mice for all treatments when compared with positive controls. From the result of the histopathologic examination, pancreatic β-cells improve utterly close to the control condition (-). In the qualitative immunohistochemical examination, there was a difference in the stained pancreatic β-cells marked by yellow density. Meanwhile, the quantitative observation did not show any improvement against normal condition control (-) (p<0.05).Conclusion: The combination of egg whites and fermented soybean significantly decreased the blood glucose levels, and the occurrence of the Langerhans island cells was nearly normal.

Diabetes Breakthroughs: Januvia and Janumet

2014 ◽  
Author(s):  
Eugene H. Cordes
Keyword(s):  
Blood Glucose ◽  
Orange Juice ◽  
Critical Role ◽  
Peptide Hormone ◽  
The Body ◽  
Medium Size ◽  
Maple Syrup ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Simple Carbohydrates

I do not recommend this, but let’s just suppose that for breakfast you had a waffle drenched in maple syrup, a large glass of orange juice, and coffee with two teaspoons of sugar. What happens next? Your breakfast is full of carbohydrates. The waffle contains complex carbohydrates (starches) from the flour, and the orange juice, syrup, and sugared coffee contain simple carbohydrates (sugars). The sugar in orange juice and syrup is mostly fructose, and that in your coffee is sucrose. In the intestines, the starches are slowly broken down into the sugar glucose; the sucrose is split into equal amounts of glucose and fructose. The fructose can be converted to glucose in the liver. The sugars from the orange juice, syrup, and coffee enter the blood quickly; those from the starches in the waffle enter more slowly. However, they all act to increase blood glucose levels. A basic principle of human physiology is summed up in one word—homeostasis, which simply means that when the normal metabolic status of the human body is changed in some way, the body responds by restoring normality. When something changes, the body fights back to eliminate or minimize the change. This is what happens when blood glucose is elevated in response to a meal. Here is how. The pancreas is a medium-size organ in the abdomen that secretes enzymes into the gut to aid in digestion, and endocrine hormones into the bloodstream to control some aspects of metabolism. The pancreas responds to sugar entering the bloodstream by secreting the peptide hormone insulin into the circulation. Insulin is made in specialized cells of the pancreas known as the beta cells of the islets of Langerhans. Insulin has a critical role in the regulation of blood glucose levels. Acting through its receptor, insulin causes glucose in the blood to be taken up by muscle and fat cells, reducing the blood glucose level.

scholarly journals Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia

2020 ◽  
Vol 11 ◽  
pp. 204201882096506
Author(s):  
Basma Haris ◽  
Saras Saraswathi ◽  
Khalid Hussain
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Therapeutic Effect ◽  
Glucagon Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Glucose Levels ◽  
Blood Glucose Levels

Hyperinsulinaemic hypoglycaemia (HH) is a biochemical finding of low blood glucose levels due to the dysregulation of insulin secretion from pancreatic β-cells. Under normal physiological conditions, glucose metabolism is coupled to β-cell insulin secretion so that blood glucose levels are maintained within the physiological range of 3.5–5.5 mmol/L. However, in HH this coupling of glucose metabolism to insulin secretion is perturbed so that insulin secretion becomes unregulated. HH typically occurs in the neonatal, infancy and childhood periods and can be due to many different causes. Adults can also present with HH but the causes in adults tend to be different. Somatostatin (SST) is a peptide hormone that is released by the delta cells (δ-cells) in the pancreas. It binds to G protein-coupled SST receptors to regulate a variety of location-specific and selective functions such as hormone inhibition, neurotransmission and cell proliferation. SST plays a potent role in the regulation of both insulin and glucagon secretion in response to changes in glucose levels by negative feedback mechanism. The half-life of SST is only 1–3 min due to quick degradation by peptidases in plasma and tissues. Thus, a direct continuous intravenous or subcutaneous infusion is required to achieve the therapeutic effect. These limitations prompted the discovery of SST analogues such as octreotide and lanreotide, which have longer half-lives and therefore can be administered as injections. SST analogues are used to treat different forms of HH in children and adults and therapeutic effect is achieved by suppressing insulin secretion from pancreatic β-cells by complex mechanisms. These treatments are associated with several side effects, especially in the newborn period, with necrotizing enterocolitis being the most serious side effect and hence SS analogues should be used with extreme caution in this age group.

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