A Novel Role for Somatostatin in the Survival of Mouse Pancreatic Beta Cells

Damsteegt, Erin L.; Hassan, Zoheb; Hewawasam, Nirun Videesha; Sarnsamak, Kittiwadee; Jones, Peter M.; Hauge-Evans, Astrid C.

doi:10.33594/000000035

Cited by 15 publications

(5 citation statements)

References 52 publications

(84 reference statements)

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“…Somatostatin also have influences on β cell. It can modulate the apoptosis and proliferation of mouse β cells in response to stress (Damsteegt et al, 2019). In addition, δ cell can direct transdifferentiate β cell therefore plays a role in β cell mass.…”

Section: δ Cell and Somatostatinmentioning

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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Section: δ Cell and Somatostatinmentioning

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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“…In addition, the close neighborhood to the vascular system might be an advantage of the bile duct as an application way to perform re-endothelization. In the end, the re-colonization of the neoorgan with endothelial cells or other co-populations will be crucial for a successful in vivo implantation without thrombosis [28,30,33,34,36,[40][41][42][43][44][45].…”

Section: Discussionmentioning

confidence: 99%

Perfusion-Based Recellularization of Rat Livers with Islets of Langerhans

et al. 2022

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Purpose Artificial organs might serve as alternative solutions for whole organ transplantation. Decellularization of a liver provides a non-immunogenic matrix with the advantage of three afferent systems, the portal vein, the hepatic artery and the bile duct. This study aims to evaluate the recellularization of rat livers with islets of Langerhans via the bile duct and the portal vein for the comparison of different perfusion routes. Methods Rat livers were decellularized in a pressure-controlled perfusion manner and repopulated with intact isolated islets of Langerhans via either the portal vein or the bile duct. Results Repopulation via the portal vein showed islet clusters stuck within the vascular system demonstrated by ellipsoid borders of thick reticular tissue around the islet cluster in Azan staining. After recellularization via the bile duct, islets were distributed close to the vessels within the parenchymal space and without a surrounding reticular layer. Large clusters of islets had a diameter of up to 1000 µm without clear shapes. Conclusion We demonstrated the bile duct to be superior to the portal vein for repopulation of a decellularized rat liver with islets of Langerhans. This technique may serve as a bioengineering platform to generate an implantable and functional endocrine neo-pancreas and provide scaffolds with the anatomic benefit of three afferent systems to facilitate co-population of cells.

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“…Outside of paracrine control of glucose homeostasis, delta-cell-derived somatostatin may also enhance beta-cell survival, as tissue culture of isolated mouse islets or MIN6 beta-cells in the presence of exogenous somatostatin reduced the presence of biochemical markers of stress and apoptosis caused by lipotoxicity, pro-inflammatory cytokines, or hypoglycemic conditions [108]. In addition, a recent study of human delta-cells identified the co-expression and presence in secretory granules with somatostatin of an alternatively spliced insulin gene product that encodes the insulin signal peptide and the B-chain [109].…”

Section: Delta-cellsmentioning

confidence: 99%

The Importance of Intra-Islet Communication in the Function and Plasticity of the Islets of Langerhans during Health and Diabetes

Hill,

Hill

2024

IJMS

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Islets of Langerhans are anatomically dispersed within the pancreas and exhibit regulatory coordination between islets in response to nutritional and inflammatory stimuli. However, within individual islets, there is also multi-faceted coordination of function between individual beta-cells, and between beta-cells and other endocrine and vascular cell types. This is mediated partly through circulatory feedback of the major secreted hormones, insulin and glucagon, but also by autocrine and paracrine actions within the islet by a range of other secreted products, including somatostatin, urocortin 3, serotonin, glucagon-like peptide-1, acetylcholine, and ghrelin. Their availability can be modulated within the islet by pericyte-mediated regulation of microvascular blood flow. Within the islet, both endocrine progenitor cells and the ability of endocrine cells to trans-differentiate between phenotypes can alter endocrine cell mass to adapt to changed metabolic circumstances, regulated by the within-islet trophic environment. Optimal islet function is precariously balanced due to the high metabolic rate required by beta-cells to synthesize and secrete insulin, and they are susceptible to oxidative and endoplasmic reticular stress in the face of high metabolic demand. Resulting changes in paracrine dynamics within the islets can contribute to the emergence of Types 1, 2 and gestational diabetes.

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A Novel Role for Somatostatin in the Survival of Mouse Pancreatic Beta Cells

Abstract: This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission.

Cited by 15 publications

References 52 publications

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

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

Perfusion-Based Recellularization of Rat Livers with Islets of Langerhans

The Importance of Intra-Islet Communication in the Function and Plasticity of the Islets of Langerhans during Health and Diabetes

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