Physiologic mechanisms for reduced apolipoprotein A-I concentrations associated with low levels of high density lipoprotein cholesterol in patients with normal plasma lipids.
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Low plasma concentrations of high density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apoA-I) are major risk factors for coronary heart disease (CHD). Low HDL levels are common in patients with hypertriglyceridemia, but they also occur in those with normal plasma lipids; the latter include obese patients and cigarette smokers, though other patients with low HDL levels are neither obese nor smokers. The present study was designed to define metabolic causes of low apoA-I levels in normal-weight, normolipidemic patients. ApoA-I tracer studies were carried out in two groups of normolipidemic patients having low HDL levels to determine input rates and residence times for ApoA-I; these patients included 11 nonobese nonsmokers and 11 nonobese cigarette smokers. Their results were compared to those of 20 normal-weight, normolipidemic controls with normal HDL levels and 12 obese nonsmokers also having low HDL. In all three groups manifesting low HDL-cholesterol and low apoA-I levels, residence times for plasma apoA-I were reduced by approximately 30%, compared to control subjects with normal HDL levels. In contrast, average input rates for apoA-I were similar among the three low-HDL patients and control subjects. No differences in apoA-I kinetics were observed among any of the three groups with low apoA-I concentrations. Within each of the four groups of the study, however, input rates for apoA-I were highly correlated with plasma concentrations of apoA-I. Thus, for individuals with normal levels of plasma lipids, both residence times and input rates for apoA-I appeared to be important determinants of apoA-I levels. Residence times for apoA-I were reduced in almost all patients with low apoA-I levels, regardless of concomitant factors, whereas input rates were highly variable among individuals.
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Small HDL in hypertriglyceridemia is associated with hypercatabolism of apolipoprotein A-I and seems related to elevated hepatic lipase activity in central obesity and insulin resistance.
“Small HDL in hypertriglyceridemia is associated with hypercatabolism of apolipoprotein A-I (47, 48), and it seems to be related to elevated hepatic lipase activity in central obesity and insulin resistance (49).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [47]
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- Authors
- Gylling, H., Vega, G., & Grundy, S.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- ORCID
- Gylling, H
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 1992-10
- Volume
- 33
- Issue
- 10
- Pages
- 1527-1539
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2136110856
- Cited by
- 67
- References
- 80
- Citations by year
- 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2012: 2
- FWCI
- 8.31
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Lipid Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Heart, Lung, and Blood Institute (HL-292-52)
- National Center for Research Resources (MO-IRR00633)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- apolipoprotein A-I, HDL cholesterol, normolipidemic patients, cigarette smoking, obesity, coronary heart disease risk, plasma lipids
- MeSH terms
- Aged, Humans, Iodine Radioisotopes, Lipids, Cholesterol, HDL, Male, Middle Aged, Obesity, Risk Factors, Apolipoprotein A-I
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