Potential Contribution of Short Chain Fatty Acids to Hepatic Apolipoprotein A-I Production.

Abstract

Apolipoprotein A-I (ApoA-I) is the major protein of high density lipoprotein (HDL) particles and has a crucial role in reverse cholesterol transport (RCT). It has been postulated that elevating production of de novo ApoA-I might translate into the formation of new functional HDL particles that could lower cardiovascular disease (CVD) risk via RCT. During inflammation, serum ApoA-I concentrations are reduced, which contributes to the development of dysfunctional HDL particles as Serum Amyloid A (SAA) overtakes the position of ApoA-I within the HDL particles. Therefore, instead of elevating serum HDL cholesterol concentrations, rescuing lower serum ApoA-I concentrations could be beneficial in both normal and inflamed conditions. Several nutritional compounds, amongst others short chain fatty acids (SCFAs), have shown their capacity to modulate hepatic lipoprotein metabolism. In this review we provide an overview of HDL and more specific ApoA-I metabolism, SCFAs physiology and the current knowledge regarding the influence of SCFAs on ApoA-I expression and synthesis in human liver cells. We conclude that the current evidence regarding the effect of SCFAs on ApoA-I transcription and secretion is promising, however there is a need to investigate which dietary fibres could lead to increased SCFAs formation and consequent elevated ApoA-I concentrations.

• Authors: Herman E Popeijus, Willem Zwaan, Jehad Z Tayyeb, Jogchum Plat
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 22 Issue 11 (Jun 01 2021) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 34206021 (Publication Type: Journal Article, Review)

Chemical References

• APOA1 protein, human
• Apolipoprotein A-I
• Fatty Acids, Volatile
• Serum Amyloid A Protein
• Cholesterol

Topics

• Apolipoprotein A-I (genetics, metabolism)
• Cholesterol (genetics, metabolism)
• Fatty Acids, Volatile (genetics, metabolism)
• Humans
• Inflammation (genetics, metabolism, pathology)
• Liver (metabolism)
• Serum Amyloid A Protein (genetics, metabolism)