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Nutrients
Special Issues
Nutrition, Genes and Signaling Pathways
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Nutrition, Genes and Signaling Pathways

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (1 August 2019) | Viewed by 11942

Special Issue Editor

Prof. Dr. Edwin Mariman

E-Mail Website
Guest Editor
Department of Human Biology, NUTRIM – School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands
Interests: Nutrition; Obesity; Weight regain after weight loss; Energy intake regulation; Adipose tissue; Genomics and proteomics; Cellular metabolism; Genetic predisposition

Special Issue Information

Dear Colleagues,

Besides being a source of energy and of structural components of cells and tissues, nutrition contains active substances that regulate the expression of the genes involved in a diverse set of signaling pathways related to the intake and processing of nutrients. This ranges from nutrient sensing and the central regulation of food intake to balancing the proper handling of nutrients in the body through digestion or storage. New information regularly becomes available showing which genes and nutrient–gene interactions play crucial roles and how genetic variation can influence signaling processes. Such knowledge might eventually be used for clinical applications by modifying nutrition to activate specific signaling pathways to promote and preserve health. This Special Issue of Nutrients, entitled “Nutrition, Genes and Signaling Pathways” welcomes manuscripts both in the form of original research and reviews, providing novel information on signaling as a joint effort of nutrition and genes. The focus is on food sensing and food intake regulation, but manuscripts on other related topics are also welcome.

Prof. Dr. Edwin Mariman
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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • Food intake regulation
  • Food sensing
  • Nutrient–gene interaction
  • Signaling pathways
  • Genetic variation
  • Personalized diet
  • Weight regulation

Published Papers (3 papers)

