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Nutrients
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The Effect of Lipids and Lipoproteins on Metabolic Health
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The Effect of Lipids and Lipoproteins on Metabolic Health

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 3904

Special Issue Editor

Dr. Alessandro Cavarape

E-Mail Website
Guest Editor
Clinica Medica, Department of Medicine (DAME), University of Udine, 33100 Udine, Italy
Interests: diabetes mellitus; cardiovascular diseases; chronic complications of diabetes; peripheral artery disease

Special Issue Information

Dear Colleagues,

The introduction of highly effective drugs for the treatment of dyslipidemias and to substantially reduce cardiovascular risk has revitalized interest in lipids and lipoprotein Lp (a) as correctable cardiovascular risk factors. In addition to their traditional role in atherogenesis, in recent years, further evidence has also emerged regarding the role of lipids and lipoproteins in the pathogenesis of various diseases. Alterations in lipoprotein metabolism is an emerging area of ​​research that may partially explain the observed relationship between dyslipidemia, immune cell activation, inflammation, and atherosclerosis. Alterations in the metabolism of lipoproteins and the probably elevated levels of lipoprotein (a) which are able to increase the mechanisms of inflammation are also correlated with the pathogenesis of other chronic developmental diseases, such as liver diseases, cognitive impairment, diseases related to obesity, and others. Numerous innovative drugs that act on the metabolism of lipoproteins and lipoprotein(a) are currently being tested. The emerging pathophysiological knowledge and promising therapeutic options open new perspectives not only on the prevention of atherogenesis and cardiovascular diseases but also on of numerous other chronic diseases. For this Special Issue on the role of lipids and lipoproteins in metabolic health, we invite the submission of research articles and reviews of experimental and clinical research with the aim of highlighting the most recent developments in the most innovative pathophysiological aspects of the metabolism of lipids and lipoprotein Lp (a), providing an updated review of the state of the art in this promising area of ​​research.

Dr. Alessandro Cavarape
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. Nutrients 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 2900 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

  • lipids
  • lipoproteins
  • lipoprotein(a)
  • cholesterol
  • dyslipidemias
  • cardiovascular diseases
  • atherosclerosis
  • chronic diseases
  • metabolic diseases
  • inflammation

Published Papers (2 papers)

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Research

15 pages, 3671 KiB  
Article
High-Density Lipoprotein Is Located Alongside Insulin in the Islets of Langerhans of Normal and Rodent Models of Diabetes
by Sahar Mohsin, Haba Elabadlah, Mariam K. Alotaiba, Suhail AlAmry, Shamma J. Almehairbi, Maha M. K. Harara, Aisha M. H. Almuhsin, Saeed Tariq, Frank Christopher Howarth and Ernest A. Adeghate
Nutrients 2024, 16(2), 313; https://doi.org/10.3390/nu16020313 - 20 Jan 2024
Cited by 1 | Viewed by 1407
Abstract
Recent studies have implicated pre-beta and beta lipoproteins (VLDL and LDL) in the etiopathogenesis of complications of diabetes mellitus (DM). In contrast, alpha lipoprotein (HDL) is protective of the beta cells of the pancreas. This study examined the distribution of HDL in the [...] Read more.
Recent studies have implicated pre-beta and beta lipoproteins (VLDL and LDL) in the etiopathogenesis of complications of diabetes mellitus (DM). In contrast, alpha lipoprotein (HDL) is protective of the beta cells of the pancreas. This study examined the distribution of HDL in the islets of Langerhans of murine models of type 1 diabetic rats (streptozotocin (STZ)-induced DM in Wistar rats) and type 2 models of DM rats (Goto–Kakizaki (GK), non-diabetic Zucker lean (ZL), and Zucker diabetic and fatty (ZDF)). The extent by which HDL co-localizes with insulin or glucagon in the islets of the pancreas was also investigated. Pancreatic tissues of Wistar non-diabetic, diabetic Wistar, GK, ZL, and ZDF rats were processed for immunohistochemistry. Pancreatic samples of GK rats fed with either a low-fat or a high-fat diet were prepared for transmission immune-electron microscopy (TIEM) to establish the cytoplasmic localization of HDL in islet cells. HDL was detected in the core and periphery of pancreatic islets of Wistar non-diabetic and diabetic, GK, ZL, and ZDF rats. The average total of islet cells immune positive for HDL was markedly (<0.05) reduced in GK and ZDF rats in comparison to Wistar controls. The number of islet cells containing HDL was also remarkably (p < 0.05) reduced in Wistar diabetic rats and GK models fed on high-fat food. The co-localization study using immunofluorescence and TIEM techniques showed that HDL is detected alongside insulin within the secretory granules of β-cells. HDL did not co-localize with glucagon. This observation implies that HDL may contribute to the metabolism of insulin. Full article
(This article belongs to the Special Issue The Effect of Lipids and Lipoproteins on Metabolic Health)
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9 pages, 275 KiB  
Article
Low-Density Lipoprotein Cholesterol, Structural Atherosclerosis, and Functional Atherosclerosis in Older Japanese
by Yuji Shimizu, Hirotomo Yamanashi, Yukiko Honda, Fumiaki Nonaka, Jun Miyata, Shin-Ya Kawashiri, Yuko Noguchi, Seiko Nakamichi, Yasuhiro Nagata and Takahiro Maeda
Nutrients 2023, 15(1), 183; https://doi.org/10.3390/nu15010183 - 30 Dec 2022
Cited by 3 | Viewed by 1999
Abstract
Aggressive endothelial repair results in the progression of both structural and functional atherosclerosis, while insufficient endothelial repair worsens functional but not structural atherosclerosis. Aging increases the risk of inadequate endothelial repair. Since low-density lipoprotein cholesterol (LDLc) activates endothelial repair, LDLc may be positively [...] Read more.
Aggressive endothelial repair results in the progression of both structural and functional atherosclerosis, while insufficient endothelial repair worsens functional but not structural atherosclerosis. Aging increases the risk of inadequate endothelial repair. Since low-density lipoprotein cholesterol (LDLc) activates endothelial repair, LDLc may be positively associated with structural atherosclerosis but inversely associated with functional atherosclerosis in older individuals. This cross-sectional study analyzed 1458 participants aged 60 to 79 years. We defined structural atherosclerosis as a carotid intima-media thickness (CIMT) of at least 1.1 mm and functional atherosclerosis as a cardio-ankle vascular index (CAVI) of at least 9.0. LDLc was significantly positively associated with structural atherosclerosis and significantly inversely associated with functional atherosclerosis, independently of known cardiovascular risk factors. For 1 standard increment of LDLc (28 mg/dL for men and 29 mg/dL for women), the odds ratios and 95% confidence intervals after adjustment for known cardiovascular risk factors were 1.28 (1.10, 1.50) for structural atherosclerosis and 0.85 (0.75, 0.96) for functional atherosclerosis. LDLc activates endothelial repair, which results in the development of structural atherosclerosis but maintains endothelial function in older individuals. To evaluate atherosclerosis in clinical practice, the combination of structural and functional assessment of atherosclerosis could be informative. Full article
(This article belongs to the Special Issue The Effect of Lipids and Lipoproteins on Metabolic Health)
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