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Gene-Diet Interactions in Obesity
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Gene-Diet Interactions in Obesity

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

Deadline for manuscript submissions: closed (31 March 2019) | Viewed by 13626

Special Issue Editors

Dr. Gerard Aragonès

E-Mail Website1 Website2
Guest Editor
Nutrigenomics Research Group, Department of Biochemistry and Biotechnology, Universitat Rovira i Virgili, 43007 Tarragona, Spain
Interests: adipose expandability; bioactive compounds; biological rhythms; chrononutrition; energy metabolism; epigenetics; functional foods; gut microbiota; hypothalamic dysfunction; leptin; nutrigenomics; obesity; polyphenols; xenohormesis
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Ibars

E-Mail Website
Guest Editor
1. Nutrigenomics Research Group, Department of Biochemistry and Biotechnology, Universitat Rovira i Virgili, Tarragona, Spain
2. Visiting Scholar, Department of Animal Sciences, Human and Animal Physiology, Wageningen University, Wageningen, The Netherlands
Interests: bioactive compounds; brain regulation of energy metabolism; mitochondria; leptin; signalling pathways; obesity; metabolic syndrome

Special Issue Information

Dear Colleagues,

Since antiquity, we have the knowledge that diet is key for health. In the late 20th century the study of the interactions between genes and nutrients, known as Nutrigenomics, started to show enormous potential against disease. To date, this strategy has been successfully used to prevent the development of particular monogenic diseases such as phenylketonuria, celiac disease and familial hypercholesterolemia. Nevertheless, there is a lack of solid evidence regarding multifactorial diseases such as cancer, obesity, cardiovascular disease and diabetes. Furthermore, not only nutrients play a role in health. Dietary components with bioactive properties such as phytochemicals showed beneficial effects in several disease models.

Thus far, it remains a challenge to elucidate the role of diet regarding its composition in macronutrients, micronutrients and non-nutrients in order to optimize its use to benefit human health.

This Special Issue welcomes manuscripts from human and animal studies focused on evaluating the influence of diet and individual dietary components on gene regulation in both physiological and non-physiological conditions (such us obesity, diabetes, hypertension or cancer), as well as in vitro studies aimed to elucidate the potential molecular mechanisms of diet and gene interactions.

Dr. Gerard Aragonès

Dr. Maria Ibars

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

  • nutrients
  • bioactive compounds
  • transcriptomics
  • cardiovascular disease
  • obesity
  • cancer
  • inflammation
  • diabetes
  • neuroendocrinology

Published Papers (4 papers)

