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Molecular Metabolic Regulation in Diabetes 2.0
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Molecular Metabolic Regulation in Diabetes 2.0

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

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 31198

Special Issue Editors

Prof. Dr. Adam Krętowski

E-Mail Website
Guest Editor
Department of Endocrinology, Diabetology and Internal Medicine, Clinical Research Centre, and Clinical Research Support Centre of Medical University of Białystok, Białystok, Poland
Interests: diabetes; obesity; insulin resistance; endocrinology; genetics, diet
Special Issues, Collections and Topics in MDPI journals
Dr. Lukasz Szczerbinski

E-Mail Website
Guest Editor
Department of Endocrinology, Diabetology and Internal Medicine,Medical University of Białystok, Białystok, Poland
Interests: diabetes; insulin resistance; NAFLD; obesity; exercise; genetics; bariatric surgery

Special Issue Information

Dear Colleagues,

Diabetes is a complex disease characterized by elevation in plasma glucose which is caused by impaired insulin secretion, insulin resistance or a combination of both. The disease is highly heterogeneous and currently divided among types and subtypes. These include the most prevalent type of diabetes mellitus, type 2 diabetes (T2D), which accounts for over 90% of all diabetes cases, type 1 diabetes (T1D), gestational diabetes mellitus (GDM), and other more specific types like latent autoimmune diabetes in adults (LADA), maturity onset diabetes of the young (MODY), and neonatal diabetes. Diabetes is already a global epidemic whose extraordinary global burden, as estimated by the International Diabetes Federation (IDF) in 2017, was 425 million adults aged 20–79 years with diabetes, representing 8.8% of the global population. Diabetes emerges from a combination of both environmental and genetic factors which can interact to influence disease outcomes. Type 1 diabetes and LADA are pathophysiologically linked to the autoimmune process of insulin-producing β-cells. Type 2 diabetes, on the other hand, is caused by a combination of abnormalities in β-cell function and insulin sensitivity. In the literature, these cardinal abnormalities comprise the “ominous octet”, representing the most significant eight pathophysiological disturbances leading to β-cell dysfunction or insulin resistance. However, their underlying molecular basis and their complications are still not fully understood. Thus, there is a pressing need to elucidate these mechanisms whose identification may lead to the discovery of new therapies and to the reduction of complications and mortality related to diabetes.

This Special Issue will focus on reviews and original data manuscripts that concern (1) molecular mechanisms of diabetes development including insulin resistance and β-cell dysfunction; (2) studies on molecular mechanisms related to carbohydrate and lipid metabolism; (3) pathophysiology of diabetes complications; (4) genetics of diabetes; and (5) molecular targets for new therapeutics for diabetes.

Prof. Adam Krętowski
Dr. Lukasz Szczerbinski
Guest Editors

Manuscript Submission Information

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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.

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Keywords

  • Diabetes
  • Obesity
  • Autoimmunity
  • Insulin resistance
  • β-cell function
  • NAFLD
  • Genetics
  • Metabolomics
  • Proteomics
  • Inflammation
  • Metabolic syndrome
  • Gene expression
  • Lipid metabolism
  • Lipidomics
  • Carbohydrates metabolism
  • Gut hormones

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Published Papers (6 papers)

