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Special Issue "Molecular Diagnostic and Therapeutic Advances of Type 2 Diabetes and Its Complications"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 April 2023 | Viewed by 344

Special Issue Editors

Prof. Dr. Stephen Atkin
E-Mail Website
Guest Editor
Royal College of Surgeons in Ireland Bahrain, Adliya 15503, Bahrain
Interests: type 2 diabetes; obesity; polycystic ovary syndrome; insulin resistance
Prof. Dr. Thozhukat Sathyapalan
E-Mail Website
Guest Editor
Academic Endocrinology, Diabetes and Metabolism, Hull York Medical School, University of Hull, Hull HU6 7RU, UK
Interests: diabetes; obesity; nutrition; insulin resistance; glucose variability; polycystic ovary syndrome (PCOS); metabolic diseases; lipid metabolism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Alexandra Butler
E-Mail Website
Guest Editor
Royal College of Surgeons in Ireland Bahrain, Adliya 15503, Bahrain
Interests: type 1 diabetes; type 2 diabetes; islet cell biology; obesity

Special Issue Information

Dear Colleagues,

This Special Issue focuses on advances in the underlying molecular mechanisms in the development and progression of type 2 diabetes from prediabetes and their interplay with obesity. It also welcomes articles on the molecular mechanisms which underpin the development and evolution of both macrovascular complications, including cardiovascular disease, dyslipidemia, and non-alcoholic fatty liver disease, as well as the microvascular complications of retinopathy, nephropathy, and neuropathy. Original and review articles addressing the molecular basis of novel biomarkers as well as therapeutic options in the management of type 2 diabetes and its complications are also considered in this Special Issue.

Prof. Dr. Stephen Atkin
Prof. Dr. Thozhukat Sathyapalan
Prof. Dr. Alexandra Butler
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Keywords

  • type 2 diabetes
  • obesity
  • diabetes complications
  • cardiovascular disease
  • dyslipidemia
  • non-alcoholic fatty liver disease
  • metabolic syndrome
  • retinopathy
  • nephropathy
  • neuropathy
  • pharmacotherapy
  • insulin resistance

Published Papers (1 paper)

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Research

Article
MicroRNA Changes Up to 24 h following Induced Hypoglycemia in Type 2 Diabetes
Int. J. Mol. Sci. 2022, 23(23), 14696; https://doi.org/10.3390/ijms232314696 - 24 Nov 2022
Viewed by 267
Abstract
Hypoglycemia, as a complication of type 2 diabetes (T2D), causes increased morbidity and mortality but the physiological response underlying hypoglycemia has not been fully elucidated. Small noncoding microRNA (miRNA) have multiple downstream biological effects. This pilot exploratory study was undertaken to determine if [...] Read more.
Hypoglycemia, as a complication of type 2 diabetes (T2D), causes increased morbidity and mortality but the physiological response underlying hypoglycemia has not been fully elucidated. Small noncoding microRNA (miRNA) have multiple downstream biological effects. This pilot exploratory study was undertaken to determine if induced miRNA changes would persist and contribute to effects seen 24 h post-hypoglycemia. A parallel, prospective study design was employed, involving T2D (n = 23) and control (n = 23) subjects. The subjects underwent insulin-induced hypoglycemia (2 mmol/L; 36 mg/dL); blood samples were drawn at baseline, upon the induction of hypoglycemia, and 4 h and 24 h post-hypoglycemia, with a quantitative polymerase chain reaction analysis of miRNA undertaken. The baseline miRNAs did not differ. In the controls, 15 miRNAs were downregulated and one was upregulated (FDR < 0.05) from the induction of hypoglycemia to 4 h later while, in T2D, only four miRNAs were altered (downregulated), and these were common to both cohorts (miR-191-5p; miR-143-3p; let-7b-5p; let-7g-5p), correlated with elevated glucagon levels, and all were associated with energy balance. From the induction of hypoglycemia to 24 h, 14 miRNAs were downregulated and 5 were upregulated (FDR < 0.05) in the controls; 7 miRNAs were downregulated and 7 upregulated (FDR < 0.05) in T2D; a total of 6 miRNAs were common between cohorts, 5 were downregulated (miR-93-5p, let-7b-5p, miR-191-5p, miR-185-5p, and miR-652-3p), and 1 was upregulated (miR-369-3p). An ingenuity pathway analysis indicated that many of the altered miRNAs were associated with metabolic and coagulation pathways; however, of the inflammatory proteins expressed, only miR-143-3p at 24 h correlated positively with tumor necrosis factor-α (TNFa; p < 0.05 and r = 0.46) and negatively with toll-like receptor-4 (TLR4; p < 0.05 and r = 0.43). The MiRNA levels altered by hypoglycemia reflected changes in counter-regulatory glucagon and differed between cohorts, and their expression at 24 h suggests miRNAs may potentiate and prolong the physiological response. Trial registration: ClinicalTrials.gov NCT03102801. Full article
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