Acylation-stimulating protein is a surrogate biomarker for acute myocardial infarction: Role of statins

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

BACKGROUND:

Acylation-stimulating protein (ASP) is an adipokine synthesized within adipocytes environment due to adipocyte differentiation.

AIM:

The aim of this study was to assess changes in ASP levels in patients with acute myocardial infarction (MI) and to correlate these variations with disease variables.

SUBJECTS AND METHODS:

A total number of 111 patients previously and currently treated with rosuvastatin or atorvastatin presented with acute MI in a Coronary Care Unit, were divided into three groups, Group A: Thirty-nine patients treated with atorvastatin, Group B: Thirty patients treated with rosuvastatin, compared to 42 patients presented with MI not previously treated with statins were enrolled in this study. ASP and troponin-I levels and lipid profile were estimated in each group.

RESULTS:

The effects of atorvastatin and rosuvastatin compared to nonstatins-treated group on the anthropometric and biochemical variables in patients with acute MI showed significant difference in all biochemical and anthropometric parameters P < 0.05. Serum ASP (nmol/l) levels were higher in control patients 57.25 ± 9.15 compared to atorvastatin-treated patients 48.43 ± 7.42 and rosuvastatin-treated patients 49.33 ± 6.52 P = 0.0124.

CONCLUSION:

ASP levels are elevated in patients with acute MI and regarded as surrogate biomarker for acute MI also; therapy with statins leads to significant reduction in ASP levels compared to nonstatins-treated patients that presented with acute MI.

Related collections

Most cited references 28

Record: found
Abstract: found
Article: not found

Critical review of acylation-stimulating protein physiology in humans and rodents.

L. Chen, Katherine Cianflone, Q. Z. Xia (2003)

In the last few years, there has been increasing interest in the physiological role of acylation-stimulating protein (ASP). Recent studies in rats and mice, in particular in C3 (-/-) mice that are ASP deficient, have advanced our understanding of the role of ASP. Of note, the background strain of the mice influences the phenotype of delayed postprandial triglyceride clearance in ASP-deficient mice. Administration of ASP in all types of lean and obese mice studied to date, however, enhances postprandial triglyceride clearance. On the other hand, regardless of the background strain, ASP-deficient mice demonstrate reduced body weight, reduced leptin and reduced adipose tissue mass, suggesting that ASP deficiency results in protection against development of obesity. In humans, a number of studies have examined the relationship between ASP, obesity, diabetes and dyslipidemia as well as the influence of diet, exercise and pharmacological therapy. While many of these studies have small subject numbers, interesting observations may help us to better understand the parameters that may influence ASP production and ASP action. The aim of the present review is to provide a comprehensive overview of the recent literature on ASP, with particular emphasis on those studies carried out in rodents and humans.

0 comments Cited 46 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Complement C3 and cleavage products in cardiometabolic risk.

Altan Onat, Gunay Can, Reza Rezvani … (2011)

This review summarizes available evidence on the role of serum complement component 3 (C3), produced by liver, adipocytes and activated macrophages at inflammation sites, and C3 cleavage products linking lipoproteins and metabolism to immunity. C3 and cleavage products are modified in several associated metabolic disorders including obesity, insulin resistance, type-2 diabetes, dyslipidemia, and cardiovascular diseases. Circulating C3 is independently and linearly associated with serum triglycerides, C-reactive protein (CRP), waist circumference and in some populations inversely with current smoking. The complement cascade is activated during myocardial ischemia and likely mediates immune and inflammatory responses in ischemic myocardium. Serum complement activation is elevated in unstable rather than stable angina pectoris suggesting added contribution to damage extension in acute coronary syndromes. In logistic regression models for incident metabolic syndrome (MetS), increasing C3 concentrations predicted MetS in women, after adjusting for continuous values of 3 major MetS components and other confounders, with a relative risk similar in magnitude to an established component suggesting elevated C3 likely constitutes part of the cluster of MetS in women. C3 interacts with MetS in men for independently conferring risk of incident type-2 diabetes and coronary heart disease (CHD). In women, though C3 is equally predictive of cardiometabolic risk, it is less so additively to MetS components or to CRP. Evidence suggests that circulating C3 might serve as a signal for an immune process that enhances - via mediation of increased apolipoprotein (apo) E levels - the development of dysfunctional apoA-I particles rendering them diabetogenic and atherogenic in populations prone to MetS or subsets of populations harboring impaired glucose tolerance. C3 activation also leads to production of chemoattractants C3a and C5a, and acylation stimulating protein (ASP, C3adesArg), a lipogenic hormone, which contribute additionally to the metabolic phenotypes generated. These observations have clinical and public health implications. Copyright © 2011. Published by Elsevier B.V.

