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Biomedicines
Special Issues
Pathophysiological and Therapeutic Perspectives of Type-1 Diabetes
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Pathophysiological and Therapeutic Perspectives of Type-1 Diabetes

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 5743

Special Issue Editor

Dr. Srinivas Nammi

E-Mail Website
Guest Editor
Discipline of Medical Sciences, School of Science and NICM-Health Research Institute, Western Sydney University, Sydney, NSW 2751, Australia
Interests: chronic kidney disease; fatty liver disease; herbal pharmacology; insulin resistance; lipid disorders; metabolic syndrome; obesity; pharmacokinetics and drug interactions; type 2 diabetes and its complications

Special Issue Information

Dear Colleagues,

Knowledge on the pathogenesis and natural history of type 1 diabetes has substantially grown in the last few decades. It is an auto-immune condition characterized by the destruction of the pancreatic beta cells, leading to absolute insulin deficiency. The destruction of β-cells is triggered by genetic, environmental and immunologic factors that destroy the endocrine cells of the pancreas, leading to insulin deficiency. Furthermore, inflammation (e.g., interleukin-1 mediated) may play a significant role in islet β-cells loss in type-1 diabetes. Patients with type 1 diabetes may also, coincidentally, have pathophysiologic elements of type 2 diabetes. In the past, the poor metabolic control of type 1 diabetes prevented most of these patients from gaining weight. Intensive therapy now commonly used to manage type 1 diabetes has resulted in approximately 20% to 30% of type 1 diabetic patients becoming overweight or obese. Insulin resistance and other features of type 2 diabetes may be exhibited in overweight patients with type 1 diabetes, especially those who also have a family history of type 2 diabetes. Over time, the complications of type 1 diabetes can affect major organs in the body, including heart, blood vessels, nerves, eyes and kidneys.

We invite scientists to contribute both original research articles and reviews that highlight the development of pathophysiological pathways of type-1 diabetes and current therapeutic perspectives. Both basic and translational research papers are welcome.

Dr. Srinivas Nammi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (2 papers)

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Research

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16 pages, 3183 KiB  
Article
Bezafibrate Reduces Elevated Hepatic Fumarate in Insulin-Deficient Mice
by Andras Franko, Martin Irmler, Cornelia Prehn, Silke S. Heinzmann, Philippe Schmitt-Kopplin, Jerzy Adamski, Johannes Beckers, Jürgen-Christoph von Kleist-Retzow, Rudolf Wiesner, Hans-Ulrich Häring, Martin Heni, Andreas L. Birkenfeld and Martin Hrabě de Angelis
Biomedicines 2022, 10(3), 616; https://doi.org/10.3390/biomedicines10030616 - 6 Mar 2022
Cited by 9 | Viewed by 2921
Abstract
Glucotoxic metabolites and pathways play a crucial role in diabetic complications, and new treatment options which improve glucotoxicity are highly warranted. In this study, we analyzed bezafibrate (BEZ) treated, streptozotocin (STZ) injected mice, which showed an improved glucose metabolism compared to untreated STZ [...] Read more.
Glucotoxic metabolites and pathways play a crucial role in diabetic complications, and new treatment options which improve glucotoxicity are highly warranted. In this study, we analyzed bezafibrate (BEZ) treated, streptozotocin (STZ) injected mice, which showed an improved glucose metabolism compared to untreated STZ animals. In order to identify key molecules and pathways which participate in the beneficial effects of BEZ, we studied plasma, skeletal muscle, white adipose tissue (WAT) and liver samples using non-targeted metabolomics (NMR spectroscopy), targeted metabolomics (mass spectrometry), microarrays and mitochondrial enzyme activity measurements, with a particular focus on the liver. The analysis of muscle and WAT demonstrated that STZ treatment elevated inflammatory pathways and reduced insulin signaling and lipid pathways, whereas BEZ decreased inflammatory pathways and increased insulin signaling and lipid pathways, which can partly explain the beneficial effects of BEZ on glucose metabolism. Furthermore, lysophosphatidylcholine levels were lower in the liver and skeletal muscle of STZ mice, which were reverted in BEZ-treated animals. BEZ also improved circulating and hepatic glucose levels as well as lipid profiles. In the liver, BEZ treatment reduced elevated fumarate levels in STZ mice, which was probably due to a decreased expression of urea cycle genes. Since fumarate has been shown to participate in glucotoxic pathways, our data suggests that BEZ treatment attenuates the urea cycle in the liver, decreases fumarate levels and, in turn, ameliorates glucotoxicity and reduces insulin resistance in STZ mice. Full article
(This article belongs to the Special Issue Pathophysiological and Therapeutic Perspectives of Type-1 Diabetes)
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Review

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11 pages, 1316 KiB  
Review
Setting the Stage for Insulin Granule Dysfunction during Type-1-Diabetes: Is ER Stress the Culprit?
by Aishwarya A. Makam, Anusmita Biswas, Lakshmi Kothegala and Nikhil R. Gandasi
Biomedicines 2022, 10(11), 2695; https://doi.org/10.3390/biomedicines10112695 - 25 Oct 2022
Cited by 4 | Viewed by 2247
Abstract
Type-1-diabetes (T1D) is a multifactorial disorder with a global incidence of about 8.4 million individuals in 2021. It is primarily classified as an autoimmune disorder, where the pancreatic β-cells are unable to secrete sufficient insulin. This leads to elevated blood glucose levels (hyperglycemia). [...] Read more.
Type-1-diabetes (T1D) is a multifactorial disorder with a global incidence of about 8.4 million individuals in 2021. It is primarily classified as an autoimmune disorder, where the pancreatic β-cells are unable to secrete sufficient insulin. This leads to elevated blood glucose levels (hyperglycemia). The development of T1D is an intricate interplay between various risk factors, such as genetic, environmental, and cellular elements. In this review, we focus on the cellular elements, such as ER (endoplasmic reticulum) stress and its consequences for T1D pathogenesis. One of the major repercussions of ER stress is defective protein processing. A well-studied example is that of islet amyloid polypeptide (IAPP), which is known to form cytotoxic amyloid plaques when misfolded. This review discusses the possible association between ER stress, IAPP, and amyloid formation in β-cells and its consequences in T1D. Additionally, ER stress also leads to autoantigen generation. This is driven by the loss of Ca++ ion homeostasis. Imbalanced Ca++ levels lead to abnormal activation of enzymes, causing post-translational modification of β-cell proteins. These modified proteins act as autoantigens and trigger the autoimmune response seen in T1D islets. Several of these autoantigens are also crucial for insulin granule biogenesis, processing, and release. Here, we explore the possible associations between ER stress leading to defects in insulin secretion and ultimately β-cell destruction. Full article
(This article belongs to the Special Issue Pathophysiological and Therapeutic Perspectives of Type-1 Diabetes)
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