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14 pages, 1431 KiB

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

by Erika Cione, Pierluigi Plastina, Attilio Pingitore, Mariarita Perri, Maria Cristina Caroleo, Alessia Fazio, Renger Witkamp and Jocelijn Meijerink

Nutrients 2019, 11(4), 915; https://doi.org/10.3390/nu11040915 - 24 Apr 2019

Cited by 20 | Viewed by 4745

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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19 pages, 24489 KiB

Open AccessArticle

Hyperglycemia Affects miRNAs Expression Pattern during Adipogenesis of Human Visceral Adipocytes—Is Memorization Involved?

by Justyna Strycharz, Ewa Świderska, Adam Wróblewski, Marta Podolska, Piotr Czarny, Janusz Szemraj, Aneta Balcerczyk, Józef Drzewoski, Jacek Kasznicki and Agnieszka Śliwińska

Nutrients 2018, 10(11), 1774; https://doi.org/10.3390/nu10111774 - 15 Nov 2018

Cited by 7 | Viewed by 4396

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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28 pages, 2978 KiB

Open AccessReview

Analysis of Association between Vitamin D Deficiency and Insulin Resistance

by Izabela Szymczak-Pajor and Agnieszka Śliwińska

Nutrients 2019, 11(4), 794; https://doi.org/10.3390/nu11040794 - 06 Apr 2019

Cited by 176 | Viewed by 20016

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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