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Obesity, Genes, and Obesity-Related Disorders
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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: closed (31 December 2021) | Viewed by 18517

Special Issue Editor

Prof. Dr. Grażyna Nowicka

E-Mail Website
Guest Editor
Department of Biochemistry and Pharmacogenomics, Faculty of Pharmacy, Medical University of Warsaw, Banacha 1B, 02-097 Warsaw, Poland
Interests: non-communicable and diet-related diseases including obesity and obesity-related disorders: pathogenesis; genetic–environmental factor interactions; risk assessment; prevention and treatment; human nutrition; nutritional biochemistry and nutrigenomics
Special Issues, Collections and Topics in MDPI journals

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 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

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

Published Papers (5 papers)

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Research

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19 pages, 3893 KiB  
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
by Adam Wróblewski, Justyna Strycharz, Ewa Świderska, Aneta Balcerczyk, Janusz Szemraj, Józef Drzewoski and Agnieszka Śliwińska
Int. J. Mol. Sci. 2021, 22(13), 6964; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136964 - 28 Jun 2021
Cited by 10 | Viewed by 2721
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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15 pages, 2568 KiB  
Article
Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice
by Qianhui Zeng, Nannan Wang, Yaru Zhang, Yuxuan Yang, Shuangshuang Li, Rong Zheng, Jin Chai, Tong Qiao and Siwen Jiang
Int. J. Mol. Sci. 2021, 22(10), 5390; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105390 - 20 May 2021
Cited by 5 | Viewed by 2129
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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Review

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24 pages, 1558 KiB  
Review
Renal Cell Cancer and Obesity
by Anna Gluba-Brzózka, Jacek Rysz, Janusz Ławiński and Beata Franczyk
Int. J. Mol. Sci. 2022, 23(6), 3404; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063404 - 21 Mar 2022
Cited by 16 | Viewed by 4043
Abstract
Cancers are a frequent cause of morbidity and mortality. There are many risk factors for tumours, including advanced age, personal or family history of cancer, some types of viral infections, exposure to radiation and some chemicals, smoking and alcohol consumption, as well as [...] Read more.
Cancers are a frequent cause of morbidity and mortality. There are many risk factors for tumours, including advanced age, personal or family history of cancer, some types of viral infections, exposure to radiation and some chemicals, smoking and alcohol consumption, as well as obesity. Increasing evidence suggest the role of obesity in the initiation and progression of various cancers, including renal cell carcinoma. Since tumours require energy for their uncontrollable growth, it appears plausible that their initiation and development is associated with the dysregulation of cells metabolism. Thus, any state characterised by an intake of excessive energy and nutrients may favour the development of various cancers. There are many factors that promote the development of renal cell carcinoma, including hypoxia, inflammation, insulin resistance, excessive adipose tissue and adipokines and others. There are also many obesity-related alterations in genes expression, including DNA methylation, single nucleotide polymorphisms, histone modification and miRNAs that can promote renal carcinogenesis. This review focuses on the impact of obesity on the risk of renal cancers development, their aggressiveness and patients’ survival. Full article
(This article belongs to the Special Issue Obesity, Genes, and Obesity-Related Disorders)
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12 pages, 526 KiB  
Review
Crosstalk between Melanin Concentrating Hormone and Endocrine Factors: Implications for Obesity
by Eva Prida, Sara Fernández-González, Verónica Pena-León, Raquel Pérez-Lois, Johan Fernø, Luisa María Seoane, Mar Quiñones and Omar Al Massadi
Int. J. Mol. Sci. 2022, 23(5), 2436; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052436 - 23 Feb 2022
Cited by 7 | Viewed by 3870
Abstract
Melanin-concentrating hormone (MCH) is a 19aa cyclic peptide exclusively expressed in the lateral hypothalamic area, which is an area of the brain involved in a large number of physiological functions and vital processes such as nutrient sensing, food intake, sleep-wake arousal, memory formation, [...] Read more.
Melanin-concentrating hormone (MCH) is a 19aa cyclic peptide exclusively expressed in the lateral hypothalamic area, which is an area of the brain involved in a large number of physiological functions and vital processes such as nutrient sensing, food intake, sleep-wake arousal, memory formation, and reproduction. However, the role of the lateral hypothalamic area in metabolic regulation stands out as the most relevant function. MCH regulates energy balance and glucose homeostasis by controlling food intake and peripheral lipid metabolism, energy expenditure, locomotor activity and brown adipose tissue thermogenesis. However, the MCH control of energy balance is a complex mechanism that involves the interaction of several neuroendocrine systems. The aim of the present work is to describe the current knowledge of the crosstalk of MCH with different endocrine factors. We also provide our view about the possible use of melanin-concentrating hormone receptor antagonists for the treatment of metabolic complications. In light of the data provided here and based on its actions and function, we believe that the MCH system emerges as an important target for the treatment of obesity and its comorbidities. Full article
(This article belongs to the Special Issue Obesity, Genes, and Obesity-Related Disorders)
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27 pages, 1584 KiB  
Review
The Interplay between Insulin Resistance, Inflammation, Oxidative Stress, Base Excision Repair and Metabolic Syndrome in Nonalcoholic Fatty Liver Disease
by Sylwia Ziolkowska, Agata Binienda, Maciej Jabłkowski, Janusz Szemraj and Piotr Czarny
Int. J. Mol. Sci. 2021, 22(20), 11128; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011128 - 15 Oct 2021
Cited by 60 | Viewed by 4787
Abstract
One of the most common chronic liver disorders, affecting mainly people in Western countries, is nonalcoholic fatty liver disease (NAFLD). Unfortunately, its pathophysiological mechanism is not fully understood, and no dedicated treatment is available. Simple steatosis can lead to nonalcoholic steatohepatitis and even [...] Read more.
One of the most common chronic liver disorders, affecting mainly people in Western countries, is nonalcoholic fatty liver disease (NAFLD). Unfortunately, its pathophysiological mechanism is not fully understood, and no dedicated treatment is available. Simple steatosis can lead to nonalcoholic steatohepatitis and even to fibrosis, cancer, and cirrhosis of the liver. NAFLD very often occurs in parallel with type 2 diabetes mellitus and in obese people. Furthermore, it is much more likely to develop in patients with metabolic syndrome (MS), whose criteria include abdominal obesity, elevated blood triacylglycerol level, reduced high-density lipoprotein cholesterol level, increased blood pressure, and high fasting glucose. An important phenomenon in MS is also insulin resistance (IR), which is very common in NAFLD. Liver IR and NAFLD development are linked through an interaction between the accumulation of free fatty acids, hepatic inflammation, and increased oxidative stress. The liver is particularly exposed to elevated levels of reactive oxygen species due to a large number of mitochondria in hepatocytes. In these organelles, the main DNA repair pathway is base excision repair (BER). The present article will illustrate how impairment of BER may be related to the development of NAFLD. Full article
(This article belongs to the Special Issue Obesity, Genes, and Obesity-Related Disorders)
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