Fasting Triglycerides and Peroxisomal Function (B109)

Maintaining low fasting triglycerides is essential to optimal health. High fasting triglycerides are indicative of mitochondrial or peroxisomal impairment, the two organelles responsible for fatty acid metabolism in our cells. 

To access the FREE seminars with full presentations and videos please visit Dr. Goodenowe’s resource site here. This is the article for seminar B109, Blood Tests and Biomarkers (Series B).

Peroxisomes and mitochondria are physically distinct organelles that are in all cells of the body (except red blood cells). Although their biochemical purposes are very distinct, they are highly synchronized. As mentioned above, mitochondria are the most important and most highly conserved of all human organelles. The primary purpose of the peroxisome is to help regulate and maintain constant mitochondrial function. It does this by adjusting fatty acid and fatty acid derived acetyl-CoA load to the mitochondria. Both mitochondria and peroxisomes contain β-oxidation enzymes to break down fatty acids into acetyl-CoA, but only mitochondria have a citric acid cycle to create CO2 and an electron transport chain to create ATP. Unlike mitochondria which are purely catabolic, peroxisomes are flexible and anabolic. The by-products created from its β-oxidation activities are used as building blocks for other biochemical pathways. 

Peroxisomes can metabolize a wide array of saturated and polyunsaturated fatty acids. Normally only 20-30% of palmitic acid (16:0), the pure energy saturated fatty acid used by mitochondria, is metabolized in the peroxisome; however, the amount of palmitic acid metabolized in the peroxisome depends on mitochondrial function/capacity. Regardless of the size or type of the starting fatty acid, peroxisomal β-oxidation is never complete, it stops at a medium chain fatty acid (8:0). These medium chain fatty acids are either transported to the mitochondria for final and complete oxidation or converted to fatty alcohols in the peroxisome to make plasmalogens. 

The acetyl-CoA created by peroxisomal β-oxidation is not used as an energy source. It is the primary carbon source for cholesterol synthesis, plasmalogen synthesis, and fatty acid synthesis. Peroxisomes are where plasmalogens, DHA, and EPA are made.  

Combined peroxisomal and mitochondrial fatty acid oxidation capacity is what regulates fatty acid metabolism. Impairments in either of these systems results in elevated fasted blood triglyceride levels. Impaired peroxisomal function due to aging or toxicity results in decreased biosynthesis of plasmalogens and DHA and increased levels of pro-inflammatory very long chain fatty acids (VLCFA). This also creates mitochondrial overload and stress which results in mitochondria switching to an anabolic source of acetyl-CoA, which is a pro-cancer phenotype.  

In contrast, an overloaded peroxisomal system due to mitochondrial insufficiency results in excess DHA and plasmalogen biosynthesis, increased VLCFA, and increased oxidative stress. 

ProdromeScan measures selected ethanolamine and choline plasmalogen species along with their phosphatidyl counterparts to measure overall plasmalogen biosynthesis. It also measures substrates and products of β-oxidation as well as total fasting triglycerides to get a thorough assessment of peroxisomal function. 

Dr. Goodenowe explains the relevant research and literature regarding blood fasting triglyceride levels and peroxisomal function in seminar B109 – Fasting Triglycerides and Peroxisomal Function. 

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