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Micronutrients in Metabolic Health 2.0
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Micronutrients in Metabolic Health 2.0

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 January 2024) | Viewed by 5424

Special Issue Editor

Dr. Adaikala Antonysunil

E-Mail Website
Guest Editor
School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham NG11 8NS, UK
Interests: nutriepigenomics; micronutrients
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

This Special Issue is the continuation of our previous Special Issue "Micronutrients in Metabolic Health".

Obesity and type 2 diabetes (T2D) are major public health problems, and genome-wide association studies only explain a small fraction of the heritability of these disorders (less than 2% for obesity and 5–10% for T2D). These low heritability estimates suggest that lifestyle factors via epigenetic mechanisms could explain the missing heritability and play a key role in these diseases. Nutritional imbalances and pre- or postnatal macro- or micro-nutrient intake could lead to epigenetic reprogramming, which is associated with increased obesity, T2D, gestational diabetes, and cardiovascular disease. More importantly, recent studies have demonstrated that micronutrient deficiency during pregnancy can induce distinctive changes in the epigenome and increase metabolic risk. By contrast, sufficient nutrient intake has been shown to improve epigenetic markers and mitigate disease risk. However, there is still a limited understanding of mechanisms of these micronutrients that can regulate a large collection of coding and noncoding transcripts involved in metabolic pathways in these metabolic diseases. Hence, the goal of this Special Issue is to broaden the molecular understanding of the roles of micronutrients and epigenetic mechanisms, through which we hope to uncover strategies for targeting epigenetic plasticity; in the future, this may offer novel and realistic opportunities to prevent and treat obesity and related disorders. We invite authors to submit original research and review articles describing basic and translational findings, with a special focus on “Micronutrients in Metabolic Health 2.0”.

Dr. Adaikala Antonysunil
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

  • micronutrients
  • vitamin B12
  • vitamin D
  • epigenetics
  • obesity
  • type 2 diabetes
  • gestational diabetes
  • insulin resistance
  • cardiovasular disease
  • maternal and fetal programming

Published Papers (2 papers)

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19 pages, 3353 KiB  
Article
Triple-Isotope Tracing for Pathway Discernment of NMN-Induced NAD+ Biosynthesis in Whole Mice
by Anthony A. Sauve, Qinghui Wang, Ning Zhang, Seolhee Kang, Abigail Rathmann and Yue Yang
Int. J. Mol. Sci. 2023, 24(13), 11114; https://doi.org/10.3390/ijms241311114 - 05 Jul 2023
Cited by 3 | Viewed by 4883
Abstract
Numerous efforts in basic and clinical studies have explored the potential anti-aging and health-promoting effects of NAD+-boosting compounds such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Despite these extensive efforts, our understanding and characterization of their whole-body pharmacodynamics, impact on [...] Read more.
Numerous efforts in basic and clinical studies have explored the potential anti-aging and health-promoting effects of NAD+-boosting compounds such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Despite these extensive efforts, our understanding and characterization of their whole-body pharmacodynamics, impact on NAD+ tissue distribution, and mechanism of action in various tissues remain incomplete. In this study, we administered NMN via intraperitoneal injection or oral gavage and conducted a rigorous evaluation of NMN’s pharmacodynamic effects on whole-body NAD+ homeostasis in mice. To provide more confident insights into NMN metabolism and NAD+ biosynthesis across different tissues and organs, we employed a novel approach using triple-isotopically labeled [18O-phosphoryl-18O-carbonyl-13C-1-ribosyl] NMN. Our results provide a more comprehensive characterization of the NMN impact on NAD+ concentrations and absolute amounts in various tissues and the whole body. We also demonstrate that mice primarily rely on the nicotinamide and NR salvage pathways to generate NAD+ from NMN, while the uptake of intact NMN plays a minimal role. Overall, the tissue-specific pharmacodynamic effects of NMN administration through different routes offer novel insights into whole-body NAD+ homeostasis, laying a crucial foundation for the development of NMN as a therapeutic supplement in humans. Full article
(This article belongs to the Special Issue Micronutrients in Metabolic Health 2.0)
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Review

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22 pages, 685 KiB  
Review
Vitamin D and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Novel Mechanistic Insights
by Ioanna Aggeletopoulou, Efthymios P. Tsounis and Christos Triantos
Int. J. Mol. Sci. 2024, 25(9), 4901; https://doi.org/10.3390/ijms25094901 - 30 Apr 2024
Viewed by 153
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent condition characterized by abnormal fat accumulation in the liver, often associated with metabolic disorders. Emerging evidence suggests a potential link between vitamin D deficiency and the development and progression of MASLD. The current [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent condition characterized by abnormal fat accumulation in the liver, often associated with metabolic disorders. Emerging evidence suggests a potential link between vitamin D deficiency and the development and progression of MASLD. The current review provides a concise overview of recent studies uncovering novel mechanistic insights into the interplay between vitamin D and MASLD. Several epidemiological studies have highlighted a significant association between low vitamin D levels and an increased risk of MASLD. Vitamin D, traditionally known for its role in bone health, has now been recognized as a key player in various physiological processes, including immune regulation and inflammation. Experimental studies using animal models have demonstrated that vitamin D deficiency exacerbates liver steatosis and inflammation, suggesting a potential protective role against MASLD. Mechanistically, vitamin D appears to modulate MASLD through multiple pathways. Firstly, the vitamin D receptor (VDR) is abundantly expressed in liver cells, indicating a direct regulatory role in hepatic function. Activation of the VDR has been shown to suppress hepatic lipid accumulation and inflammation, providing a mechanistic basis for the observed protective effects. Additionally, vitamin D influences insulin sensitivity, a critical factor in MASLD pathogenesis. Improved insulin sensitivity may mitigate the excessive accumulation of fat in the liver, thus attenuating MASLD progression. In parallel, vitamin D exhibits anti-inflammatory properties by inhibiting pro-inflammatory cytokines implicated in MASLD pathophysiology. Experimental evidence suggests that the immunomodulatory effects of vitamin D extend to the liver, reducing inflammation and oxidative stress, key drivers of MASLD, and the likelihood of hepatocyte injury and fibrosis. Understanding the complex interplay between vitamin D and MASLD provides a basis for exploring targeted therapeutic strategies and preventive interventions. As vitamin D deficiency is a modifiable risk factor, addressing this nutritional concern may prove beneficial in mitigating the burden of MASLD and associated metabolic disorders. Full article
(This article belongs to the Special Issue Micronutrients in Metabolic Health 2.0)
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