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Advances in Genetics of Regeneration in Metabesity
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Advances in Genetics of Regeneration in Metabesity

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 July 2018) | Viewed by 30688

Special Issue Editors

Dr. Benoit Gauthier

E-Mail Website
Guest Editor
Andalusian Center for Molecular Biology and Regenerative Medicine CABIMER, 41001 Sevilla, Spain
Interests: islet physiology; genetics of diabetes; cell regeneration; drug development
Special Issues, Collections and Topics in MDPI journals
Dr. Francisco-Javier Bermúdez-Silva

E-Mail Website
Guest Editor
Instituto de Investigación Biomédica de Málaga (IBIMA), 29001 Málaga, Spain
Interests: diabetes; islets; inflammation; cannabinoids; EVOO

Special Issue Information

Dear Colleagues,

‘Metabesity’ was recently coined to define the armada of metabolic diseases that include diabetes, obesity, metabolic syndrome, cardiovascular disease, neurodegenerative disorders and accelerated aging. These diseases share both metabolic and inflammatory roots. A major hallmark of metabesity is the continuous destruction of specialized cells (neurons, cardiomyocytes, beta cells, hepatocytes, etc.) leaving affected individuals weakened. An active research area looking for new therapeutic options to cure metabesity or at least improve life quality of patients is focused on harnessing the regenerative capacity, as well as enhanced survival of cells and tissues. Understanding the underlying molecular mechanisms and, specifically, how genes govern such processes will advance us closer to the therapeutic goal of rebuilding ones own damaged tissue.

In this Special Issue, we welcome original research or review articles on any topic related to “Advances in Genetics of Regeneration in Metabesity”. We look forward to your contributions.

Dr. Benoit Gauthier
Dr. Francisco-Javier Bermúdez-Silva
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. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • Regeneration
  • Metabolic diseases
  • Genetic networks
  • Genes
  • Transgenic
  • Animal model
  • Inflammation
  • Regenerative Medicine
  • Cell therapy

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Published Papers (6 papers)

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Editorial

Jump to: Research, Review, Other

3 pages, 200 KiB  
Editorial
Advances in Genetics of Regeneration in Metabesity
by Benoit R. Gauthier and Francisco J. Bermúdez-Silva
Genes 2019, 10(5), 383; https://doi.org/10.3390/genes10050383 - 20 May 2019
Cited by 2 | Viewed by 2777
Abstract
‘Metabesity’ is a recent term comprising a wide range of diseases with underlying metabolic disarrangements at its root, and whose aetiology lies in complex relationships among genes and the obesogenic environment to which individuals are currently exposed in most countries. Of note, epigenetic [...] Read more.
‘Metabesity’ is a recent term comprising a wide range of diseases with underlying metabolic disarrangements at its root, and whose aetiology lies in complex relationships among genes and the obesogenic environment to which individuals are currently exposed in most countries. Of note, epigenetic changes are increasingly being reported to play an outstanding role in carrying deleterious information that, together with susceptibility genes, boost the development of metabesity in subsequent generations. In this context, it is noteworthy to mention that the transition from the pre-industrial era to the current high-technology society and global economy, even after suffering two world wars, has been very fast. By contrast, evolution-driven processes, such as biological ones, are slow. In fact, there is a general consensus that at the metabolic level, adipogenic processes and thrifty pathways prevail over those promoting energy expenditure in a way that currently leads to metabolic diseases by excessive energy storage. In such an imbalanced social–biological scenario, genes that were beneficial in the past have shifted to becoming detrimental, i.e., favouring metabesity, which is quickly growing to reach pandemic proportions. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)

