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Special Issue "Nutrition and Insulin Resistance–Beyond Energy Metabolism"

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

Deadline for manuscript submissions: closed (28 February 2019)

Special Issue Editor

Guest Editor
Dr. Yan Lam

Department of Biochemistry and Microbiology and New Jersey Institute for Food, Nutrition & Health, Rutgers University, New Brunswick, New Jersey 08901, USA
Website | E-Mail
Phone: +1-848-932-5673
Interests: gut microbiota; obesity; insulin resistance; omega-3 polyunsaturated fatty acids

Special Issue Information

Dear Colleagues,

Over the past few decades we have seen a rapid change in the disease landscape and many attributes this to environmental factors, particularly nutrition. Beyond the classic effects of macronutrients on energy homeostasis, nutrition has a broader implication on human health by modulating insulin sensitivity. Recent research suggest that insulin resistance is a key mechanistic driver of many debilitating diseases ranging from type 2 diabetes, cardiovascular, autoimmune to neurodegenerative diseases. This puts nutrition at the forefront of innovative prevention and/or treatment of many medical conditions. The current Special Issue gathers reviews of recent research from various disciplines to delineate the role of nutrition in the development of insulin resistance and disease pathophysiology, and potentially provide insights into nutraceutical-based strategies to curb global epidemics such as obesity.

Dr. Yan Lam
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 papers will be 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 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 2000 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

  • Insulin resistance
  • Inflammation
  • Gut microbiota
  • Nutrition

Published Papers (3 papers)

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Research

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Open AccessArticle
Capsaicin Analogues Derived from n-3 Polyunsaturated Fatty Acids (PUFAs) Reduce Inflammatory Activity of Macrophages and Stimulate Insulin Secretion by β-Cells In Vitro
Nutrients 2019, 11(4), 915; https://doi.org/10.3390/nu11040915
Received: 22 March 2019 / Revised: 15 April 2019 / Accepted: 20 April 2019 / Published: 24 April 2019
Cited by 1 | PDF Full-text (1431 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
In this study, two capsaicin analogues, N-eicosapentaenoyl vanillylamine (EPVA) and N-docosahexaenoyl vanillylamine (DHVA), were enzymatically synthesized from their corresponding n-3 long chain polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both dietary relevant components. The compounds significantly reduced [...] Read more.
In this study, two capsaicin analogues, N-eicosapentaenoyl vanillylamine (EPVA) and N-docosahexaenoyl vanillylamine (DHVA), were enzymatically synthesized from their corresponding n-3 long chain polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both dietary relevant components. The compounds significantly reduced the production of some lipopolysaccharide (LPS)-induced inflammatory mediators, including nitric oxide (NO), macrophage-inflammatory protein-3α (CCL20) and monocyte chemoattractant protein-1 (MCP-1 or CCL2), by RAW264.7 macrophages. Next to this, only EPVA increased insulin secretion by pancreatic INS-1 832/13 β-cells, while raising intracellular Ca2+ and ATP concentrations. This suggests that the stimulation of insulin release occurs through an increase in the intracellular ATP/ADP ratio in the first phase, while is calcium-mediated in the second phase. Although it is not yet known whether EPVA is endogenously produced, its potential therapeutic value for diabetes treatment merits further investigation. Full article
(This article belongs to the Special Issue Nutrition and Insulin Resistance–Beyond Energy Metabolism)
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Graphical abstract

