scholarly journals Impact of prematurity for pancreatic islet and beta-cell development

2018 ◽  
Vol 238 (3) ◽  
pp. R161-R171 ◽  
Author(s):  
Frank H Bloomfield

As increasing numbers of babies born preterm survive into adulthood, it is becoming clear that, in addition to the well-described risks of neurodevelopmental sequelae, there also are increased risks for non-communicable diseases, including diabetes. Epidemiological studies indicate that risks are increased even for birth at late preterm and early term gestations and for both type 1 and type 2 diabetes. Thus, factors related to preterm birth likely affect development of the fetal and neonatal beta-cell in addition to effects on peripheral insulin sensitivity. These factors could operate prior to preterm birth and be related to the underlying cause of preterm birth, to the event of being born preterm itself, to the postnatal care of the preterm neonate or to a combination of these exposures. Experimental evidence indicates that factors may be operating during all these critical periods to contribute to altered development of beta-cell mass in those born preterm. Greater understanding of how these factors impact upon development of the pancreas may lead to interventions or management approaches that mitigate the increased risk of later diabetes.

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 213
Author(s):  
Taylor Marie Richards ◽  
Aixia Sun ◽  
Hasaan Hayat ◽  
Neil Robertson ◽  
Zhaoda Zhang ◽  
...  

Islet transplantation has great potential as a cure for type 1 diabetes. At present; the lack of a clinically validated non-invasive imaging method to track islet grafts limits the success of this treatment. Some major clinical imaging modalities and various molecular probes, which have been studied for non-invasive monitoring of transplanted islets, could potentially fulfill the goal of understanding pathophysiology of the functional status and viability of the islet grafts. In this current review, we summarize the recent clinical studies of a variety of imaging modalities and molecular probes for non-invasive imaging of transplanted beta cell mass. This review also includes discussions on in vivo detection of endogenous beta cell mass using clinical imaging modalities and various molecular probes, which will be useful for longitudinally detecting the status of islet transplantation in Type 1 diabetic patients. For the conclusion and perspectives, we highlight the applications of multimodality and novel imaging methods in islet transplantation.


2016 ◽  
Vol 73 (19) ◽  
pp. 3623-3637 ◽  
Author(s):  
Krishna Prasadan ◽  
Chiyo Shiota ◽  
Xiao Xiangwei ◽  
David Ricks ◽  
Joseph Fusco ◽  
...  

2019 ◽  
Vol 10 ◽  
Author(s):  
Gabriela Alves Bronczek ◽  
Jean Franciesco Vettorazzi ◽  
Gabriela Moreira Soares ◽  
Mirian Ayumi Kurauti ◽  
Cristiane Santos ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Lucien Marchand ◽  
Audrey Jalabert ◽  
Emmanuelle Meugnier ◽  
Kathleen Van den Hende ◽  
Nicole Fabien ◽  
...  

Background.The use of miRNAs as biomarkers for Type 1 Diabetes (T1D) risk is attractive as T1D is usually diagnosed in front of acute symptoms. As miR-375 is highly expressed in the endocrine pancreas, we postulated that its circulating level might reflect beta cell alterations and might be altered in the blood of T1D patients recently diagnosed.Methods.Sera were obtained from 22 T1D children at onset of the disease, before subcutaneous insulin treatment, and from 10 nondiabetic pediatric controls. MiR-375 seric level was quantified by stem-loop RT-PCR-based assay. MiRNAs regulations in isolated human islets in response to high glucose concentrations were determined by TaqMan Low-Density Array.Results.The abundance of miR-375, among the 410 miRNAs detected in human islets, mirrored its well-established role in rodent islet biology. Upregulated miRNAs targeted genes involved in islet homeostasis and regulation of beta cell mass. Downregulated miRNAs, including miR-375, were involved in pancreas secretion and protein turnover. Seric level of miR-375 was lower in T1D children versus age-matched controls, without any correlations with HbA1c, glycaemia, and number of autoantibodies.Conclusion.Altered circulating level of miR-375 at onset of T1D might be a general biomarker of metabolic alterations and inflammation associated with the disease.


