Cited by 96Lipoproteins and Cardiovascular HealthLipid metabolism and disordersCholesterol and Lipid Metabolism

Effects of Statins on Triglyceride Metabolism

Open access
Ginsberg, Henry N·1998·The American Journal of Cardiology

Abstract

Hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or "statins," have been extremely efficacious in decreasing low-density lipoprotein (LDL) cholesterol levels in patients with hypercholesterolemia and in treating patients with dysbetalipoproteinemia, a relatively rare form of hyperlipidemia. Clinical trials have indicated that statins can significantly lower very-low-density lipoprotein (VLDL) triglyceride levels, although the central mechanism of action of statins-i.e., increasing the number of LDL receptors-would appear to suggest that they would have no significant effect on VLDL levels. Through a review of published data from animal and human studies, this article addresses the important clinical question of how drugs that inhibit the rate-limiting enzyme for cholesterol can affect triglyceride metabolism.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/s0002-9149(98)00035-6

Cites

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Statins reduce plasma TG concentrations, with modest clinically meaningful reductions, particularly in individuals with elevated baseline TG and comorbid metabolic conditions such as type 2 diabetes and obesity.

    “While statins are primarily prescribed for their potent LDL-C-lowering effects, they also exert a modest yet clinically meaningful impact on TG levels and TRLs, making them foundational therapy in patients with high TG and elevated cardiovascular risk [68].”

    From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [68]

    The Abstract reports that statins lower plasma triglycerides and can reduce VLDL triglycerides by 35–45% in patients with significant hypertriglyceridemia; it also describes their potent LDL-lowering effects. The Conclusions frame extending statin use to a wider group with high triglycerides and coronary risk as a possibility warranting further study, not an established basis for calling them foundational therapy in that group. The passages do not establish a particular benefit in people with type 2 diabetes or obesity. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Statins decrease hepatic VLDL synthesis, upregulate LDL receptors, and enhance clearance of apoB-containing lipoproteins, including remnant particles.

    “From a mechanistic standpoint, statins decrease hepatic VLDL synthesis, upregulate LDL receptors, and enhance clearance of apoB-containing lipoproteins, including remnant particles [68].”

    From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [68]

    The Conclusions (page unavailable) say statins appear to inhibit VLDL assembly and secretion, and the Abstract says they increase hepatic LDL receptors. The review discusses increased remnant removal as a possible mechanism and reports remnant clearance in dysbetalipoproteinemia, but its Conclusions note no increase in VLDL or LDL apoB fractional clearance in the authors’ own studies. The claim presents enhanced clearance of apoB-containing lipoproteins as a general, established effect without that qualification. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

No references could be resolved yet.

