Apolipoprotein B

Not just a biomarker but a causal factor in hepatic endoplasmic reticulum stress and insulin resistance

Qiaozhu Su, Angela C. Rutledge, Mark Dekker, Khosrow Adeli

Research output: Contribution to journalReview article

4 Citations (Scopus)

Abstract

Insulin resistance is associated with dyslipidemia, which is initiated largely by the overproduction of VLDL particles. VLDL particles are produced in the liver via lipidation of nascent ApoB molecules in the endoplasmic reticulum (ER). In insulin-resistant states, excess flux of free fatty acids to the liver can lead to ApoB accumulation in the ER, causing ER stress. Recent studies reveal a critical role of hepatic ER stress and the unfolded protein response in the development of insulin resistance. This review summarizes the intersections between the three branches of unfolded protein response signaling and hepatic lipogenesis, presents recent findings regarding lipid-induced ER stress and the role of ApoB in the development of hepatic ER stress and insulin resistance, and briefly discusses the clinical utility of ApoB as a potential drug target.

Original languageEnglish (US)
Pages (from-to)267-276
Number of pages10
JournalClinical Lipidology
Volume5
Issue number2
DOIs
StatePublished - Apr 1 2010

Fingerprint

Endoplasmic Reticulum Stress
Apolipoproteins B
Insulin Resistance
Biomarkers
Liver
Unfolded Protein Response
Endoplasmic Reticulum
Lipogenesis
Dyslipidemias
Heat-Shock Proteins
Nonesterified Fatty Acids
Insulin
Lipids
Pharmaceutical Preparations

Keywords

  • ApoB
  • Dyslipidemia
  • Endoplasmic reticulum stress
  • Insulin resistance
  • Lipid
  • Unfolded protein response

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine

Cite this

Apolipoprotein B : Not just a biomarker but a causal factor in hepatic endoplasmic reticulum stress and insulin resistance. / Su, Qiaozhu; Rutledge, Angela C.; Dekker, Mark; Adeli, Khosrow.

In: Clinical Lipidology, Vol. 5, No. 2, 01.04.2010, p. 267-276.

Research output: Contribution to journalReview article

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