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Research

17 pages, 3482 KiB  
Article
Hyperglycemia Changes Expression of Key Adipogenesis Markers (C/EBPα and PPARᵞ)and Morphology of Differentiating Human Visceral Adipocytes
by Ewa Świderska, Marta Podolska, Justyna Strycharz, Marzena Szwed, Halina Abramczyk, Beata Brożek-Płuska, Adam Wróblewski, Janusz Szemraj, Ireneusz Majsterek, Józef Drzewoski and Agnieszka Śliwińska
Nutrients 2019, 11(8), 1835; https://doi.org/10.3390/nu11081835 - 8 Aug 2019
Cited by 12 | Viewed by 3983
Abstract
Disturbances in adipose tissue significantly contribute to the development of metabolic disorders, which are connected with hyperglycemia (HG) and underlain by epigenetics-based mechanisms. Therefore, we aimed to evaluate the effect of hyperglycemia on proliferating, differentiating and maturating human visceral pre/adipocytes (HPA-v). Three stages [...] Read more.
Disturbances in adipose tissue significantly contribute to the development of metabolic disorders, which are connected with hyperglycemia (HG) and underlain by epigenetics-based mechanisms. Therefore, we aimed to evaluate the effect of hyperglycemia on proliferating, differentiating and maturating human visceral pre/adipocytes (HPA-v). Three stages of cell culture were conducted under constant or variable glycemic conditions. Adipogenesis progress was assessed using BODIPY 505/515 staining. Lipid content typical for normal and hyperglycemic conditions of adipocytes was analyzed using Raman spectroscopy and imaging. Expression of adipogenic markers, PPARγ and C/EBPα, was determined at the mRNA and protein levels. We also examined expression of miRNAs proven to target PPARγ (miR-34a-5p) and C/EBPα (miR-137-3p), employing TaqMan Low-Density Arrays (TLDA) cards. Hyperglycemia altered morphology of differentiating HPA-v in relation to normoglycemia by accelerating the formation of lipid droplets and making their numbers and volume increase. Raman results confirmed that the qualitative and quantitative lipid composition under normal and hyperglycemic conditions were different, and that the number of lipid droplets increased in (HG)-treated cells. Expression profiles of both examined genes markedly changed either during adipogenesis under physiological and hyperglycemic conditions, orat particular stages of adipogenesis upon chronic and/or variable glycemia. Expression levels of PPARγ seemed to correspond to some expression changes of miR-34a-5p. miR-137-3p, whose expression was rather stable throughout the culture, did not seem to affect C/EBPα. Our observations revealed that chronic and intermittent hyperglycemia change the morphology of visceral pre/adipocytes during adipogenesis. Moreover, hyperglycemia may utilize miR-34a-5p to induce some expression changes in PPARγ. Full article
(This article belongs to the Special Issue Nutrition, Genes and Signaling Pathways)
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10 pages, 1778 KiB  
Article
Bone Protective Effect of Extra-Virgin Olive Oil Phenolic Compounds by Modulating Osteoblast Gene Expression
by Lucía Melguizo-Rodríguez, Francisco Javier Manzano-Moreno, Rebeca Illescas-Montes, Javier Ramos-Torrecillas, Elvira de Luna-Bertos, Concepción Ruiz and Olga García-Martínez
Nutrients 2019, 11(8), 1722; https://doi.org/10.3390/nu11081722 - 25 Jul 2019
Cited by 37 | Viewed by 4287
Abstract
The phenolic compounds of extra-virgin olive oil can act at various levels to protect individuals against cardiovascular and neurodegenerative diseases, cancer, and osteoporosis, among others. Polyphenols in extra-virgin olive oil can stimulate the proliferation of osteoblasts, modify their antigen profile, and promote alkaline [...] Read more.
The phenolic compounds of extra-virgin olive oil can act at various levels to protect individuals against cardiovascular and neurodegenerative diseases, cancer, and osteoporosis, among others. Polyphenols in extra-virgin olive oil can stimulate the proliferation of osteoblasts, modify their antigen profile, and promote alkaline phosphatase synthesis. The objective of this work was to determine the effect of different extra-virgin olive oil phenolic compounds on the gene expression of osteoblast-related markers. The cells of the MG63 osteoblast line were cultured for 24 h with 10−6 M of the phenolic compounds ferulic acid, caffeic acid, coumaric acid, apigenin, or luteolin. The expression of studied markers was quantified using quantitative real-time polymerase chain reaction (q-RT-PCR). The expression by MG63 osteoblasts of growth and differentiation/maturation markers was modified after 24 h of treatment with 10−6 M of the phenolic compounds under study, most of which increased the gene expression of the transforming growth factor β1 (TGF-β1), TGF-β receptor 1,2 and 3 (TGF-βR1, TGF-βR2, TGF-βR3), bone morphogenetic protein 2 and 7 (BMP2, BMP7), run-related transcription factor 2 (RUNX-2), Alkaline phosphatase (ALP), Osteocalcin (OSC), Osterix (OSX), Collagen type I (Col-I) and osteoprotegerin (OPN). The extra-virgin olive oil phenolic compounds may have a beneficial effect on bone by modulating osteoblast physiology, which would support their protective effect against bone pathologies. Full article
(This article belongs to the Special Issue Nutrition, Genes and Signaling Pathways)
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16 pages, 1799 KiB  
Article
HM-Chromanone Isolated from Portulaca Oleracea L. Protects INS-1 Pancreatic β Cells against Glucotoxicity-Induced Apoptosis
by Jae Eun Park, Youngwan Seo and Ji Sook Han
Nutrients 2019, 11(2), 404; https://doi.org/10.3390/nu11020404 - 14 Feb 2019
Cited by 16 | Viewed by 3335
Abstract
In this study, we investigated whether (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone, a homoisoflavonoid compound isolated from Portulaca oleracea L., protects INS-1 pancreatic β cells against glucotoxicity-induced apoptosis. Treatment with high glucose (30 mM) induced apoptosis in INS-1 pancreatic β cells; however, the level of cell [...] Read more.
In this study, we investigated whether (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone, a homoisoflavonoid compound isolated from Portulaca oleracea L., protects INS-1 pancreatic β cells against glucotoxicity-induced apoptosis. Treatment with high glucose (30 mM) induced apoptosis in INS-1 pancreatic β cells; however, the level of cell viability was significantly increased by treatment with (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone. Treatment with 10–20 µM of (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone dose-dependently increased cell viability and significantly decreased the intracellular level of reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), and nitric oxide levels in INS-1 pancreatic β cells pretreated with high glucose. These effects were associated with increased anti-apoptotic Bcl-2 protein expression, while reducing pro-apoptotic Bax, cytochrome C, and caspase 9 protein expression. Treatment with (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone reduced the apoptosis previously induced by high-level glucose-treatment, according to annexin V/propidium iodide staining. These results demonstrate that (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone may be useful as a potential therapeutic agent to protect INS-1 pancreatic β cells against high glucose-induced apoptosis. Full article
(This article belongs to the Special Issue Nutrition, Genes and Signaling Pathways)
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