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Novel Insights into Biochemical and Molecular Nutrition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (28 November 2023) | Viewed by 6789

Special Issue Editors


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Guest Editor
1. School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan
2. Master Program in Global Health and Health Security, College of Public Health, Taipei Medical University, Taipei 11031, Taiwan
3. Nutrition Research Center, Taipei Medical University Hospital, Taipei 11031, Taiwan
4. TMU Research Center for Digestive Medicine, Taipei Medical University, Taipei 11031, Taiwan
Interests: human nutrition; functional foods; intestinal health; chronic diseases; cancers
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Special Issue Information

Dear Colleagues,

Nutrition has become an important subject and a critical issue for health. Aspects of nutrition, such as biochemical and molecular, affect the outcome of health-related research. Many scientists have contributed to the research on biochemical and molecular nutrition. These fruitful results have been beneficial to health and basic research. However, we need more input of the novel insights into biochemical and molecular nutrition to obtain decent results and stronger scientific evidence. Therefore, this Special Issue aims to present a collection of articles focused on novel insights into biochemical and molecular nutrition, including the mechanisms and consequences, both in vivo and in vitro. Additionally, the links between nutrition and health or diseases can be investigated in aspects of biochemical and molecular nutrition. These may be associated with health promotion, disease prevention, disease therapy, or recovery in the population at any age after therapy. You are most welcome to share findings relevant to novel insights into biochemical and molecular nutrition that were obtained in your lab using reliable animal models and/or established cell models, and even through human studies.

Moreover, considering the health merits of modern therapies, this Special Issue will cover a wide variety of areas, including the repurposing of well-known nutrients or molecules, with the aim of developing useful nutrients or molecules for the novel insights into biochemical and molecular nutrition from different aspects. Various forms of manuscripts are welcomed for submission to this Special Issue, including reviews and original research articles, among others. We look forward to receiving contributions from all over the world.

Dr. Juei-Tang Cheng
Prof. Dr. Jane C.-J. Chao
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. 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.

Published Papers (4 papers)

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Research

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25 pages, 4888 KiB  
Article
Abrupt Photoperiod Changes Differentially Modulate Hepatic Antioxidant Response in Healthy and Obese Rats: Effects of Grape Seed Proanthocyanidin Extract (GSPE)
by Antonio J. Cortés-Espinar, Néstor Ibarz-Blanch, Jorge R. Soliz-Rueda, Enrique Calvo, Francisca Isabel Bravo, Miquel Mulero and Javier Ávila-Román
Int. J. Mol. Sci. 2023, 24(23), 17057; https://doi.org/10.3390/ijms242317057 - 02 Dec 2023
Viewed by 846
Abstract
Disruptions of the light/dark cycle and unhealthy diets can promote misalignment of biological rhythms and metabolic alterations, ultimately leading to an oxidative stress condition. Grape seed proanthocyanidin extract (GSPE), which possesses antioxidant properties, has demonstrated its beneficial effects in metabolic-associated diseases and its [...] Read more.
Disruptions of the light/dark cycle and unhealthy diets can promote misalignment of biological rhythms and metabolic alterations, ultimately leading to an oxidative stress condition. Grape seed proanthocyanidin extract (GSPE), which possesses antioxidant properties, has demonstrated its beneficial effects in metabolic-associated diseases and its potential role in modulating circadian disruptions. Therefore, this study aimed to assess the impact of GSPE administration on the liver oxidant system of healthy and diet-induced obese rats undergoing a sudden photoperiod shift. To this end, forty-eight photoperiod-sensitive Fischer 344/IcoCrl rats were fed either a standard (STD) or a cafeteria diet (CAF) for 6 weeks. A week before euthanizing, rats were abruptly transferred from a standard photoperiod of 12 h of light/day (L12) to either a short (6 h light/day, L6) or a long photoperiod (18 h light/day, L18) while receiving a daily oral dose of vehicle (VH) or GSPE (25 mg/kg). Alterations in body weight gain, serum and liver biochemical parameters, antioxidant gene and protein expression, and antioxidant metabolites were observed. Interestingly, GSPE partially ameliorated these effects by reducing the oxidative stress status in L6 through an increase in GPx1 expression and in hepatic antioxidant metabolites and in L18 by increasing the NRF2/KEAP1/ARE pathway, thereby showing potential in the treatment of circadian-related disorders by increasing the hepatic antioxidant response in a photoperiod-dependent manner. Full article
(This article belongs to the Special Issue Novel Insights into Biochemical and Molecular Nutrition)
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13 pages, 1583 KiB  
Article
Identification of Optimal Reference Genes for qRT-PCR Normalization for Physical Activity Intervention and Omega-3 Fatty Acids Supplementation in Humans
by Agata Grzybkowska, Katarzyna Anczykowska, Jędrzej Antosiewicz, Szczepan Olszewski, Magdalena Dzitkowska-Zabielska and Maja Tomczyk
Int. J. Mol. Sci. 2023, 24(7), 6734; https://doi.org/10.3390/ijms24076734 - 04 Apr 2023
Viewed by 1425
Abstract
The quantitative polymerase chain reaction (qRT-PCR) technique gives promising opportunities to detect and quantify RNA targets and is commonly used in many research fields. This study aimed to identify suitable reference genes for physical exercise and omega-3 fatty acids supplementation intervention. Forty healthy, [...] Read more.
The quantitative polymerase chain reaction (qRT-PCR) technique gives promising opportunities to detect and quantify RNA targets and is commonly used in many research fields. This study aimed to identify suitable reference genes for physical exercise and omega-3 fatty acids supplementation intervention. Forty healthy, physically active men were exposed to a 12-week eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation and standardized endurance training protocol. Blood samples were collected before and after the intervention and mRNA levels of six potential reference genes were tested in the leukocytes of 18 eligible participants using the qRT-PCR method: GAPDH (Glyceraldehyde-3-phosphate dehydrogenase), ACTB (Beta actin), TUBB (Tubulin Beta Class I), RPS18 (Ribosomal Protein S18), UBE2D2 (Ubiquitin-conjugating enzyme E2 D2), and HPRT1 (Hypoxanthine Phosphoribosyltransferase 1). The raw quantification cycle (Cq) values were then analyzed using RefFinder, an online tool that incorporates four different algorithms: NormFinder, geNorm, BestKeeper, and the comparative delta-Ct method. Delta-Ct, NormFinder, BestKeeper, and RefFinder comprehensive ranking have found GAPDH to be the most stably expressed gene. geNorm has identified TUBB and HPRT as the most stable genes. All algorithms have found ACTB to be the least stably expressed gene. A combination of the three most stably expressed genes, namely GAPDH, TUBB, and HPRT, is suggested for obtaining the most reliable results. Full article
(This article belongs to the Special Issue Novel Insights into Biochemical and Molecular Nutrition)
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Review

