Microalga Decreases Plasma Cholesterol by Down-regulation of Intestinal NPC1L1, Hepatic LDL Receptor, and HMG-CoA Reductase

Jingnan Chen, Yue Jiang*, Ka Ying Ma, Feng Chen, Zhen Yu Chen*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

30 Citations (Scopus)

Abstract

The present study examined the cholesterol-lowering activity of algal powder (AP), algal lipids (AL), and algal residue (AR) and their interaction with genes of transporters, receptors, and enzymes involved in cholesterol absorption and metabolism. In this experiment, 48 hamsters were fed either control diet or one of the three experimental diets containing 2% AP, 1.0% AL, or 1.0% AR for 6 weeks. Plasma total cholesterol (TC) and non-high-density- lipoprotein-cholesterol (non-HDL-C) were significantly decreased in the AP and AL groups but not in the AR group compared with those in the control hamsters. It was found that the cholesterol-lowering activity of AP and AL was associated with down-regulation of hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, low-density lipoprotein receptor (LDLR), and intestinal Niemann-Pick C1-like 1 (NPC1L1) transporter. It was concluded that the alga possessed the cholesterol-lowering activity and its lipids were the active ingredients. The mechanisms underlying the cholesterol-lowering activity of algae were mediated most likely by increasing the sterol excretion and decreasing the cholesterol absorption and synthesis.

Original languageEnglish
Pages (from-to)6790-6797
Number of pages8
JournalJournal of Agricultural and Food Chemistry
Volume59
Issue number12
Early online date23 May 2011
DOIs
Publication statusPublished - 22 Jun 2011

User-Defined Keywords

  • HMG-CoA reductase
  • LDL receptor
  • microalga
  • NPC1L1
  • total cholesterol

Fingerprint

Dive into the research topics of 'Microalga Decreases Plasma Cholesterol by Down-regulation of Intestinal NPC1L1, Hepatic LDL Receptor, and HMG-CoA Reductase'. Together they form a unique fingerprint.

Cite this