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Special Issue "Obesity, Genes, and Obesity-Related Disorders"

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: 31 December 2021.

Special Issue Editor

Prof. Dr. Grażyna Nowicka
E-Mail Website
Guest Editor
Chair in Biochemistry and Clinical Chemistry and Head of Department of Biochemistry and Pharmacogenomics, Faculty of Pharmacy, Medical University of Warsaw, Warsaw, Poland
Interests: biochemistry and molecular medicine; molecular and cellular mechanisms of disease pathogenesis; biomarkers in disease diagnosis; assessment of therapy effectiveness; pharmacogenomics and nutrigenomics; diet related disorders; atherosclerosis; obesity; obesity associated metabolic disorders; cancers

Special Issue Information

Dear Colleagues,

Obesity is one of the biggest health issues in today’s society. It is well accepted that increased adiposity is associated with metabolic disturbances, the development of low grade inflammatory processes, hypertension, diabetes, an enhanced risk of coronary heart disease, and certain cancers. In addition to the obvious environmental influences, there is considerable evidence to support the roles of genetic factors and epigenetic mechanisms in different pathways involved in obesity development. Excessive accumulation of adipose tissue drives disturbances in adipocyte metabolism and cross-talk between adipocytes and other cells, resulting in the development of obesity-associted diseases. In addition, eating behavior, a major factor in the development of obesity, involves a complex interplay of physiological, psychological, social and genetic factors.  

For this Special Issue, we seek papers focused on mechanisms associated with the development of obesity and obesity-related diseases, including cell-to cell metabolic cross-talk as well as cross-talk among the brain, gastrointestinal tract, microbiome, and adipose tissue and the molecular mechanisms underlying these processes. New insights into molecular mechanisms related to changes in eating behaviors leading to obesity are also of importance. There is no doubt that further knowledge is required for the future development of clinically relevant guidelines and strategies to enhance obesity prevention and treatment.

Prof. Dr. Grażyna Nowicka
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 papers will be 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

  • adipose tissue
  • genetic variants
  • gene expression
  • DNA damage
  • epigenetics
  • appetite control
  • food craving
  • metabolic disorders
  • cancer

Published Papers (2 papers)

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Research

Article
Chronic and Transient Hyperglycemia Induces Changes in the Expression Patterns of IL6 and ADIPOQ Genes and Their Associated Epigenetic Modifications in Differentiating Human Visceral Adipocytes
Int. J. Mol. Sci. 2021, 22(13), 6964; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136964 - 28 Jun 2021
Cited by 2 | Viewed by 628
Abstract
Adipokines secreted by hypertrophic visceral adipose tissue (VAT) instigate low-grade inflammation, followed by hyperglycemia (HG)-related metabolic disorders. The latter may develop with the participation of epigenetic modifications. Our aim was to assess how HG influences selected epigenetic modifications and the expression of interleukin [...] Read more.
Adipokines secreted by hypertrophic visceral adipose tissue (VAT) instigate low-grade inflammation, followed by hyperglycemia (HG)-related metabolic disorders. The latter may develop with the participation of epigenetic modifications. Our aim was to assess how HG influences selected epigenetic modifications and the expression of interleukin 6 (IL-6) and adiponectin (APN; gene symbol ADIPOQ) during the adipogenesis of human visceral preadipocytes (HPA-v). Adipocytes (Ads) were chronically or transiently HG-treated during three stages of adipogenesis (proliferation, differentiation, maturation). We measured adipokine mRNA, protein, proven or predicted microRNA expression (RT-qPCR and ELISA), and enrichment of H3K9/14ac, H3K4me3, and H3K9me3 at gene promoter regions (chromatin immunoprecipitation). In chronic HG, we detected different expression patterns of the studied adipokines at the mRNA and protein levels. Chronic and transient HG-induced changes in miRNA (miR-26a-5p, miR-26b-5p, let-7d-5p, let-7e-5p, miR-365a-3p, miR-146a-5p) were mostly convergent to altered IL-6 transcription. Alterations in histone marks at the IL6 promoter were also in agreement with IL-6 mRNA. The open chromatin marks at the ADIPOQ promoter mostly reflected the APN transcription during NG adipogenesis, while, in the differentiation stage, HG-induced changes in all studied marks were in line with APN mRNA levels. In summary, HG dysregulated adipokine expression, promoting inflammation. Epigenetic changes coexisted with altered expression of adipokines, especially for IL-6; therefore, epigenetic marks induced by transient HG may act as epi-memory in Ads. Such changes in the epigenome and expression of adipokines could be instrumental in the development of inflammation and metabolic deregulation of VAT. Full article
(This article belongs to the Special Issue Obesity, Genes, and Obesity-Related Disorders)
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Article
Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice
Int. J. Mol. Sci. 2021, 22(10), 5390; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105390 - 20 May 2021
Viewed by 538
Abstract
Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in [...] Read more.
Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity. Full article
(This article belongs to the Special Issue Obesity, Genes, and Obesity-Related Disorders)
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