Alteration of the Copy Number of Mitochondrial DNA in Leukocytes of Patients with Hyperlipidemia
Abstract
A bstract: Lipid metabolism in leukocytes may be disturbed by mitochondrial dysfunction caused by depletion of mitochondrial DNA (mtDNA) in response to an increase of oxidative stress in blood circulation. It is possible that alteration in mtDNA copy number of the leukocyte is involved in the impairment of the scavenging of oxidatively modified plasma proteins such as oxidized low‐density lipoprotein (oxLDL). To test this hypothesis, we recruited 91 healthy subjects and 63 patients with hyperlipidemia (LDL >130 mg/dL) for this study. The copy number of mtDNA in the leukocyte and the titer of oxLDL IgG autoantibody (oLAB) were determined as indices of the oxidative stress response of immune cells. The results revealed a significant higher level of plasma oxLDL, lower titer of oLAB, and decreased copy number of mtDNA in patients with hyperlipidemia (P <0.05). In the analysis of partial correlations under age control, we found that an increase in the copy number of mtDNA was positively correlated with an increase in the level of oLAB (P <0.005, r= 0.3002) and a decrease in the oxLDL level (P <0.05, r=−0.2654) in healthy subjects but not in patients. Based on the results obtained from this case‐control study, we conclude that the increase of mtDNA copy number might provide the leukocyte an increased capability of scavenging oxLDL, possibly by enhanced generation of oLAB in healthy subjects, but not in hyperlipidemic patients who had lower mtDNA copy numbers in their leukocytes. Taken together, these findings suggest that an alteration of mtDNA copy number in the leukocyte may be one of the risk factors for hyperlipidemia.
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Reduced mtDNA copy number is observed in cardiovascular risk factors independent of atherosclerosis, such as hyperlipidaemia.
“Finally, a reduction in mtDNA copy number has also been observed in cardiovascular risk factors independent of atherosclerosis, such as hyperlipidaemia179.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [179]
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Mitochondrial and metabolic dysfunction in ageing and age-related diseases
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- Authors
- LIU, C., KUO, C., CHENG, W., HUANG, C., LEE, C., & WEI, Y.
- Affiliations
- Changhua Christian Hospital (TW)
- National Yang Ming University (TW)
- Corresponding author
- WEI, YAU‐HUEI
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2005-05
- Volume
- 1042
- Issue
- 1
- Pages
- 70-75
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2045264023
- Cited by
- 41
- References
- 15
- Citations by year
- 2024: 4 · 2023: 1 · 2022: 1 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 3 · 2015: 2 · 2014: 5 · 2013: 2 · 2012: 6
- FWCI
- 0.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Council
- National Health Research Institutes
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- mitochondrial DNA copy number, hyperlipidemia, leukocytes, oxidative stress, oxidized LDL, lipid metabolism, mitochondrial dysfunction
- MeSH terms
- DNA, Mitochondrial, Female, Humans, Hyperlipidemias, Leukocytes, Lipoproteins, LDL, Male, Middle Aged, Gene Dosage
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