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18 pages, 1434 KiB  
Review
Modulation of Tau Pathology in Alzheimer’s Disease by Dietary Bioactive Compounds
by Huahua Shi and Yan Zhao
Int. J. Mol. Sci. 2024, 25(2), 831; https://doi.org/10.3390/ijms25020831 - 09 Jan 2024
Viewed by 1167
Abstract
Tau is a microtubule-associated protein essential for microtubule assembly and stability in neurons. The abnormal intracellular accumulation of tau aggregates is a major characteristic of brains from patients with Alzheimer’s disease (AD) and other tauopathies. In AD, the presence of neurofibrillary tangles (NFTs), [...] Read more.
Tau is a microtubule-associated protein essential for microtubule assembly and stability in neurons. The abnormal intracellular accumulation of tau aggregates is a major characteristic of brains from patients with Alzheimer’s disease (AD) and other tauopathies. In AD, the presence of neurofibrillary tangles (NFTs), which is composed of hyperphosphorylated tau protein, is positively correlated with the severity of the cognitive decline. Evidence suggests that the accumulation and aggregation of tau cause synaptic dysfunction and neuronal degeneration. Thus, the prevention of abnormal tau phosphorylation and elimination of tau aggregates have been proposed as therapeutic strategies for AD. However, currently tau-targeting therapies for AD and other tauopathies are limited. A number of dietary bioactive compounds have been found to modulate the posttranslational modifications of tau, including phosphorylation, small ubiquitin-like modifier (SUMO) mediated modification (SUMOylation) and acetylation, as well as inhibit tau aggregation and/or promote tau degradation. The advantages of using these dietary components over synthetic substances in AD prevention and intervention are their safety and accessibility. This review summarizes the mechanisms leading to tau pathology in AD and highlights the effects of bioactive compounds on the hyperphosphorylation, aggregation and clearance of tau protein. The potential of using these bioactive compounds for AD prevention and intervention is also discussed. Full article
(This article belongs to the Special Issue Novel Insights into Biochemical and Molecular Nutrition)
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29 pages, 2466 KiB  
Review
Molecular Mechanisms of Neuroprotection by Ketone Bodies and Ketogenic Diet in Cerebral Ischemia and Neurodegenerative Diseases
by Jiwon Jang, Su Rim Kim, Jo Eun Lee, Seoyeon Lee, Hyeong Jig Son, Wonchae Choe, Kyung-Sik Yoon, Sung Soo Kim, Eui-Ju Yeo and Insug Kang
Int. J. Mol. Sci. 2024, 25(1), 124; https://doi.org/10.3390/ijms25010124 (registering DOI) - 21 Dec 2023
Cited by 1 | Viewed by 2766
Abstract
Ketone bodies (KBs), such as acetoacetate and β-hydroxybutyrate, serve as crucial alternative energy sources during glucose deficiency. KBs, generated through ketogenesis in the liver, are metabolized into acetyl-CoA in extrahepatic tissues, entering the tricarboxylic acid cycle and electron transport chain for ATP production. [...] Read more.
Ketone bodies (KBs), such as acetoacetate and β-hydroxybutyrate, serve as crucial alternative energy sources during glucose deficiency. KBs, generated through ketogenesis in the liver, are metabolized into acetyl-CoA in extrahepatic tissues, entering the tricarboxylic acid cycle and electron transport chain for ATP production. Reduced glucose metabolism and mitochondrial dysfunction correlate with increased neuronal death and brain damage during cerebral ischemia and neurodegeneration. Both KBs and the ketogenic diet (KD) demonstrate neuroprotective effects by orchestrating various cellular processes through metabolic and signaling functions. They enhance mitochondrial function, mitigate oxidative stress and apoptosis, and regulate epigenetic and post-translational modifications of histones and non-histone proteins. Additionally, KBs and KD contribute to reducing neuroinflammation and modulating autophagy, neurotransmission systems, and gut microbiome. This review aims to explore the current understanding of the molecular mechanisms underpinning the neuroprotective effects of KBs and KD against brain damage in cerebral ischemia and neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Full article
(This article belongs to the Special Issue Novel Insights into Biochemical and Molecular Nutrition)
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