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Epigenetics of Diabetes and Related Complications 2.0

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

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 21270

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Special Issue Editors

Dr. Claudia Miele

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Guest Editor

URT Istituto per l’Endocrinologia e l’Oncologia Sperimentale “Gaetano Salvatore” CNR, Naples, Italy
Interests: signal transduction; glucose metabolism; type 2 diabetes; insulin resistance; beta-cell function; glucotoxicity; epigenetic of type 2 diabetes; diabetes and cognitive diseases; diabetes and cancer
Special Issues, Collections and Topics in MDPI journals

Dr. Cecilia Nigro

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Co-Guest Editor

URT Genomica del Diabete - Istituto per l’Endocrinologia e l’Oncologia Sperimentale “Gaetano Salvatore” CNR, Naples, Italy
Interests: diabetes mellitus; dicarbonyl stress; glucose homeostasis; insulin resistance; mouse models, vascular complications; diabetes epigenetics

Special Issue Information

A growing body of evidence suggests that dynamic alterations in the epigenome (i.e., DNA methylation, histone markers, and non-coding RNAs) play a causative role in the activation of the molecular events responsible for diabetes progression and associated complications. These events can be induced by metabolic changes, such as hyperglycaemia, and can be responsible for a long-lasting impairment of vascular and cardiac function, even after intensive glycemic control. Indeed, diabetes complications can be affected by glucose levels that were experienced years earlier, a phenomenon called metabolic memory. Notably, the adverse epigenetic profile acquired over the life course can be transmitted to the offspring, and may contribute to early cardiovascular phenotypes in younger generations.

Unveiling the epigenetic landscape in diabetic subjects and people at risk of developing diabetes is beneficial to the provision of tools for personalized epigenetic-based therapies.

The aim of this Special Issue is to provide a collection of original research and review articles aimed at advancing our knowledge of the epigenetics of diabetes and its implications in classic diabetes complications and co-morbidities.

Dr. Claudia Miele
Guest Editor
Dr. Cecilia Nigro
Co-Guest Editor

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Keywords

diabetes mellitus
epigenetics
glycation stress
histone markers
metabolic memory
methylation
ncRNA
vascular complications
cognitive disease
cancer risk

Published Papers (5 papers)

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Research

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18 pages, 4835 KiB

Open AccessArticle

Distinctive Microbial Signatures and Gut-Brain Crosstalk in Pediatric Patients with Coeliac Disease and Type 1 Diabetes Mellitus

by Parul Singh, Arun Rawat, Bara Al-Jarrah, Saras Saraswathi, Hoda Gad, Mamoun Elawad, Khalid Hussain, Mohammed A. Hendaus, Wesam Al-Masri, Rayaz A. Malik, Souhaila Al Khodor and Anthony K. Akobeng

Int. J. Mol. Sci. 2021, 22(4), 1511; https://doi.org/10.3390/ijms22041511 - 3 Feb 2021

Cited by 10 | Viewed by 2779

Abstract

Coeliac disease (CD) and Type 1 diabetes mellitus (T1DM) are immune-mediated diseases. Emerging evidence suggests that dysbiosis in the gut microbiome plays a role in the pathogenesis of both diseases and may also be associated with the development of neuropathy. The primary goal in this cross-sectional pilot study was to identify whether there are distinct gut microbiota alterations in children with CD (n = 19), T1DM (n = 18) and both CD and T1DM (n = 9) compared to healthy controls (n = 12). Our second goal was to explore the relationship between neuropathy (corneal nerve fiber damage) and the gut microbiome composition. Microbiota composition was determined by 16S rRNA gene sequencing. Corneal confocal microscopy was used to determine nerve fiber damage. There was a significant difference in the overall microbial diversity between the four groups with healthy controls having a greater microbial diversity as compared to the patients. The abundance of pathogenic proteobacteria Shigella and E. coli were significantly higher in CD patients. Differential abundance analysis showed that several bacterial amplicon sequence variants (ASVs) distinguished CD from T1DM. The tissue transglutaminase antibody correlated significantly with a decrease in gut microbial diversity. Furthermore, the Bacteroidetes phylum, specifically the genus Parabacteroides was significantly correlated with corneal nerve fiber loss in the subjects with neuropathic damage belonging to the diseased groups. We conclude that disease-specific gut microbial features traceable down to the ASV level distinguish children with CD from T1DM and specific gut microbial signatures may be associated with small fiber neuropathy. Further research on the mechanisms linking altered microbial diversity with neuropathy are warranted. Full article

