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Nutritional Bioactive Compounds and Diabetic Neuropathy

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Micronutrients and Human Health".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 5027

Special Issue Editor


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Guest Editor
Department of Pharmacology, School of Medicine, University of Malaga, Malaga, Spain
Interests: cardiovascular disease; diabetes; antioxidants; oxidative stress; inflammatory biomarkers

Special Issue Information

Dear Colleagues,

Diabetes mellitus is a true social and health problem throughout the world. Approximately 460 million people suffer from diabetes mellitus. Long-term complications involve the vascular system, both in arteries (macroangiopathy) and in small vessels (diabetic microangiopathy), among which are those of the retina, kidney and nervous tissue (diabetic neuropathy).

Diabetic neuropathy affects both peripheral (legs, feet), visceral and central nervous tissue (including retina). This damage is generated by long-term high glucose levels; however, despite being a direct alteration of the nervous tissue, there is no doubt that the involvement of the blood vessels is a factor that jointly affects the nervous tissue.

Oxidative stress is one of the main mechanisms that initiate and promote the evolution of diabetic neuropathy. For this reason, in addition to the intensive control of blood glucose levels, antioxidants are postulated as possible useful compounds in the prevention of said neuropathy.

Diet is not only useful to control blood glucose levels, but it is also a source of antioxidant compounds, which have been shown to be effective in preventing cardiovascular disease, including type 2 diabetes mellitus.

In this Special Issue, we encourage investigators to contribute original research and review articles that address biochemical, functional and clinical evidence, which provide a greater understanding of the role that various nutrients can play in the pathophysiology and evolution of diabetic neuropathy.

Dr. José Pedro De La Cruz Cortes
Guest Editor

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Keywords

  • diabetes
  • neuropathy
  • antioxidants
  • bioactive compounds
  • micronutrients

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Published Papers (2 papers)

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Research

13 pages, 4826 KiB  
Article
Neuroprotective Effect of 3′,4′-Dihydroxyphenylglycol in Type-1-like Diabetic Rats—Influence of the Hydroxytyrosol/3′,4′-dihydroxyphenylglycol Ratio
by María Dolores Rodríguez-Pérez, Inmaculada Pérez de Algaba, Esther Martín-Aurioles, María Monsalud Arrebola, Laura Ortega-Hombrados, Cristina Verdugo, María África Fernández-Prior, Alejandra Bermúdez-Oria, José Pedro De La Cruz and José Antonio González-Correa
Nutrients 2022, 14(6), 1146; https://doi.org/10.3390/nu14061146 - 8 Mar 2022
Cited by 8 | Viewed by 2212
Abstract
The aim of this study was to assess the possible neuroprotective effect of 3′,4′-dihydroxyphenylglycol (DHPG), a polyphenol from extra virgin olive oil (EVOO), in an experimental model of diabetes and whether this effect is modified by the presence of another EVOO polyphenol, hydroxytyrosol [...] Read more.
The aim of this study was to assess the possible neuroprotective effect of 3′,4′-dihydroxyphenylglycol (DHPG), a polyphenol from extra virgin olive oil (EVOO), in an experimental model of diabetes and whether this effect is modified by the presence of another EVOO polyphenol, hydroxytyrosol (HT). The neuroprotective effect was assessed in a hypoxia–reoxygenation model in brain slices and by quantifying retinal nerve cells. The animals were distributed as follows: (1) normoglycemic rats (NDR), (2) diabetic rats (DR), (3) DR treated with HT (5 mg/kg/day p.o.), (4) DR treated with DHPG (0.5 mg/kg/day), or (5) with 1 mg/kg/day, (6) DR treated with HT plus DHPG 0.5 mg/kg/day, or (7) HT plus 1 mg/kg/day p.o. DHPG. Diabetic animals presented higher levels of oxidative stress variables and lower numbers of neuronal cells in retinal tissue. The administration of DHPG or HT reduced most of the oxidative stress variables and brain lactate dehydrogenase efflux (LDH) as an indirect index of cellular death and also reduced the loss of retinal cells. The association of DHPG+HT in the same proportions, as found in EVOO, improved the neuroprotective and antioxidant effects of both polyphenols. Full article
(This article belongs to the Special Issue Nutritional Bioactive Compounds and Diabetic Neuropathy)
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15 pages, 2530 KiB  
Article
The Citrus Flavonoid Hesperetin Encounters Diabetes-Mediated Alzheimer-Type Neuropathologic Changes through Relieving Advanced Glycation End-Products Inducing Endoplasmic Reticulum Stress
by Mei-Chou Lai, Wayne-Young Liu, Shorong-Shii Liou and I-Min Liu
Nutrients 2022, 14(4), 745; https://doi.org/10.3390/nu14040745 - 10 Feb 2022
Cited by 19 | Viewed by 2405
Abstract
The present study investigates whether hesperetin, a citrus flavonoid, can encounter advanced glycation end-product (AGE)-induced Alzheimer’s disease-like pathophysiological changes with the underlying mechanisms. SH-SY5Y cells pretreated with hesperetin before stimulation with AGEs (200 μg/mL) were assessed in the following experiments. Hesperetin (40 μmol/L) [...] Read more.
The present study investigates whether hesperetin, a citrus flavonoid, can encounter advanced glycation end-product (AGE)-induced Alzheimer’s disease-like pathophysiological changes with the underlying mechanisms. SH-SY5Y cells pretreated with hesperetin before stimulation with AGEs (200 μg/mL) were assessed in the following experiments. Hesperetin (40 μmol/L) elevated the reduced cell viability induced by AGEs. Hesperetin ameliorated reactive oxygen species overproduction and the downregulation of superoxide dismutase, glutathione peroxidase, and catalase, triggered by AGEs. Amyloid precursor protein upregulation, accompanied by the increased production of Aβ, caused by AGEs, was reversed by hesperetin. However, hesperetin lowered β-site APP-cleaving enzyme 1 expression, inducing insulin-degrading and neprilysin expression. In addition, hesperetin downregulated the expressions of the AGEs-induced endoplasmic reticulum (ER) stress proteins, including 78-kDa glucose-regulated protein and C/EBP homologous protein, and lowered the phosphorylation of protein kinase R-like ER kinase and activating transcription factor 4. Hesperetin-pretreated cells had a minor apoptotic DNA fragmentation. Hesperetin is able to upregulate Bcl-2 protein expression, downregulate Bax expression, and decrease caspase-12/-9/-3 activity as well, indicating that it inhibits ER stress-mediated neuronal apoptosis. There is a similar effect between hesperetin and positive rosiglitazone control against Aβ aggravation of SH-SY5Y cell injury induced by AGEs. Thus, hesperetin might be a potential agent for treating glycation-induced Aβ neurotoxicity. Full article
(This article belongs to the Special Issue Nutritional Bioactive Compounds and Diabetic Neuropathy)
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