Research works printed but not linked: 17

  1. Dixon JL, Ginsberg HN. Regulation of hepatic secretion of apolipoprotein B-containing lipoproteins: information obtained from cultured liver cells. J Lipid Res 1993;34:167-179.
  2. Bennett MK, Lopez JM, Sanchez HB, Osborne TF. Sterol regulation of fatty acid synthase promoter: coordinate feedback regulation of two major lipid path- ways. J Biol Chem 1995;270:25578 -25583.
  3. Lopez JM, Bennett MK, Sanchez HB, Rosenfeld JM, Osborne TF. Sterol regulation of acetyl coenzyme A carboxylase: a mechanism for coordinate control of cellular lipid. Proc Natl Acad Sci USA 1996;93:1049 -1053.
  4. Kawabe Y, Sato R, Matsumoto A, Honda M, Wada Y, Yazaki Y, Endo A, Takano T, Itakura H, Kodama T. Regulation of fatty acid synthase expression by cholesterol in human cultured cells. Biochem Biophys Res Com 1996;219:515- 520.
  5. Humble E, al-Shurbaji A, Lund E, Berglund L. Studies on rat liver phosphati- date phosphohydrolase and plasma lipids: effect of HMG-CoA reductase inhib- itors. Biochim Biophys Acta 1994;1214:32-38.
  6. Yanagita T, Yamamoto K, Ishida S, Sonda K, Morito F, Saku K, Sakai T. Effects of simvastatin, a cholesterol synthesis inhibitor, on phosphatidylcholine synthesis in HepG2 cells. Clin Ther 1994;16:200 -208.
  7. Khan B, Wilcox HG, Heimberg M. Cholesterol is required for secretion of very low density lipoprotein by rat liver. Biochem J 1989;258:807-816.
  8. Kasim SE, LeBoeuf RC, Khilnani S, Tallapaka L, Dayananda D, Jen KC. Mechanisms of triglyceride-lowering effect of an HMG-CoA reductase inhibitor in a hypertriglyceridemic animal model, the Zucker obese rat. J Lipid Res 1992;33:1-7.
  9. 34B THE AMERICAN JOURNAL OF CARDIOLOGYா VOL. 81 (4A) FEBRUARY 26, 1998
  10. Krause BR, Newton RS. Lipid-lowering activity of atorvastatin and lovastatin in rodent species: triglyceride-lowering in rats correlates with efficacy in LDL animal models. Atherosclerosis 1997;117:237-244.
  11. Kasim SE, Elovson J, Khilnani S, Almario RU, Jen KL. Effect of lovastatin on the secretion of very low density lipoprotein lipids and apolipoprotein B in the hypertriglyceridemic Zucker obese rat. Atherosclerosis 1993;104:147-152.
  12. Maeda E, Yoshino G, Matsushita M, Nagata K, Morita M, Naka Y, Kazumi T. Effect of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor on triglyceride kinetics in chronically streptozotocin-diabetic rats. Metabolism 1993; 42:52-57.
  13. Shiomi M, Ito T. Pravastatin sodium, a competitive inhibitor of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreases the cholesterol content of newly secreted very-low-density lipoprotein in Watanabe heritable hyperlipidemic rabbits. Metabolism 1994;43:559 -564.
  14. Huff MW, Telford DE. Regulation of low density lipoprotein apoprotein B metabolism by lovastatin and cholestyramine in miniature pigs: effects on LDL composition and synthesis of LDL subfractions. Metabolism 1989;38:256 -264.
  15. Ginsberg HN, Le N, Short MP, Ramakrishnan R, Desnick RJ. Suppression of apolipoprotein B production during treatment of cholesteryl ester storage disease with lovastatin: implications for regulation of apolipoprotein B synthesis. J Clin Invest 1987;80:1692-1697.
  16. Arad Y, Ramakrishnan R, Ginsberg HN. Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production. J Lipid Res 1990;31:567-582.
  17. Arad Y, Ramakrishnan R, Ginsberg H. Effects of lovastatin therapy on very-low-density lipoprotein triglyceride metabolism in subjects with combined hyperlipidemia: evidence for reduced assembly and secretion of triglyceride-rich lipoproteins. Metabolism 1992;41:487-493.

Cited by

Sorted by citations

Authors
Ginsberg, H. N.
Affiliations
Columbia University (US)
Corresponding author
Ginsberg, Henry N
Venue
The American Journal of Cardiology
Publisher
Elsevier BV
Published
1998-02
Volume
81
Issue
4
Pages
32B-35B
ISSN
0002-9149 (ISSN-L)
OpenAlex
W2047597521
Cited by
96
References
0
Citations by year
2026: 4 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 2 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 1
FWCI
6.65
Type
journal article
Language
en
Open access
Locations
  • The American Journal of Cardiology (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Keywords
statins, triglyceride metabolism, VLDL triglycerides, LDL cholesterol, hypercholesterolemia, dysbetalipoproteinemia, LDL receptor, cholesterol biosynthesis
MeSH terms
Animals, Hypolipidemic Agents, Humans, Hypercholesterolemia, Hyperlipoproteinemia Type III, Cholesterol, LDL, Lipoproteins, VLDL, Receptors, LDL, Triglycerides, Hydroxymethylglutaryl-CoA Reductase Inhibitors

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