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Pathophysiology of hypertriglyceridemia

H C Hassing1, R P Surendran, H L Mooij

  • 1Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.

Biochimica Et Biophysica Acta
|December 20, 2011
PubMed

Insights

Triglycerides (TG) are increasingly recognized as independent cardiovascular disease (CVD) risk factors, despite current guideline exclusions. Understanding TG pathophysiology reveals new therapeutic targets for hypertriglyceridemia.

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Metabolic Diseases

Background:

  • The role of triglycerides (TG) in cardiovascular disease (CVD) risk is debated.
  • International guidelines currently exclude TG from CVD risk calculators.
  • Recent evidence suggests plasma TG is an independent risk factor for CVD.

Purpose of the Study:

  • To review novel insights into triglyceride pathophysiology.
  • To explore potential new drug targets for hypertriglyceridemia.
  • To discuss future therapeutic strategies for triglyceride homeostasis.

Main Methods:

  • Review of current literature on triglyceride metabolism.
  • Discussion of mechanisms of hypertriglyceridemia: VLDL production, chylomicron synthesis, LPL-mediated lipolysis, and remnant clearance.
  • Focus on the roles of GPIHBP1, apolipoproteins, and heparin sulfate proteoglycans.

Main Results:

  • Hypertriglyceridemia arises from hepatic VLDL production, intestinal chylomicron synthesis, impaired LPL lipolysis, or defective remnant clearance.
  • GPIHBP1 and apolipoproteins are key players in lipolysis.
  • Heparin sulfate proteoglycans are crucial for hepatic remnant clearance.

Conclusions:

  • Understanding triglyceride pathophysiology is essential for developing novel therapies.
  • Targeting lipolysis and remnant clearance pathways offers promise for improving triglyceride homeostasis.
  • Further research is needed to integrate TG levels into CVD risk assessment and management.

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