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Research

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16 pages, 2696 KiB  
Article
Long-Chain Acylcarnitines Decrease the Phosphorylation of the Insulin Receptor at Tyr1151 Through a PTP1B-Dependent Mechanism
by Karlis Vilks, Melita Videja, Marina Makrecka-Kuka, Martins Katkevics, Eduards Sevostjanovs, Aiga Grandane, Maija Dambrova and Edgars Liepinsh
Int. J. Mol. Sci. 2021, 22(12), 6470; https://doi.org/10.3390/ijms22126470 - 16 Jun 2021
Cited by 8 | Viewed by 2807
Abstract
The accumulation of lipid intermediates may interfere with energy metabolism pathways and regulate cellular energy supplies. As increased levels of long-chain acylcarnitines have been linked to insulin resistance, we investigated the effects of long-chain acylcarnitines on key components of the insulin signalling pathway. [...] Read more.
The accumulation of lipid intermediates may interfere with energy metabolism pathways and regulate cellular energy supplies. As increased levels of long-chain acylcarnitines have been linked to insulin resistance, we investigated the effects of long-chain acylcarnitines on key components of the insulin signalling pathway. We discovered that palmitoylcarnitine induces dephosphorylation of the insulin receptor (InsR) through increased activity of protein tyrosine phosphatase 1B (PTP1B). Palmitoylcarnitine suppresses protein kinase B (Akt) phosphorylation at Ser473, and this effect is not alleviated by the inhibition of PTP1B by the insulin sensitizer bis-(maltolato)-oxovanadium (IV). This result indicates that palmitoylcarnitine affects Akt activity independently of the InsR phosphorylation level. Inhibition of protein kinase C and protein phosphatase 2A does not affect the palmitoylcarnitine-mediated inhibition of Akt Ser473 phosphorylation. Additionally, palmitoylcarnitine markedly stimulates insulin release by suppressing Akt Ser473 phosphorylation in insulin-secreting RIN5F cells. In conclusion, long-chain acylcarnitines activate PTP1B and decrease InsR Tyr1151 phosphorylation and Akt Ser473 phosphorylation, thus limiting the cellular response to insulin stimulation. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
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16 pages, 3510 KiB  
Article
Role of TSPO/VDAC1 Upregulation and Matrix Metalloproteinase-2 Localization in the Dysfunctional Myocardium of Hyperglycaemic Rats
by Micaela Gliozzi, Federica Scarano, Vincenzo Musolino, Cristina Carresi, Miriam Scicchitano, Stefano Ruga, Maria Caterina Zito, Saverio Nucera, Francesca Bosco, Jessica Maiuolo, Roberta Macrì, Lorenza Guarnieri, Rocco Mollace, Anna Rita Coppoletta, Caterina Nicita, Annamaria Tavernese, Ernesto Palma, Carolina Muscoli and Vincenzo Mollace
Int. J. Mol. Sci. 2020, 21(20), 7432; https://doi.org/10.3390/ijms21207432 - 9 Oct 2020
Cited by 14 | Viewed by 2861
Abstract
Clinical management of diabetic cardiomyopathy represents an unmet need owing to insufficient knowledge about the molecular mechanisms underlying the dysfunctional heart. The aim of this work is to better clarify the role of matrix metalloproteinase 2 (MMP-2) isoforms and of translocator protein (TSPO)/voltage-dependent [...] Read more.
Clinical management of diabetic cardiomyopathy represents an unmet need owing to insufficient knowledge about the molecular mechanisms underlying the dysfunctional heart. The aim of this work is to better clarify the role of matrix metalloproteinase 2 (MMP-2) isoforms and of translocator protein (TSPO)/voltage-dependent anion-selective channel 1 (VDAC1) modulation in the development of hyperglycaemia-induced myocardial injury. Hyperglycaemia was induced in Sprague-Dawley rats through a streptozocin injection (35 mg/Kg, i.p.). After 60 days, cardiac function was analysed by echocardiography. Nicotinamide Adenine Dinucleotide Phosphate NADPH oxidase and TSPO expression was assessed by immunohistochemistry. MMP-2 activity was detected by zymography. Superoxide anion production was estimated by MitoSOX™ staining. Voltage-dependent anion-selective channel 1 (VDAC-1), B-cell lymphoma 2 (Bcl-2), and cytochrome C expression was assessed by Western blot. Hyperglycaemic rats displayed cardiac dysfunction; this response was characterized by an overexpression of NADPH oxidase, accompanied by an increase of superoxide anion production. Under hyperglycaemia, increased expression of TSPO and VDAC1 was detected. MMP-2 downregulated activity occurred under hyperglycemia and this profile of activation was accompanied by the translocation of intracellular N-terminal truncated isoform of MMP-2 (NT-MMP-2) from mitochondria-associated membrane (MAM) into mitochondria. In the onset of diabetic cardiomyopathy, mitochondrial impairment in cardiomyocytes is characterized by the dysregulation of the different MMP-2 isoforms. This can imply the generation of a “frail” myocardial tissue unable to adapt itself to stress. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
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Review

