CoChat
Sign Up
Cited by 277Lipoproteins and Cardiovascular HealthParaoxonase enzyme and polymorphismsLipid metabolism and disorders

Genetic Cholesteryl Ester Transfer Protein Deficiency Is Extremely Frequent in the Omagari Area of Japan: Marked Hyperalphalipoproteinemia Caused by CETP Gene Mutation Is Not Associated With Longevity

Hirano, Ken-ichi, Yamashita, Shizuya, Nakajima, Norimichi, Arai, Takeshi, Maruyama, Takao, Yoshida, Yu, Ishigami, Masato, Sakai, Naohiko +2 more·1997·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/01.atv.17.6.1053
Open this paper in CoChat — free account

Abstract

Abstract Low levels of HDL cholesterol have been clearly demonstrated to be associated with an increased incidence of coronary heart disease, strongly suggesting that HDL particles have an antiatherogenic function. However, little information has been available concerning the atherogenicity of a marked hyperalphalipoproteinemia (HALP). There is no agreement about whether plasma cholesteryl ester transfer protein (CETP) deficiency is associated with an antiatherogenic state or not, although this disorder was reported to be one of the major causes of marked HALP. In the current study, we have found a unique area (Omagari City, Akita Prefecture, Japan) where CETP deficiency caused by a G-to-A mutation at the 5′ splice donor site of intron 14 in the CETP gene is extremely frequent. In Omagari City, the mutation was detected more than 20 times more frequently and the prevalence of a marked HALP with plasma HDL cholesterol ≥2.58 mmol/L (100 mg/dL) was 5 to 10 times higher than in other areas of Japan. This discovery has made it possible to perform a large population-based study concerning the atherogenicity of a marked elevation of HDL cholesterol in a genetically more homogeneous population. There was a statistically significant U-shaped relationship between HDL cholesterol levels and the incidence of ischemic changes in electrocardiograms. In cases of HDL cholesterol <1.81 mmol/L (70 mg/dL), the incidence increased in proportion to the levels of HDL cholesterol. The frequency of the CETP gene mutation was higher in patients with coronary heart disease than in healthy control subjects. In subjects aged >80 years, the prevalence of both marked HALP and the intron 14 splicing defect was significantly lower than in the younger generation. The current study indicated for the first time that a marked HALP caused by CETP gene mutation may not represent a longevity syndrome, suggesting the importance of reevaluation of the clinical significance and pathophysiology of a marked HALP.

Integrity signals

Registry

Crossref · 10.1161/01.atv.17.6.1053

Cites

40 of 40 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Hirano, K.-I., Yamashita, S., Nakajima, N., Arai, T., Maruyama, T., Yoshida, Y., Ishigami, M., Sakai, N., Kameda-Takemura, K., & Matsuzawa, Y.
Affiliations
  • The University of Osaka (JP)
  • From the Second Department of Internal Medicine, Osaka University Medical School (K-i.H., S.Y., T.A., T.M., Y.Y., M.I., N.S., K.K.-T., Y.M.), and the Nakajima Clinic, Akita (N.N.), Japan.
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1997-06
Volume
17
Issue
6
Pages
1053-1059
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/01.atv.17.6.1053
OpenAlex
W2151720705
Cited by
275
References
40
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 7 · 2020: 4 · 2019: 2 · 2018: 5 · 2017: 5 · 2016: 9 · 2015: 11 · 2014: 9 · 2013: 11 · 2012: 15
FWCI
14.93
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords
hyperalphalipoproteinemia, HDL cholesterol, coronary artery disease, atherogenicity, genetic prevalence
MeSH terms
Aged, Carrier Proteins, Female, Glycoproteins, Humans, Japan, Lipid Metabolism, Inborn Errors, Lipoproteins, HDL, Longevity, Male, Middle Aged, Cholesterol Ester Transfer Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review