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Cited by 531Lipid metabolism and disordersDiabetes, Cardiovascular Risks, and LipoproteinsCholesterol and Lipid Metabolism

The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.

Regulation of Plasma Triglycerides in Insulin Resistance and Diabetes

Ginsberg, Henry N., Zhang, Yuan-Li, Hernandez-Ono, Antonio·2005·Archives of Medical Research
DOI 10.1016/j.arcmed.2005.01.005
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Abstract

Increased plasma levels of triglycerides (TG) in very low density lipoproteins (VLDL) are not only common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus (T2DM) but are the central pathophysiologic feature of the abnormal lipid profile. Overproduction of VLDL leads to increased plasma levels of TG which, via an exchange process mediated by cholesterol ester transfer protein (CETP), results in low levels of high density lipoprotein (HDL) cholesterol and apolipoprotein A-I, and the generation of small, dense, cholesterol ester depleted low density lipoproteins (LDL). Increased assembly and secretion of VLDL by the liver results from the complex, post-transcriptional regulation of apolipoprotein B (apoB) metabolism in the liver. In the presence of low levels of hepatic TG and cholesterol, much of the constitutively synthesized apoB is degraded by both proteasomal and non-proteasomal pathways. When excess TG, and to a lesser extent, cholesterol, are present, and in the presence of active microsomal triglycerides transfer protein, apoB is targeted for secretion. The major sources of TG in the liver: uptake of fatty acids (FA) released by lipolysis of adipose tissue TG, uptake of TGFA in VLDL and chylomicrons remnants, and hepatic de novo lipogenesis (the synthesis of FA from glucose) are all abnormally increased in insulin resistance. Treatment of the dyslipidemia in insulin resistant individuals and patients with T2DM has been successful in reducing cardiovascular disease; LDL cholesterol, TG, and HDL cholesterol are all appropriate targets for therapy when diet, exercise, and weight loss do not achieve goals.

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  1. Ginsberg, 1998, Lipoprotein physiology. Chapter 1
  2. Taghibiglou, 2002, Hepatic very low density lipoprotein-ApoB overproduction is associated with attenuated hepatic insulin signaling and overexpression of protein-tyrosine phosphatase 1B in a fructose-fed hamster model of insulin resistance, J Biol Chem, 277, 793, 10.1074/jbc.M106737200 · DOI

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Metadata

Authors
Ginsberg, H. N., Zhang, Y.-L., & Hernandez-Ono, A.
Affiliations
Columbia University (US)
Corresponding author
Ginsberg, Henry N.
ORCID
Ginsberg, Henry N.
Venue
Archives of Medical Research
Publisher
Elsevier BV
Published
2005-05
Volume
36
Issue
3
Pages
232-240
ISSN
  • 0066-6769 (ISSN-L)
  • 0188-4409
DOI
10.1016/j.arcmed.2005.01.005
OpenAlex
W2095612977
Cited by
531
References
57
Citations by year
2026: 11 · 2025: 19 · 2024: 24 · 2023: 27 · 2022: 26 · 2021: 27 · 2020: 34 · 2019: 24 · 2018: 25 · 2017: 27 · 2016: 33 · 2015: 31 · 2014: 20 · 2013: 28 · 2012: 24
FWCI
4.58
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Archives of Medical Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Keywords
plasma triglycerides, insulin resistance, type 2 diabetes, dyslipidemia, VLDL secretion, apolipoprotein B, hepatic triglyceride metabolism, cholesteryl ester transfer protein, HDL cholesterol, small dense LDL, microsomal triglyceride transfer protein, hepatic de novo lipogenesis, lipolysis, cardiovascular disease, lipid-lowering therapy
MeSH terms
Adipose Tissue, Animals, Apolipoproteins B, Cholesterol, Chylomicrons, Diabetes Mellitus, Type 2, Fatty Acids, Humans, Insulin Resistance, Lipoproteins, Lipoproteins, HDL, Lipoproteins, VLDL, Liver, Models, Biological, Triglycerides, Apolipoprotein A-I, Lipid Metabolism

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