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21 pages, 3958 KiB  
Review
Maturity Onset Diabetes of the Young—New Approaches for Disease Modelling
by Dawid Skoczek, Józef Dulak and Neli Kachamakova-Trojanowska
Int. J. Mol. Sci. 2021, 22(14), 7553; https://doi.org/10.3390/ijms22147553 - 14 Jul 2021
Cited by 20 | Viewed by 10912
Abstract
Maturity-onset diabetes of the young (MODY) is a genetically heterogeneous group of monogenic endocrine disorders that is characterised by autosomal dominant inheritance and pancreatic β-cell dysfunction. These patients are commonly misdiagnosed with type 1 or type 2 diabetes, as the clinical symptoms largely [...] Read more.
Maturity-onset diabetes of the young (MODY) is a genetically heterogeneous group of monogenic endocrine disorders that is characterised by autosomal dominant inheritance and pancreatic β-cell dysfunction. These patients are commonly misdiagnosed with type 1 or type 2 diabetes, as the clinical symptoms largely overlap. Even though several biomarkers have been tested none of which could be used as single clinical discriminator. The correct diagnosis for individuals with MODY is of utmost importance, as the applied treatment depends on the gene mutation or is subtype-specific. Moreover, in patients with HNF1A-MODY, additional clinical monitoring can be included due to the high incidence of vascular complications observed in these patients. Finally, stratification of MODY patients will enable better and newer treatment options for MODY patients, once the disease pathology for each patient group is better understood. In the current review the clinical characteristics and the known disease-related abnormalities of the most common MODY subtypes are discussed, together with the up-to-date applied diagnostic criteria and treatment options. Additionally, the usage of pluripotent stem cells together with CRISPR/Cas9 gene editing for disease modelling with the possibility to reveal new pathophysiological mechanisms in MODY is discussed. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
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22 pages, 433 KiB  
Review
The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
by Witold Bauer, Attila Gyenesei and Adam Krętowski
Int. J. Mol. Sci. 2021, 22(14), 7493; https://doi.org/10.3390/ijms22147493 - 13 Jul 2021
Cited by 15 | Viewed by 3798
Abstract
Type 1 Diabetes (T1D) results from autoimmune destruction of insulin producing pancreatic ß-cells. This disease, with a peak incidence in childhood, causes the lifelong need for insulin injections and necessitates careful monitoring of blood glucose levels. However, despite the current insulin therapies, it [...] Read more.
Type 1 Diabetes (T1D) results from autoimmune destruction of insulin producing pancreatic ß-cells. This disease, with a peak incidence in childhood, causes the lifelong need for insulin injections and necessitates careful monitoring of blood glucose levels. However, despite the current insulin therapies, it still shortens life expectancy due to complications affecting multiple organs. Recently, the incidence of T1D in childhood has increased by 3–5% per year in most developed Western countries. The heterogeneity of the disease process is supported by the findings of follow-up studies started early in infancy. The development of T1D is usually preceded by the appearance of autoantibodies targeted against antigens expressed in the pancreatic islets. The risk of T1D increases significantly with an increasing number of positive autoantibodies. The order of autoantibody appearance affects the disease risk. Genetic susceptibility, mainly defined by the human leukocyte antigen (HLA) class II gene region and environmental factors, is important in the development of islet autoimmunity and T1D. Environmental factors, mainly those linked to the changes in the gut microbiome as well as several pathogens, especially viruses, and diet are key modulators of T1D. The aim of this paper is to expand the understanding of the aetiology and pathogenesis of T1D in childhood by detailed description and comparison of factors affecting the progression from the islet autoimmunity to T1D in children. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
15 pages, 653 KiB  
Review
Calcium-Deficiency during Pregnancy Affects Insulin Resistance in Offspring
by Junji Takaya
Int. J. Mol. Sci. 2021, 22(13), 7008; https://doi.org/10.3390/ijms22137008 - 29 Jun 2021
Cited by 11 | Viewed by 6540
Abstract
Prenatal malnutrition is known to affect the phenotype of the offspring through changes in epigenetic regulation. Growing evidence suggests that epigenetics is one of the mechanisms by which nutrients and minerals affect metabolic traits. Although the perinatal period is the time of highest [...] Read more.
Prenatal malnutrition is known to affect the phenotype of the offspring through changes in epigenetic regulation. Growing evidence suggests that epigenetics is one of the mechanisms by which nutrients and minerals affect metabolic traits. Although the perinatal period is the time of highest phenotypic plasticity, which contributes largely to developmental programming, there is evidence of nutritional influence on epigenetic regulation during adulthood. Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Cortisol, the most important glucocorticoid, is considered to lead to insulin resistance and metabolic syndrome. 11β-hydroxysteroid dehydrogenase-1 is a key enzyme that catalyzes the intracellular conversion of cortisone to physiologically active cortisol. This brief review aims to identify the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in the offspring. Those findings demonstrate that maternal Ca deficiency during pregnancy may affect the epigenetic regulation of gene expression and thereby induce different metabolic phenotypes. We aim to address the need for Ca during pregnancy and propose the scaling-up of clinical and public health approaches that improved pregnancy outcomes. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
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18 pages, 2404 KiB  
Review
Biological Activity of c-Peptide in Microvascular Complications of Type 1 Diabetes—Time for Translational Studies or Back to the Basics?
by Aleksandra Ryk, Aleksandra Łosiewicz, Arkadiusz Michalak and Wojciech Fendler
Int. J. Mol. Sci. 2020, 21(24), 9723; https://doi.org/10.3390/ijms21249723 - 20 Dec 2020
Cited by 13 | Viewed by 3398
Abstract
People with type 1 diabetes have an increased risk of developing microvascular complications, which have a negative impact on the quality of life and reduce life expectancy. Numerous studies in animals with experimental diabetes show that c-peptide supplementation exerts beneficial effects on diabetes-induced [...] Read more.
People with type 1 diabetes have an increased risk of developing microvascular complications, which have a negative impact on the quality of life and reduce life expectancy. Numerous studies in animals with experimental diabetes show that c-peptide supplementation exerts beneficial effects on diabetes-induced damage in peripheral nerves and kidneys. There is substantial evidence that c-peptide counteracts the detrimental changes caused by hyperglycemia at the cellular level, such as decreased activation of endothelial nitric oxide synthase and sodium potassium ATPase, and increase in formation of pro-inflammatory molecules mediated by nuclear factor kappa-light-chain-enhancer of activated B cells: cytokines, chemokines, cell adhesion molecules, vascular endothelial growth factor, and transforming growth factor beta. However, despite positive results from cell and animal studies, no successful c-peptide replacement therapies have been developed so far. Therefore, it is important to improve our understanding of the impact of c-peptide on the pathophysiology of microvascular complications to develop novel c-peptide-based treatments. This article aims to review current knowledge on the impact of c-peptide on diabetic neuro- and nephropathy and to evaluate its potential therapeutic role. Full article
(This article belongs to the Special Issue Molecular Metabolic Regulation in Diabetes 2.0)
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