2018 ◽  
Author(s):  
Peter Seiron ◽  
Anna Wiberg ◽  
Lars Krogvold ◽  
Frode Lars Jahnsen ◽  
Knut Dahl-Jørgensen ◽  
...  

AbstractInsulin deficiency in type 1 diabetes (T1D) is generally considered a consequence of specific beta-cell loss. Since healthy pancreatic islets consist of ~65% beta cells, this would lead to reduced islet size if the beta cells are not replaced by other cells or tissue. The number of islets per pancreas volume (islet density) would not be affected.In this study, we compared the islet density, size, and size distribution in subjects with recent-onset or long-standing T1D, with that in matched non-diabetic subjects. Results show that subjects with T1D, regardless of disease duration, had a dramatically reduced islet number per mm2, while the islet size was similar in all groups. Insulin-negative islets in T1D subjects were dominated by glucagon-positive cells that frequently had lost the alpha-cell transcription factor ARX while instead expressing PDX1, normally expressed in beta cells.Based on our findings, we propose that failure during childhood to establish a sufficient islet number to reach the beta-cell mass needed to cope with episodes of increased insulin demand contributes to T1D susceptibility. Exhaustion induced by relative lack of beta cells could then potentially drive beta-cell dedifferentiation to alpha-cells, explaining the preserved islet size observed in T1D compared to controls.


2021 ◽  
Vol 249 (2) ◽  
pp. T1-T11
Author(s):  
Pieter-Jan Martens ◽  
Conny Gysemans ◽  
Chantal Mathieu

Type 1 diabetes is one of the most common chronic diseases in children and adolescents, but remains unpreventable and incurable. The discovery of insulin, already 100 years ago, embodied a lifesaver for people with type 1 diabetes as it allowed the replacement of all functions of the beta cell. Nevertheless, despite all technological advances, the majority of type 1 diabetic patients fail to reach the recommended target HbA1c levels. The disease-associated complications remain the true burden of affected individuals and necessitate the search for disease prevention and reversal. The recognition that type 1 diabetes is a heterogeneous disease with an etiology in which both the innate and adaptive immune system as well as the insulin-producing beta cells intimately interact, has fostered the idea that treatment to specific molecular or cellular characteristics of the patient groups will be needed. Moreover, robust and reliable biomarkers to detect type 1 diabetes in the early (pre-symptomatic) phases are wanted to preserve functional beta cell mass. The pitfalls of past therapeutics along with the perspectives of current therapies can open up the path for future research.


2008 ◽  
Vol 52 (2) ◽  
pp. 407-415 ◽  
Author(s):  
Carlos Eduardo Barra Couri ◽  
Júlio César Voltarelli

Type 1 diabetes mellitus is the result of the autoimmune response against pancreatic beta-cell(s). At the time of clinical diagnosis near 70% of beta-cell mass is been destroyed as a consequence of the auto-destruction that begins months or even years before the clinical diagnosis. Although marked reduction of chronic complications was seen after development and progression of insulin therapy over the years for type 1 diabetic population, associated risks of chronic end-organ damage and hypoglycemia still remain. Besides tight glucose control, beta-cell mass preservation and/or increase are known to be other important targets in management of type 1 diabetes as long as it reduces chronic microvascular complications in the eyes, kidneys and nerves. Moreover, the larger the beta-cell mass, the lower the incidence of hypoglycemic events. In this article, we discuss some insights about beta-cell regeneration, the importance of regulation of the autoimmune process and what is being employed in human type 1 diabetes in regard to stem cell repertoire to promote regeneration and/or preservation of beta-cell mass.


2013 ◽  
Vol 11 (4) ◽  
pp. 200-201
Author(s):  
Wietske Woliner-van der Weg ◽  
Maarten Brom ◽  
Marcel J.R. Janssen ◽  
Martin Béhe ◽  
Wim J.G. Oyen ◽  
...  

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