(This article belongs to the Special Issue Epigenetics of Diabetes and Related Complications 2.0)

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17 pages, 1577 KiB

Open AccessArticle

Placental Epigenome-Wide Association Study Identified Loci Associated with Childhood Adiposity at 3 Years of Age

by Valérie Gagné-Ouellet, Edith Breton, Kathrine Thibeault, Carol-Ann Fortin, Véronique Desgagné, Élise Girard Tremblay, Andres Cardenas, Renée Guérin, Patrice Perron, Marie-France Hivert and Luigi Bouchard

Int. J. Mol. Sci. 2020, 21(19), 7201; https://doi.org/10.3390/ijms21197201 - 29 Sep 2020

Cited by 10 | Viewed by 2666

Abstract

The aim of this study was to identify placental DNA methylation (DNAm) variations associated with adiposity at 3 years of age. We quantified placental DNAm using the Infinium MethylationEPIC BeadChips. We assessed associations between DNAm at single-CpGs and skinfold thickness using robust linear regression models adjusted for gestational age, child’s sex, age at follow-up and cellular heterogeneity. We sought replication of DNAm association with child adiposity in an independent cohort. We quantified placental mRNA levels for annotated gene using qRT-PCR and tested for correlation with DNAm. Lower DNAm at cg22593959 and cg22436429 was associated with higher adiposity (β = −1.18, q = 0.002 and β = −0.82, q = 0.04). The cg22593959 is located in an intergenic region (chr7q31.3), whereas cg22436429 is within the TFAP2E gene (1p34.3). DNAm at cg22593959 and cg22436429 was correlated with mRNA levels at FAM3C (r_s = −0.279, p = 0.005) and TFAP2E (r_s = 0.216, p = 0.03). In an independent cohort, the association between placental DNAm at cg22593959 and childhood adiposity was of similar strength and direction (β = −3.8 ± 4.1, p = 0.36), yet non-significant. Four genomic regions were also associated with skinfold thickness within FMN1, MAGI2, SKAP2 and BMPR1B genes. We identified placental epigenetic variations associated with adiposity at 3 years of age suggesting that childhood fat accretion patterns might be established during fetal life. Full article

(This article belongs to the Special Issue Epigenetics of Diabetes and Related Complications 2.0)

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Review

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25 pages, 889 KiB

Open AccessReview

DNA Methylation and Type 2 Diabetes: Novel Biomarkers for Risk Assessment?

by Gregory Alexander Raciti, Antonella Desiderio, Michele Longo, Alessia Leone, Federica Zatterale, Immacolata Prevenzano, Claudia Miele, Raffaele Napoli and Francesco Beguinot

Int. J. Mol. Sci. 2021, 22(21), 11652; https://doi.org/10.3390/ijms222111652 - 28 Oct 2021

