Development and Characteristics of Pancreatic Epsilon Cells

Sakata, Naoaki; Yoshimatsu, Gumpei; Kodama, Shohta

doi:10.3390/ijms20081867

Cited by 30 publications

(23 citation statements)

References 85 publications

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“…It was intriguing to note that not all secretory granules of pancreatic beta cell contain both insulin-and ghrelin-positive nanoparticles. Although reports have shown that ghrelin is produced by epsilon cells of the pancreas [57,59], we did not find ghrelin-positive granules in other cell types. Other studies have reported that ghrelin co-localized sporadically with glucagon in early and late fetal periods and eventually separate later in adult life [60].…”

Section: Body Weight Gain Blood Glucose and Glucose Tolerancecontrasting

confidence: 99%

Exogenous Ghrelin Increases Plasma Insulin Level in Diabetic Rats

et al. 2020

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Ghrelin, a 28-amino acid peptide, is a strong growth hormone secretagogue and a regulator of food intake. In addition, ghrelin is thought to play a role in insulin secretion and in glucose homeostasis. A lot of contradictory data have been reported in the literature regarding the co-localization of ghrelin with other hormones in the islet of Langerhans, its role in insulin secretion and attenuation of type 2 diabetes mellitus. In this study, we investigate the effect of chronic ghrelin treatment on glucose, body weight and insulin level in normal and streptozotocin-induced diabetic male Wistar rats. We have also examined the distribution pattern and co-localization of ghrelin with insulin in pancreatic islet cells using immunohistochemistry and immune-electron microscopy and the ability of ghrelin to stimulate insulin release from the CRL11065 beta cell line. Control, non-diabetic groups received intraperitoneal injection of normal saline, while treated groups received intraperitoneal injection of 5 µg/kg body weight of ghrelin (amino acid chain 24–51) on a daily basis for a duration of four weeks. Our results show that the administration of ghrelin increases the number of insulin-secreting beta cells and serum insulin level in both normal and diabetic rats. We also demonstrated that ghrelin co-localizes with insulin in pancreatic islet cells and that the pattern of ghrelin distribution is altered after the onset of diabetes. Moreover, ghrelin at a dose of 10−6 M and 10−12 M increased insulin release from the CRL11065 beta cell line. In summary, ghrelin co-localizes with insulin in the secretory granules of pancreatic beta cells and enhances insulin production.

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Section: Body Weight Gain Blood Glucose and Glucose Tolerancecontrasting

confidence: 99%

Exogenous Ghrelin Increases Plasma Insulin Level in Diabetic Rats

et al. 2020

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“…ε cell was the fifth endocrine cells identified in pancreatic islet cells, which producing the ghrelin hormone (Wierup et al, 2002). Ghrelin functions through regulating the functions of other endocrine cells (Sakata et al, 2019). Ghrelin inhibits the secretion of insulin from β cells via paracrine interaction between δ cells and β cells.…”

Section: ε Cell and Ghrelinmentioning

confidence: 99%

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

Wei

Lin

et al. 2020

Front. Physiol.

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The clinical significance of diabetes arising in the setting of pancreatic disease (also known as diabetes of the exocrine pancreas, DEP) has drawn more attention in recent years. However, significant improvements still need to be made in the recognition, diagnosis and treatment of the disorder, and in the knowledge of the pathological mechanisms. The clinical course of DEP is different from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). DEP develops in patients with previous existing exocrine pancreatic disorders which damage both exocrine and endocrine parts of pancreas, and lead to pancreas exocrine insufficiency (PEI) and malnutrition. Therefore, damage in various exocrine and endocrine cell types participating in glucose metabolism regulation likely contribute to the development of DEP. Due to the limited amount of clinical and experimental studies, the pathological mechanism of DEP is poorly defined. In fact, it still not entirely clear whether DEP represents a distinct pathologic entity or is a form of T2DM arising when β cell failure is accelerated by pancreatic disease. In this review, we include findings from related studies in T1DM and T2DM to highlight potential pathological mechanisms involved in initiation and progression of DEP, and to provide directions for future research studies.

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“…Ghrelin is a 28-amino-acid peptide produced mainly by the neuroendocrine cells named P/D1 in humans in the oxyntic mucosa of the gastric fundus, and to a far lesser extent in the duodenum, and also in the epsilon pancreatic islet cells (69,70). Ghrelin is cleaved from the 117-amino-acid preproghrelin protein encoded by the human ghrelin gene on chromosome 3p25-26.…”

Section: The Ghrelin Leptin and Melanocortin System In An And Bnmentioning

confidence: 99%

Current Aspects of the Role of Autoantibodies Directed Against Appetite-Regulating Hormones and the Gut Microbiome in Eating Disorders

et al. 2021

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The equilibrium and reciprocal actions among appetite-stimulating (orexigenic) and appetite-suppressing (anorexigenic) signals synthesized in the gut, brain, microbiome and adipose tissue (AT), seems to play a pivotal role in the regulation of food intake and feeding behavior, anxiety, and depression. A dysregulation of mechanisms controlling the energy balance may result in eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). AN is a psychiatric disease defined by chronic self-induced extreme dietary restriction leading to an extremely low body weight and adiposity. BN is defined as out-of-control binge eating, which is compensated by self-induced vomiting, fasting, or excessive exercise. Certain gut microbiota-related compounds, like bacterial chaperone protein Escherichia coli caseinolytic protease B (ClpB) and food-derived antigens were recently described to trigger the production of autoantibodies cross-reacting with appetite-regulating hormones and neurotransmitters. Gut microbiome may be a potential manipulator for AT and energy homeostasis. Thus, the regulation of appetite, emotion, mood, and nutritional status is also under the control of neuroimmunoendocrine mechanisms by secretion of autoantibodies directed against neuropeptides, neuroactive metabolites, and peptides. In AN and BN, altered cholinergic, dopaminergic, adrenergic, and serotonergic relays may lead to abnormal AT, gut, and brain hormone secretion. The present review summarizes updated knowledge regarding the gut dysbiosis, gut-barrier permeability, short-chain fatty acids (SCFA), fecal microbial transplantation (FMT), blood-brain barrier permeability, and autoantibodies within the ghrelin and melanocortin systems in eating disorders. We expect that the new knowledge may be used for the development of a novel preventive and therapeutic approach for treatment of AN and BN.

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Development and Characteristics of Pancreatic Epsilon Cells

Cited by 30 publications

References 85 publications

Exogenous Ghrelin Increases Plasma Insulin Level in Diabetic Rats

Exogenous Ghrelin Increases Plasma Insulin Level in Diabetic Rats

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

Current Aspects of the Role of Autoantibodies Directed Against Appetite-Regulating Hormones and the Gut Microbiome in Eating Disorders

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