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Molecular Mechanisms and Signaling Pathways Involved in Insulin Producing β-Cell Function

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 1775

Special Issue Editor


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Guest Editor
Department of Endocrinology, Hadassah University Hospital, Jerusalem, Israel
Interests: pancreatic beta cell function; apoptosis; gluco-lipotoxicity; inflammation; NF-kB; diabetes

Special Issue Information

Dear Colleagues,

Insulin is the main regulator of glucose homeostasis; the normal function of pancreatic insulin-secreting beta-cells is crucial for maintaining glucose homeostasis in the organism. Diabetes mellitus is a heterogeneous group of disorders characterized by an excess in blood glucose levels or hyperglycemia. Defective insulin secretion is the cause of all forms of diabetes. 

Genetic and environmental factors can impact beta-cell dysfunction in many ways, such as impaired glucose-sensing and secretion coupling mechanisms, insufficient adaptive response to insulin resistance, increased beta-cell loss, and dedifferentiation.

Several mechanisms have been suggested to be involved in decreased beta-cell function and/or survival in Type 2 diabetes, including oxidative stress, ceramide formation, ER overload, inflammation, disturbance of the circadian-timing system, disruption of intra-islet communication, elevated blood glucagon levels, etc.

Maintaining pancreatic beta-cell function and mass is essential for normal insulin production and glucose homeostasis.

Dr. Danielle Melloul
Guest Editor

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Published Papers (1 paper)

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12 pages, 2634 KiB  
Perspective
Nrf2 and Antioxidant Response in Animal Models of Type 2 Diabetes
by R. Paul Robertson
Int. J. Mol. Sci. 2023, 24(4), 3082; https://doi.org/10.3390/ijms24043082 - 4 Feb 2023
Cited by 7 | Viewed by 1555
Abstract
This perspective examines the proposition that chronically elevated blood glucose levels caused by type 2 diabetes (T2D) harm body tissues by locally generating reactive oxygen species (ROS). A feed-forward scenario is described in which the initial onset of defective beta cell function T2D [...] Read more.
This perspective examines the proposition that chronically elevated blood glucose levels caused by type 2 diabetes (T2D) harm body tissues by locally generating reactive oxygen species (ROS). A feed-forward scenario is described in which the initial onset of defective beta cell function T2D becomes sustained and causes chronic elevations in blood glucose, which flood metabolic pathways throughout the body, giving rise to abnormally high local levels of ROS. Most cells can defend themselves via a full complement of antioxidant enzymes that are activated by ROS. However, the beta cell itself does not contain catalase or glutathione peroxidases and thereby runs a greater risk of ROS-induced damage. In this review, previously published experiments are revisited to examine the concept that chronic hyperglycemia can lead to oxidative stress in the beta cell, how this relates to the absence of beta cell glutathione peroxidase (GPx) activity, and whether this deficiency might be ameliorated by genetic enrichment of beta cell GPx and by oral antioxidants, including ebselen, a GPx mimetic. Full article
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