Cited by 18 | Viewed by 4180

Abstract

Diabetes is a severe threat to global health. Almost 500 million people live with diabetes worldwide. Most of them have type 2 diabetes (T2D). T2D patients are at risk of developing severe and life-threatening complications, leading to an increased need for medical care and reduced quality of life. Improved care for people with T2D is essential. Actions aiming at identifying undiagnosed diabetes and at preventing diabetes in those at high risk are needed as well. To this end, biomarker discovery and validation of risk assessment for T2D are critical. Alterations of DNA methylation have recently helped to better understand T2D pathophysiology by explaining differences among endophenotypes of diabetic patients in tissues. Recent evidence further suggests that variations of DNA methylation might contribute to the risk of T2D even more significantly than genetic variability and might represent a valuable tool to predict T2D risk. In this review, we focus on recent information on the contribution of DNA methylation to the risk and the pathogenesis of T2D. We discuss the limitations of these studies and provide evidence supporting the potential for clinical application of DNA methylation marks to predict the risk and progression of T2D. Full article

(This article belongs to the Special Issue Epigenetics of Diabetes and Related Complications 2.0)

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25 pages, 786 KiB

Open AccessReview

Changes Induced by Mind–Body Intervention Including Epigenetic Marks and Its Effects on Diabetes

by Hyun-Jeong Yang, Eugene Koh, Min-Kyu Sung and Hojung Kang

Int. J. Mol. Sci. 2021, 22(3), 1317; https://doi.org/10.3390/ijms22031317 - 28 Jan 2021

Cited by 9 | Viewed by 4490

Abstract

Studies have evidenced that epigenetic marks associated with type 2 diabetes (T2D) can be inherited from parents or acquired through fetal and early-life events, as well as through lifelong environments or lifestyles, which can increase the risk of diabetes in adulthood. However, epigenetic modifications are reversible, and can be altered through proper intervention, thus mitigating the risk factors of T2D. Mind–body intervention (MBI) refers to interventions like meditation, yoga, and qigong, which deal with both physical and mental well-being. MBI not only induces psychological changes, such as alleviation of depression, anxiety, and stress, but also physiological changes like parasympathetic activation, lower cortisol secretion, reduced inflammation, and aging rate delay, which are all risk factors for T2D. Notably, MBI has been reported to reduce blood glucose in patients with T2D. Herein, based on recent findings, we review the effects of MBI on diabetes and the mechanisms involved, including epigenetic modifications. Full article

(This article belongs to the Special Issue Epigenetics of Diabetes and Related Complications 2.0)

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27 pages, 6388 KiB

Open AccessReview

Exploring the Triple Interaction between the Host Genome, the Epigenome, and the Gut Microbiome in Type 1 Diabetes

by Duaa Ahmed Elhag, Manoj Kumar and Souhaila Al Khodor

Int. J. Mol. Sci. 2021, 22(1), 125; https://doi.org/10.3390/ijms22010125 - 24 Dec 2020

Cited by 10 | Viewed by 6340

Abstract

Type 1 diabetes (T1D) is an auto-immune disorder characterized by a complex interaction between the host immune system and various environmental factors in genetically susceptible individuals. Genome-wide association studies (GWAS) identified different T1D risk and protection alleles, however, little is known about the environmental factors that can be linked to these alleles. Recent evidence indicated that, among those environmental factors, dysbiosis (imbalance) in the gut microbiota may play a role in the pathogenesis of T1D, affecting the integrity of the gut and leading to systemic inflammation and auto-destruction of the pancreatic β cells. Several studies have identified changes in the gut microbiome composition in humans and animal models comparing T1D subjects with controls. Those changes were characterized by a higher abundance of Bacteroides and a lower abundance of the butyrate-producing bacteria such as Clostridium clusters IV and XIVa. The mechanisms by which the dysbiotic bacteria and/or their metabolites interact with the genome and/or the epigenome of the host leading to destructive autoimmunity is still not clear. As T1D is a multifactorial disease, understanding the interaction between different environmental factors such as the gut microbiome, the genetic and the epigenetic determinants that are linked with the early appearance of autoantibodies can expand our knowledge about the disease pathogenesis. This review aims to provide insights into the interaction between the gut microbiome, susceptibility genes, epigenetic factors, and the immune system in the pathogenesis of T1D. Full article

(This article belongs to the Special Issue Epigenetics of Diabetes and Related Complications 2.0)

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