Biochemistry · MU Pleven

26. Lipid Transport in Serum: Cholesterol Transport by Lipoproteins. Metabolism. Role of These Lipoproteins for the Development of Atherosclerosis. Atherogenic Factors.

Covers how cholesterol travels in the blood within lipoproteins, taking LDL, HDL and the VLDL to IDL to LDL pathway in turn, including their metabolism and roles. It then explains how LDL and oxidised LDL drive atherosclerosis step by step, from endothelial injury to plaque rupture, and why HDL is protective. It closes with a list of atherogenic factors and a short clinical summary of therapy goals.

Inside: 6 sections · 6 labelled pictures · 10 flashcards · 3 min

Topic 26 of 76 in the MU Pleven syllabus for Biochemistry (Medicine, Year 2). The free AceMed note covers it in 6 sections, about 388 words (3 min of reading), with 10 flashcards.

In this note

  1. Lipid Transport in Serum: Cholesterol Transport by Lipoproteins.
  2. Cholesterol Transport in Serum
  3. Metabolism of Cholesterol-Transporting Lipoproteins
  4. Role of Lipoproteins in Atherosclerosis
  5. Atherogenic Factors (Increase Risk of Atherosclerosis)
  6. Clinical Meaning

Cholesterol Transport in Serum

  • Cholesterol is essential for:
  • Cell membrane fluidity
  • Steroid hormone synthesis
  • Bile acid and vitamin D formation
  • Cholesterol is hydrophobic, so it must be transported in blood within lipoproteins.
  • Major lipoproteins involved:
  • LDL → delivers cholesterol to tissues
  • HDL → removes cholesterol from tissues
  • VLDL → IDL → LDL pathway is central to cholesterol circulation.

Metabolism of Cholesterol-Transporting Lipoproteins

A) LDL (Low-Density Lipoprotein) — “Bad Cholesterol”

  • Formed from VLDL after TAGs are removed.
  • Contains ApoB-100 → allows binding to LDL receptors on cells.
  • Delivers cholesterol to peripheral tissues for:
  • Cell membrane synthesis
  • Hormone synthesis
  • If LDL is excessive:
  • It accumulates in blood vessel walls → leading to plaques
  • Oxidized LDL is taken up by macrophages → forming foam cells → early atherosclerotic lesion.

B) HDL (High-Density Lipoprotein) — “Good Cholesterol”

  • Synthesized in liver and intestine.
  • Contains ApoA-I, which activates LCAT.
  • Collects excess cholesterol from:
  • Peripheral tissues
  • Arteries
  • Macrophages
  • Converts cholesterol → cholesteryl esters → carried back to liver.
  • This process is called Reverse Cholesterol Transport.
  • Protective effect → reduces risk of atherosclerosis.

C) VLDL → IDL → LDL Pathway

  • Liver packages triglycerides + cholesterol → VLDL.
  • LPL removes TAGs from VLDL → becomes IDL.
  • IDL is partly:
  • Taken up by liver, or
  • Further processed → LDL.
  • LDL circulates for hours → higher chance of oxidation → more atherogenic.

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