Open AccessArticle
Hyperglycemia Affects miRNAs Expression Pattern during Adipogenesis of Human Visceral Adipocytes—Is Memorization Involved?
Nutrients 2018, 10(11), 1774; https://doi.org/10.3390/nu10111774
Received: 17 October 2018 / Revised: 5 November 2018 / Accepted: 13 November 2018 / Published: 15 November 2018
Cited by 1 | PDF Full-text (24489 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
microRNAs are increasingly analyzed in adipogenesis, whose deregulation, especially visceral, contributes to the development of diabetes. Hyperglycemia is known to affect cells while occurring acutely and chronically. Therefore, we aimed to evaluate the effect of hyperglycemia on human visceral pre/adipocytes from the perspective [...] Read more.
microRNAs are increasingly analyzed in adipogenesis, whose deregulation, especially visceral, contributes to the development of diabetes. Hyperglycemia is known to affect cells while occurring acutely and chronically. Therefore, we aimed to evaluate the effect of hyperglycemia on human visceral pre/adipocytes from the perspective of microRNAs. The relative expression of 78 microRNAs was determined by TaqMan Low Density Arrays at three stages of HPA-v adipogenesis conducted under normoglycemia, chronic, and intermittent hyperglycemia (30 mM). Hierarchical clustering/Pearson correlation revealed the relationship between various microRNAs’ expression profiles, while functional analysis identified the genes and signaling pathways regulated by differentially expressed microRNAs. Hyperglycemia affected microRNAs’ expression patterns during adipogenesis, and at the stage of pre-adipocytes, differentiated and mature adipocytes compared to normoglycemia. Interestingly, the changes that were evoked upon hyperglycemic exposure during one adipogenesis stage resembled those observed upon chronic hyperglycemia. At least 15 microRNAs were modulated during normoglycemic and/or hyperglycemic adipogenesis and/or upon intermittent/chronic hyperglycemia. Bioinformatics analysis revealed the involvement of these microRNAs in cell cycle, lipid metabolism, ECM–receptor interaction, oxidative stress, signaling of insulin, MAPK, TGF-β, p53, and more. The obtained data suggests that visceral pre/adipocytes exposed to chronic/intermittent hyperglycemia develop a microRNAs’ expression pattern, which may contribute to further visceral dysfunction, the progression of diabetic phenotype, and diabetic complications possibly involving “epi”-memory. Full article
(This article belongs to the Special Issue Nutrition and Insulin Resistance–Beyond Energy Metabolism)
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Review

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Open AccessReview
Analysis of Association between Vitamin D Deficiency and Insulin Resistance
Nutrients 2019, 11(4), 794; https://doi.org/10.3390/nu11040794
Received: 27 February 2019 / Revised: 31 March 2019 / Accepted: 1 April 2019 / Published: 6 April 2019
PDF Full-text (2978 KB) | HTML Full-text | XML Full-text
Abstract
Recent evidence revealed extra skeleton activity of vitamin D, including prevention from cardiometabolic diseases and cancer development as well as anti-inflammatory properties. It is worth noting that vitamin D deficiency is very common and may be associated with the pathogenesis of insulin-resistance-related diseases, [...] Read more.
Recent evidence revealed extra skeleton activity of vitamin D, including prevention from cardiometabolic diseases and cancer development as well as anti-inflammatory properties. It is worth noting that vitamin D deficiency is very common and may be associated with the pathogenesis of insulin-resistance-related diseases, including obesity and diabetes. This review aims to provide molecular mechanisms showing how vitamin D deficiency may be involved in the insulin resistance formation. The PUBMED database and published reference lists were searched to find studies published between 1980 and 2019. It was identified that molecular action of vitamin D is involved in maintaining the normal resting levels of ROS and Ca2+, not only in pancreatic β-cells, but also in insulin responsive tissues. Both genomic and non-genomic action of vitamin D is directed towards insulin signaling. Thereby, vitamin D reduces the extent of pathologies associated with insulin resistance such as oxidative stress and inflammation. More recently, it was also shown that vitamin D prevents epigenetic alterations associated with insulin resistance and diabetes. In conclusion, vitamin D deficiency is one of the factors accelerating insulin resistance formation. The results of basic and clinical research support beneficial action of vitamin D in the reduction of insulin resistance and related pathologies. Full article
(This article belongs to the Special Issue Nutrition and Insulin Resistance–Beyond Energy Metabolism)
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