Written by Susan Sweeny Johnson, PhD, Biochemestry. 53 males who supplemented with 150 mg of CoQ10 for 14 days had a 13 % decrease in total LDL cholesterol, most of which was the very atherogenic high density LDL.
Ubiquinol (Q10H2) is the reduced form of ubiquinone (CoQ10). In the body, CoQ10 cycles between reduced and oxidized states in the electron transport chain of the mitochondria. Its function is critical for the production of cellular energy as ATP. In addition, ubiquinol is a powerful antioxidant, slowing damaging oxidation of fats and protein in the body.
Previously the authors of this paper have determined that supplementation with ubiquinol reduces the release of pro-inflammatory molecules in vitro(1). They determined that ubiquinol but not ubiquinone, had a marked effect on certain mouse genes involved in cholesterol synthesis, lipid metabolism and lipoprotein metabolism. (2)
In this new study, the authors looked at connections between ubiquinol-induced gene expression and physiological effects, primarily alterations in LDL cholesterol and red blood cell production. Fifty-three healthy males, aged 21-28 years, were given 150 mg ubiquinol per day with meals for 14 days. Plasma levels of ubiquinol increased about 4.8 fold at 14 days compared to baseline. After a four-week washout period, ubiquinol levels returned to baseline.
Samples of monocytes from the participant’s blood were analyzed for changes in expression of genes. Analysis of the 272 genes activated by ubiquinol supplementation showed that these affected genes were involved in inflammation, cell death, and cell differentiation.
Since formation of red blood cells is a process of cell differentiation, the distribution of the various types of red blood cells in the plasma of subjects after supplementation was determined to see if genetic changes could be correlated to physiological ones. Observed changes in blood cells showed a decrease in erythrocytes (mature red blood cells) (p= 0.02) and an increase in reticulocytes (immature red blood cells) (p<0.001). Thus, changes in gene expression correlated to observed physical changes.
One of the genes affected by ubiquinol supplementation plays a key role in lipid metabolism (3), thus changes in LDL cholesterol were examined. Total LDL cholesterol was reduced approximately 13% (p<0.001). Additionally, most of the reductions were in the higher density LDLs, which are most atherogenic.
Finally, the presence of inflammatory proteins in the blood was measured as the gene changes would predict. No changes in the amount of these proteins were detected.
In conclusion, altered gene expression that correlated with ubiquinol supplementation also corresponded to significant physiological changes in the plasma LDL cholesterol and red blood cell differentiation but not with the presence of inflammatory proteins.
Source: Constance Schmelzer, Petra Niklowitz, Ju¨rgen G. Okun, Dorothea Haas, Thomas Menke and Frank Do¨ring. Ubiquinol-Induced Gene Expression Signatures are Translated into Altered Parameters of Erythropoiesis and Reduced Low Density Lipoprotein Cholesterol Levels in Humans. Life, 63(1): 42–48, January 2011.
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Posted September 19, 2011.
References:
- Schmelzer, C, et al. In vitro effects of the reduced form of Coenzyme Q10 on secretion levels of TNF-alpha and chemokines in response to LPS in the human monocytic cell line THP-1. J Clin Biochem Nutr. 2009, 44: 62-66.
- Schmelzer, C., Kubo, H., Mori, M., Sawashita, J., Kitano, M., Hosoe, K.,
Boomgaarden, I., Do¨ring, F., and Higuchi, K. (2009) Supplementation with the reduced form of Coenzyme Q(10) decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator-activated receptor-alpha gene expression signature in SAMP1 mice. Mol. Nutr. Food Res. 54, 805–815. - Ricote, M., Valledor, A. F. and Glass, C. K. (2004) Decoding transcriptional programs regulated by PPARs and LXRs in the macrophage: effects on lipid homeostasis, inflammation, and atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 24, 230–239.
- See the Preventive Cardiovascular Nurses Association website.
- Heart Disease and Stroke Statistics: 2009 Update. American Heart Association. January 13, 2009.
