International Journal of Molecular Sciences

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Special Issue Editor

Special Issue Information

Dear Colleagues,

Lipid homeostasis represents the coordination and regulation of numerous complex processes that work to ensure a balance between lipid influx and efflux in order to maintain the optimal lipid status required for normal cell function. As the vehicles that provide the means to deliver and transport both cholesterol and fatty acids as energy substrates to different tissues, lipoproteins are key in maintaining this balance. Lipoprotein metabolism relies on a number of enzymes, transfer proteins, apolipoproteins, and receptors to ensure the delivery and transport of lipids to different tissues. The imbalance or deregulation of lipid homeostasis can manifest as different forms of dyslipidemias, which can contribute to or serve as markers of the physiopathology of a number of diseases, including cardiovascular and metabolic diseases, as well as neurodegenerative diseases such as Alzheimer’s disease. Despite the advances in the field of lipoprotein metabolism in the past few decades, the causal relationship between lipoproteins and these different pathologies remains under active investigation.

The aim of this Special Issue is to highlight new discoveries and present up-to-date reviews in order to further enrich our understanding of the role of lipoprotein metabolism in different physiopathologies ranging from cardiovascular and metabolic to neurodegenerative diseases, and thus identify innovative strategies or therapeutics for the prevention or treatment of these pathologies.

Original articles or focused reviews addressing these topics will be considered for publication.

Dr. Frances T. Yen
Guest Editor

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Related Special Issue

Published Papers (1 paper)

Research

18 pages, 1158 KiB

Open AccessArticle

Serum Levels of Adiponectin Are Strongly Associated with Lipoprotein Subclasses in Healthy Volunteers but Not in Patients with Metabolic Syndrome

by Iva Klobučar, Hansjörg Habisch, Lucija Klobučar, Matias Trbušić, Gudrun Pregartner, Andrea Berghold, Gerhard M. Kostner, Hubert Scharnagl, Tobias Madl, Saša Frank and Vesna Degoricija

Int. J. Mol. Sci. 2024, 25(9), 5050; https://doi.org/10.3390/ijms25095050 - 6 May 2024

Viewed by 473

Abstract

Metabolic syndrome (MS) is a widespread disease in developed countries, accompanied, among others, by decreased adiponectin serum levels and perturbed lipoprotein metabolism. The associations between the serum levels of adiponectin and lipoproteins have been extensively studied in the past under healthy conditions, yet it remains unexplored whether the observed associations also exist in patients with MS. Therefore, in the present study, we analyzed the serum levels of lipoprotein subclasses using nuclear magnetic resonance spectroscopy and examined their associations with the serum levels of adiponectin in patients with MS in comparison with healthy volunteers (HVs). In the HVs, the serum levels of adiponectin were significantly negatively correlated with the serum levels of large buoyant-, very-low-density lipoprotein, and intermediate-density lipoprotein, as well as small dense low-density lipoprotein (LDL) and significantly positively correlated with large buoyant high-density lipoprotein (HDL). In patients with MS, however, adiponectin was only significantly correlated with the serum levels of phospholipids in total HDL and large buoyant LDL. As revealed through logistic regression and orthogonal partial least-squares discriminant analyses, high adiponectin serum levels were associated with low levels of small dense LDL and high levels of large buoyant HDL in the HVs as well as high levels of large buoyant LDL and total HDL in patients with MS. We conclude that the presence of MS weakens or abolishes the strong associations between adiponectin and the lipoprotein parameters observed in HVs and disturbs the complex interplay between adiponectin and lipoprotein metabolism. Full article

(This article belongs to the Special Issue Lipoprotein Metabolism in Health and Disease 2.0)

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