Research

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11 pages, 3079 KiB  
Article
Genetic Targeting of GRP78 in the VMH Improves Obesity Independently of Food Intake
by Laura Liñares-Pose, Eva Rial-Pensado, Ánxela Estévez-Salguero, Edward Milbank, Ismael González-García, Claudia Rodríguez, Patricia Seoane-Collazo, Noelia Martinez-Sánchez, Rubén Nogueiras, Dolores Prieto, Carlos Diéguez, Cristina Contreras and Miguel López
Genes 2018, 9(7), 357; https://doi.org/10.3390/genes9070357 - 17 Jul 2018
Cited by 15 | Viewed by 4979
Abstract
Recent data have demonstrated that the hypothalamic GRP78/BiP (glucose regulated protein 78 kDa/binding immunoglobulin protein) modulates brown adipose tissue (BAT) thermogenesis by acting downstream on AMP-activated protein kinase (AMPK). Herein, we aimed to investigate whether genetic over-expression of GRP78 in the ventromedial nucleus [...] Read more.
Recent data have demonstrated that the hypothalamic GRP78/BiP (glucose regulated protein 78 kDa/binding immunoglobulin protein) modulates brown adipose tissue (BAT) thermogenesis by acting downstream on AMP-activated protein kinase (AMPK). Herein, we aimed to investigate whether genetic over-expression of GRP78 in the ventromedial nucleus of the hypothalamus (VMH: a key site regulating thermogenesis) could ameliorate very high fat diet (vHFD)-induced obesity. Our data showed that stereotaxic treatment with adenoviruses harboring GRP78 in the VMH reduced hypothalamic endoplasmic reticulum ER stress and reversed vHFD-induced obesity. Herein, we also demonstrated that this body weight decrease was more likely associated with an increased BAT thermogenesis and browning of white adipose tissue (WAT) than to anorexia. Overall, these results indicate that the modulation of GRP78 in the VMH may be a target against obesity. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)
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Review

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20 pages, 1030 KiB  
Review
Dissecting the Brain/Islet Axis in Metabesity
by Esther Fuente-Martín, Jose M. Mellado-Gil, Nadia Cobo-Vuilleumier, Alejandro Martín-Montalvo, Silvana Y. Romero-Zerbo, Irene Diaz Contreras, Abdelkrim Hmadcha, Bernat Soria, Francisco Martin Bermudo, Jose C. Reyes, Francisco J. Bermúdez-Silva, Petra I. Lorenzo and Benoit R. Gauthier
Genes 2019, 10(5), 350; https://doi.org/10.3390/genes10050350 - 8 May 2019
Cited by 12 | Viewed by 5317
Abstract
The high prevalence of type 2 diabetes mellitus (T2DM), together with the fact that current treatments are only palliative and do not avoid major secondary complications, reveals the need for novel approaches to treat the cause of this disease. Efforts are currently underway [...] Read more.
The high prevalence of type 2 diabetes mellitus (T2DM), together with the fact that current treatments are only palliative and do not avoid major secondary complications, reveals the need for novel approaches to treat the cause of this disease. Efforts are currently underway to identify therapeutic targets implicated in either the regeneration or re-differentiation of a functional pancreatic islet β-cell mass to restore insulin levels and normoglycemia. However, T2DM is not only caused by failures in β-cells but also by dysfunctions in the central nervous system (CNS), especially in the hypothalamus and brainstem. Herein, we review the physiological contribution of hypothalamic neuronal and glial populations, particularly astrocytes, in the control of the systemic response that regulates blood glucose levels. The glucosensing capacity of hypothalamic astrocytes, together with their regulation by metabolic hormones, highlights the relevance of these cells in the control of glucose homeostasis. Moreover, the critical role of astrocytes in the response to inflammation, a process associated with obesity and T2DM, further emphasizes the importance of these cells as novel targets to stimulate the CNS in response to metabesity (over-nutrition-derived metabolic dysfunctions). We suggest that novel T2DM therapies should aim at stimulating the CNS astrocytic response, as well as recovering the functional pancreatic β-cell mass. Whether or not a common factor expressed in both cell types can be feasibly targeted is also discussed. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)
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10 pages, 474 KiB  
Review
Epigenetic Control of Pancreatic Regeneration in Diabetes
by Shruti Balaji, Tiziana Napolitano, Serena Silvano, Marika Elsa Friano, Anna Garrido-Utrilla, Josipa Atlija and Patrick Collombat
Genes 2018, 9(9), 448; https://doi.org/10.3390/genes9090448 - 7 Sep 2018
Cited by 6 | Viewed by 4939
Abstract
Both type 1 and type 2 diabetes are conditions that are associated with the loss of insulin-producing β-cells within the pancreas. An active research therefore aims at regenerating these β-cells with the hope that they could restore euglycemia. The approaches classically used consist [...] Read more.
Both type 1 and type 2 diabetes are conditions that are associated with the loss of insulin-producing β-cells within the pancreas. An active research therefore aims at regenerating these β-cells with the hope that they could restore euglycemia. The approaches classically used consist in mimicking embryonic development, making use of diverse cell sources or converting pre-existing pancreatic cells. Despite impressive progresses and promising successes, it appears that we still need to gain further insight into the molecular mechanisms underlying β-cell development. This becomes even more obvious with the emergence of a relatively new field of research, epigenetics. The current review therefore focuses on the latest advances in this field in the context of β-cell (neo-)genesis research. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)
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9 pages, 510 KiB  
Review
Hyperphagia and Obesity in Prader–Willi Syndrome: PCSK1 Deficiency and Beyond?
by Bruno Ramos-Molina, María Molina-Vega, José C. Fernández-García and John W. Creemers
Genes 2018, 9(6), 288; https://doi.org/10.3390/genes9060288 - 7 Jun 2018
Cited by 9 | Viewed by 6329
Abstract
Prader–Willi syndrome (PWS) is a complex genetic disorder that, besides cognitive impairments, is characterized by hyperphagia, obesity, hypogonadism, and growth impairment. Proprotein convertase subtilisin/kexin type 1 (PCSK1) deficiency, a rare recessive congenital disorder, partially overlaps phenotypically with PWS, but both genetic [...] Read more.
Prader–Willi syndrome (PWS) is a complex genetic disorder that, besides cognitive impairments, is characterized by hyperphagia, obesity, hypogonadism, and growth impairment. Proprotein convertase subtilisin/kexin type 1 (PCSK1) deficiency, a rare recessive congenital disorder, partially overlaps phenotypically with PWS, but both genetic disorders show clear dissimilarities as well. The recent observation that PCSK1 is downregulated in a model of human PWS suggests that overlapping pathways are affected. In this review we will not only discuss the mechanisms by which PWS and PCSK1 deficiency could lead to hyperphagia but also the therapeutic interventions to treat obesity in both genetic disorders. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)
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Other