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Research

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14 pages, 2285 KiB  
Article
Proanthocyanidins Limit Adipose Accrual Induced by a Cafeteria Diet, Several Weeks after the End of the Treatment
by Iris Ginés, Katherine Gil-Cardoso, Joan Serrano, Àngela Casanova-Marti, Maria Lobato, Ximena Terra, M Teresa Blay, Anna Ardévol and Montserrat Pinent
Genes 2019, 10(8), 598; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10080598 - 08 Aug 2019
Cited by 6 | Viewed by 2626
Abstract
A dose of proanthocyanidins with satiating properties proved to be able to limit body weight increase several weeks after administration under exposure to a cafeteria diet. Here we describe some of the molecular targets and the duration of the effects. We treated rats [...] Read more.
A dose of proanthocyanidins with satiating properties proved to be able to limit body weight increase several weeks after administration under exposure to a cafeteria diet. Here we describe some of the molecular targets and the duration of the effects. We treated rats with 500 mg grape seed proanthocyanidin extract (GSPE)/kg BW for ten days. Seven or seventeen weeks after the last GSPE dose, while animals were on a cafeteria diet, we used reverse transcriptase-polymerase chain reaction (RT-PCR) to measure the mRNA of the key energy metabolism enzymes from the liver, adipose depots and muscle. We found that a reduction in the expression of adipose Lpl might explain the lower amount of adipose tissue in rats seven weeks after the last GSPE dose. The liver showed increased expression of Cpt1a and Hmgs2 together with a reduction in Fasn and Dgat2. In addition, muscle showed a higher fatty oxidation (Oxct1 and Cpt1b mRNA). However, after seventeen weeks, there was a completely different gene expression pattern. At the conclusion of the study, seven weeks after the last GSPE administration there was a limitation in adipose accrual that might be mediated by an inhibition of the gene expression of the adipose tissue Lpl. Concomitantly there was an increase in fatty acid oxidation in liver and muscle. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Obesity)
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13 pages, 1898 KiB  
Article
White Adipose Tissue Response of Obese Mice to Ambient Oxygen Restriction at Thermoneutrality: Response Markers Identified, but no WAT Inflammation
by Femke P. M. Hoevenaars, Jaap Keijer, Inge van der Stelt, Loes P. M. Duivenvoorde, Laure Herreman, Robin van Nes, David Friedecký, Maria A. Hegeman and Evert M. van Schothorst
Genes 2019, 10(5), 359; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10050359 - 10 May 2019
Cited by 2 | Viewed by 3826
Abstract
Obesity is associated with white adipose tissue (WAT) hypoxia and inflammation. We aimed to test whether mild environmental oxygen restriction (OxR, 13% O2), imposing tissue hypoxia, triggers WAT inflammation in obese mice. Thirteen weeks diet-induced obese male adult C57BL/6JOlaHsd mice housed [...] Read more.
Obesity is associated with white adipose tissue (WAT) hypoxia and inflammation. We aimed to test whether mild environmental oxygen restriction (OxR, 13% O2), imposing tissue hypoxia, triggers WAT inflammation in obese mice. Thirteen weeks diet-induced obese male adult C57BL/6JOlaHsd mice housed at thermoneutrality were exposed for five days to OxR versus normoxia. WAT and blood were isolated and used for analysis of metabolites and adipokines, WAT histology and macrophage staining, and WAT transcriptomics. OxR increased circulating levels of haemoglobin and haematocrit as well as hypoxia responsive transcripts in WAT and decreased blood glucose, indicating systemic and tissue hypoxia. WAT aconitase activity was inhibited. Macrophage infiltration as marker for WAT inflammation tended to be decreased, which was supported by down regulation of inflammatory genes S100a8, Ccl8, Clec9a, Saa3, Mgst2, and Saa1. Other down regulated processes include cytoskeleton remodelling and metabolism, while response to hypoxia appeared most prominently up regulated. The adipokines coiled-coil domain containing 3 (CCDC3) and adiponectin, as well as the putative WAT hormone cholecystokinin (CCK), were reduced by OxR on transcript (Cck, Ccdc3) and/or serum protein level (adiponectin, CCDC3). Conclusively, our data demonstrate that also in obese mice OxR does not trigger WAT inflammation. However, OxR does evoke a metabolic response in WAT, with CCDC3 and adiponectin as potential markers for systemic or WAT hypoxia. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Obesity)
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17 pages, 2294 KiB  
Article
iNOS Gene Ablation Prevents Liver Fibrosis in Leptin-Deficient ob/ob Mice
by Sara Becerril, Amaia Rodríguez, Victoria Catalán, Beatriz Ramírez, Xabier Unamuno, Javier Gómez-Ambrosi and Gema Frühbeck
Genes 2019, 10(3), 184; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10030184 - 27 Feb 2019
Cited by 12 | Viewed by 3138
Abstract
The role of extracellular matrix (ECM) remodeling in fibrosis progression in nonalcoholic fatty liver disease (NAFLD) is complex and dynamic, involving the synthesis and degradation of different ECM components, including tenascin C (TNC). The aim was to analyze the influence of inducible nitric [...] Read more.
The role of extracellular matrix (ECM) remodeling in fibrosis progression in nonalcoholic fatty liver disease (NAFLD) is complex and dynamic, involving the synthesis and degradation of different ECM components, including tenascin C (TNC). The aim was to analyze the influence of inducible nitric oxide synthase (iNOS) deletion on inflammation and ECM remodeling in the liver of ob/ob mice, since a functional relationship between leptin and iNOS has been described. The expression of molecules involved in inflammation and ECM remodeling was analyzed in the liver of double knockout (DBKO) mice simultaneously lacking the ob and the iNOS genes. Moreover, the effect of leptin was studied in the livers of ob/ob mice and compared to wild-type rodents. Liver inflammation and fibrosis were increased in leptin-deficient mice. As expected, leptin treatment reverted the obesity phenotype. iNOS deletion in ob/ob mice improved insulin sensitivity, inflammation, and fibrogenesis, as evidenced by lower macrophage infiltration and collagen deposition as well as downregulation of the proinflammatory and profibrogenic genes including Tnc. Circulating TNC levels were also decreased. Furthermore, leptin upregulated TNC expression and release via NO-dependent mechanisms in AML12 hepatic cells. iNOS deficiency in ob/ob mice improved liver inflammation and ECM remodeling-related genes, decreasing fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in hepatocytes, suggesting an important role of this alarmin in the development of NAFLD. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Obesity)
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Review

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8 pages, 236 KiB  
Review
The Influence of Diet and Obesity on Gene Expression in SLE
by Antonio La Cava
Genes 2019, 10(5), 405; https://0-doi-org.brum.beds.ac.uk/10.3390/genes10050405 - 27 May 2019
Cited by 15 | Viewed by 3608
Abstract
This review provides an overview of the known effects of diet, obesity, and the intake of different nutrients on systemic lupus erythematosus (SLE). It summarizes and discusses the studies in rodents that identified how different diets can regulate gene expression in the disease, [...] Read more.
This review provides an overview of the known effects of diet, obesity, and the intake of different nutrients on systemic lupus erythematosus (SLE). It summarizes and discusses the studies in rodents that identified how different diets can regulate gene expression in the disease, together with a description of the effects of diet on lupus patients’ inflammatory state and disease severity. The identification of selected dietary candidates that can modulate SLE onset and progression is analyzed in relation to possible targeted approaches that could ultimately ameliorate the management and prognosis of this disease. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Obesity)
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