0 comments Cited 35 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Adipocyte differentiation-related protein promotes fatty acid storage in cytosolic triglycerides and inhibits secretion of very low-density lipoproteins.

Michel Rosquete, P Stillemark-Billton, Björn Magnusson … (2006)

We investigated the role of adipocyte differentiation-related protein (ADRP) in triglyceride turnover and in the secretion of very low-density lipoprotein (VLDL) from McA-RH7777 cells and primary rat hepatocytes. An increase in the expression of ADRP increased triglyceride accumulation in cytosolic lipid droplets and prevented the incorporation of fatty acids into secretable triglycerides, thereby reducing the secretion of triglycerides as well as of apolipoprotein B-100 (apoB-100) and apoB-48 VLDL. The ability of ADRP to block the secretion of apoB-100 VLDL1 decreased with increasing quantities of fatty acids in the medium, indicating a saturable process and emphasizing the importance of sequestering of fatty acids for the effect of ADRP on VLDL secretion. Knockdown (small interfering RNA) of ADRP decreased the pool of cytosolic lipid droplets but increased only the secretion of apoB-48 VLDL1. Additionally, there was an increased flow of fatty acids into beta-oxidation. ADRP is essential for the accumulation of triglycerides in cytosolic lipid droplets. An increase in ADRP prevents the formation of VLDL by diverting fatty acids from the VLDL assembly pathway into cytosolic triglycerides, whereas a decrease of the protein increases the sorting of fatty acids to beta-oxidation and promotes the secretion of apoB-48 VLDL1.

0 comments Cited 31 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): J Lab Physicians

Journal ID (iso-abbrev): J Lab Physicians

Journal ID (publisher-id): JLP

Title: Journal of Laboratory Physicians

Publisher: Medknow Publications & Media Pvt Ltd (India )

ISSN (Print): 0974-2727

ISSN (Electronic): 0974-7826

Publication date (Print): Jul-Sep 2017

Volume: 9

Issue: 3

Pages: 163-169

Affiliations

[1] Department of Pharmacology, Toxicology and Medicine, College of Medicine, Almustansiriya University, Baghdad, Iraq

Author notes

Address for correspondence: Dr. Hayder M. Al-Kuraishy, Department of Pharmacology, Toxicology and Medicine, College of Medicine, Almustansiriya University, P.O. Box 14132, Baghdad, Iraq. E-mail: hayderm36@ 123456yahoo.com

Article

Publisher ID: JLP-9-163

DOI: 10.4103/0974-2727.208263

PMC ID: 5496293

PubMed ID: 28706385

SO-VID: b6f67ad4-585f-498f-98e9-aee17a949177

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

Acylation-stimulating protein is a surrogate biomarker for acute myocardial infarction: Role of statins

Read this article at

Abstract

BACKGROUND:

AIM:

SUBJECTS AND METHODS:

RESULTS:

CONCLUSION:

Related collections

Journal of Circulating Biomarkers

Most cited references 28

Critical review of acylation-stimulating protein physiology in humans and rodents.

Complement C3 and cleavage products in cardiometabolic risk.

Adipocyte differentiation-related protein promotes fatty acid storage in cytosolic triglycerides and inhibits secretion of very low-density lipoproteins.

Author and article information

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 220

Cited by 19

Most referenced authors 549