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Integrated and Multidisciplinary Approach to Manage Metabolic Diseases

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 2110

Special Issue Editors


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Guest Editor
CREA—Research Centre for Food and Nutrition, via Ardeatina 546, 00178 Rome, Italy
Interests: molecular biology; bioactive compounds; molecular nutrition; hormone metabolism; cancer; hormone-related diseases; nutrigenomics; nutrigenetics; metabolic disease
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
CREA—Research Centre for Food and Nutrition, via Ardeatina 546, 00178 Rome, Italy
Interests: nutritional status; health; immunological status; hormonal status; inflammatory status
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
CREA- Research Centre for Food and Nutrition, via Ardeatina 546, 00178 Rome, Italy
Interests: nutrition; health status; human observational studies and intervention trials; diet and lifestyle; bioactive compounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic syndrome is a complex clinical condition characterized by a clustering of metabolic risk factors, determined by the simultaneous occurrence of at least three of the following components: central obesity, dyslipidemia, impaired glucose metabolism, and elevated blood pressure. This cluster of conditions that occur together leads to increased risk of heart disease, stroke, and type 2 diabetes. The incidence of metabolic syndrome often occurs together with the incidence of both obesity and type 2 diabetes, even if there are no global data on metabolic syndrome. However, its prevalence could be estimated to be about one quarter of the world population.

During the last three decades, understanding of the biology of metabolic syndrome has increased. Many new pieces have been added to the puzzle, so we know that metabolic syndrome is a complex pathophysiologic state that originates primarily from an imbalance of calorie intake and energy expenditure but is also affected by genetic/epigenetic composition of the individual, lifestyle, physical activity, and other factors such as food quality, its nutrient contents, and composition of gut microbes.

The scientific community is cordially invited to contribute with original research papers or reviews to this Special Issue of Molecules, which reports an integrated and multidisciplinary approach to identify and characterize food and molecules that help to manage the metabolic syndrome.

Dr. Raffaella Comitato
Dr. Eugenia Venneria
Dr. Federica Intorre
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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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

  • obesity
  • cardiovascular disease
  • diabetes
  • food and bioactive compounds
  • human observational studies and intervention trials

Published Papers (1 paper)

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Research

18 pages, 2438 KiB  
Article
Inhibition of Endoplasmic Reticulum Stress Improves Acetylcholine-Mediated Relaxation in the Aorta of Type-2 Diabetic Rats
by Sagir Mustapha, Ahmad Khusairi Azemi, Wan Amir Nizam Wan Ahmad, Aida Hanum Ghulam Rasool, Mohd Rais Mustafa and Siti Safiah Mokhtar
Molecules 2022, 27(16), 5107; https://doi.org/10.3390/molecules27165107 - 11 Aug 2022
Cited by 2 | Viewed by 1640
Abstract
Endoplasmic reticulum (ER) stress contributes to insulin resistance and macro- and microvascular complications associated with diabetes. This study aimed to evaluate the effect of ER stress inhibition on endothelial function in the aorta of type-2 diabetic rats. Type-2 diabetes was developed in male [...] Read more.
Endoplasmic reticulum (ER) stress contributes to insulin resistance and macro- and microvascular complications associated with diabetes. This study aimed to evaluate the effect of ER stress inhibition on endothelial function in the aorta of type-2 diabetic rats. Type-2 diabetes was developed in male Sprague–Dawley rats using a high-fat diet and low-dose streptozotocin. Rat aortic tissues were harvested to study endothelial-dependent relaxation. The mechanisms for acetylcholine-mediated relaxation were investigated using pharmacological blockers, Western blotting, oxidative stress, and inflammatory markers. Acetylcholine-mediated relaxation was diminished in the aorta of diabetic rats compared to control rats; supplementation with TUDCA improved relaxation. In the aortas of control and diabetic rats receiving TUDCA, the relaxation was mediated via eNOS/PI3K/Akt, NAD(P)H, and the KATP channel. In diabetic rats, acetylcholine-mediated relaxation involved eNOS/PI3K/Akt and NAD(P)H, but not the KATP channel. The expression of ER stress markers was upregulated in the aorta of diabetic rats and reduced with TUDCA supplementation. The expression of eNOS and Akt were lower in diabetic rats but were upregulated after supplementation with TUDCA. The levels of MDA, IL-6, and SOD activity were higher in the aorta of the diabetic rats compared to control rats. This study demonstrated that endothelial function was impaired in diabetes, however, supplementation with TUDCA improved the function via eNOS/Akt/PI3K, NAD(P)H, and the KATP channel. The improvement of endothelial function was associated with increased expressions of eNOS and Akt. Thus, ER stress plays a crucial role in the impairment of endothelial-dependent relaxation. Mitigating ER stress could be a potential strategy for improving endothelial dysfunction in type-2 diabetes. Full article
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