9 pages, 358 KiB  
Brief Report
Complement Factor C3 Methylation and mRNA Expression Is Associated to BMI and Insulin Resistance in Obesity
by Daniel Castellano-Castillo, Isabel Moreno-Indias, Jose Carlos Fernandez-Garcia, Mercedes Clemente-Postigo, Manuel Castro-Cabezas, Francisco José Tinahones, María Isabel Queipo-Ortuño and Fernando Cardona
Genes 2018, 9(8), 410; https://doi.org/10.3390/genes9080410 - 13 Aug 2018
Cited by 14 | Viewed by 4727
Abstract
Epigenetic marks, and especially DNA methylation, are becoming an important factor in obesity, which could help to explain its etiology and associated comorbidities. Adipose tissue, now considered as an important endocrine organ, produces complement system factors. Complement component 3 (C3) turns [...] Read more.
Epigenetic marks, and especially DNA methylation, are becoming an important factor in obesity, which could help to explain its etiology and associated comorbidities. Adipose tissue, now considered as an important endocrine organ, produces complement system factors. Complement component 3 (C3) turns out to be an important protein in metabolic disorders, via either inflammation or the C3 subproduct acylation stimulating protein (ASP) which directly stimulates lipid storage. In this study, we analyze C3 DNA methylation in adipose tissue from subjects with a different grade of obesity. Adipose tissue samples were collected from subjects with a different degree of obesity determined by their body mass index (BMI) as: Overweight subjects (BMI ≥ 25 and <30), obese class 1/2 subjects (BMI ≥ 30 and <40) and obese class 3 subjects (BMI ≥ 40). C3 DNA methylation was measured for 7 CpGs by pyrosequencition using the Pyromark technology (Qiagen, Madrid Spain). C3 messenger RNA (mRNA) levels were analyzed by pre-designed Taqman assays (Applied biosystems, Foster City, CA, USA) and ASP/C3a was measured using a ELISA kit. The data were analyzed using the statistic package SPSS. C3 DNA methylation levels were lower in the morbid obese group. Accordingly, C3 methylation correlated negatively with BMI and leptin. However, C3 mRNA levels were more associated with insulin resistance, and positive correlations with insulin, glucose and homeostasis model assessment-estimated insulin resistance (HOMA-IR) existed. ASP correlated negatively with high density lipoprotein (HDL) cholesterol. C3 methylation levels were associated to adiposity variables, such as BMI and leptin, while the C3 mRNA levels were associated to glucose metabolism. Full article
(This article belongs to the Special Issue Advances in Genetics of Regeneration in Metabesity)
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