Where Does the Energy Come from That Powers Our Skin Cells? Answer: Acyl-Co A (ACAD) and Mitochondria

Introduction

The usual textbook description of mitochondria that a few of us are familiar with is that mitochondria are the power generating house of the cell. However, the range of functions of mitochondria and its role in the development of different pathological disorders is rather more complex. Mitochondria are cellular organelles located within out cells such as our skin cells that comprise their own deoxyribonucleic acid (DNA), also called mitochondrial DNA (mtDNA). Similar to mutations in the nuclear genome, mtDNA mutations can also lead to the onset of various pathological disorders. (Chinnery & Schon, 2003) Mitochondria and associated enzymes play an important role in the regulation of metabolism. Mitochondria also mediate signaling for the cell cycle, modulate embryonic development, and are also involved in neuronal function. (McBride et al., 2006) Mitochondrial acyl-CoA dehydrogenases (ACAD) are involved in the metabolism of amino acids and β-oxidation of fatty acids with subsequent energy production. Mitochondria play an important role in the structure and function of the skin. Mitochondrial dysfunction is associated with different skin pathologies as well as skin aging. (Lucas et al., 2011; Sreedhar et al., 2020) The following sections elaborate on the role of mitochondria in maintaining skin health and how certain ingredients in LipidTAC products can target the mitochondrial enzyme, Acyl-Co A (ACAD), to modulate skin health. 

The Key Functions of Mitochondria 

It is important to know about the key functions of mitochondria prior to the discussion about the consequences of mitochondrial dysfunction. Mitochondria provide sufficient adenosine triphosphate (ATP, cellular energy) to meet the energy requirements of the skin, which is the largest and highest turnover organ of the human body. This ATP (cellular energy) is produced by oxidative phosphorylation in the mitochondria. Mitochondria are also associated with redox homeostasis, respiration, biogenesis, cellular growth, and calcium homeostasis. On the contrary, dysfunctional mitochondria are accompanied by reduced ATP (cellular energy) levels, cell death, oxidative stress, dysfunctional oxidative phosphorylation, calcium imbalance, and altered mitochondrial biogenesis. (Sreedhar et al., 2020)

Β-Oxidation of Fatty Acids and Energy for Skin 

Cells require a constant supply of energy, in the form of ATP, to carry out metabolic functions as well as to divide into progeny cells. Since skin is a high turnover and largest organ of the human body, it requires a sufficient ATP (cellular energy) supply from mitochondria. The β-oxidation of fatty acids produces nicotinamide adenine dinucleotide (NADH) and Flavin adenine dinucleotide (FADH2). The NADH and FADH2 serve as substrates in the electron transport chain (ETC) for the production of ATP in the mitochondria. Reactions in mitochondria that yield NADH and FADH2 yield are catalyzed by ACAD (Acyl-Co A). (Fillmore et al., 2011)

Acyl-CoA (ACAD) Dehydrogenase 

ACADs are flavoenzymes found in mitochondria that catalyze the first rate-limiting step in the β-oxidation of fatty acids. These enzymes transfer electrons, derived from the CoA ester, to electron transferring protein (ETF), and subsequently ETF dehydrogenase. This is coupled with the ETC and mediates the production of ATP (cellular energy). ACADs (Acyl-Co A)  that take part in the β-oxidation of fatty acids include the following enzymes. (Swigonová et al., 2009)

  1. Short-chain acyl-CoA dehydrogenase (SCAD)
  2. Medium-chain acyl-CoA dehydrogenase (MCAD)
  3. ACAD9
  4. Long-chain acyl-CoA dehydrogenase (LCAD)
  5. Very long-chain acyl-CoA dehydrogenase (VLCAD)

Impaired activity of ACADs in the mitochondria, along with ACAD deficiency, leads to the impairment of the capacity of the mitochondria to carry out β-oxidation of fatty acids. (Schiff et al., 2015) This almost certainly influences the production of ATP (cellular energy), which is indirectly associated with the β-oxidation of fatty acids and subsequent production of NADH and FADH2

LipidTAC Products 

What can you do about impaired β-oxidation of fatty acids and reduced ATP production by the mitochondria? Are there suitable products that can target ACADs and modulate the normal function of mitochondria in providing energy to the rapidly dividing skin cells? 

The answer is yes. LipidTAC products are made with carefully tailored proportions of natural or naturally-derived ingredients, which are beneficial to the optimal health and functioning of the body structures. In this section, you will learn how LipidTAC ingredients, safflower oil and vitamin B5, are related to the activity of ACAD and β-oxidation of fatty acids. 

Vitamin B5 (Dexpanthenol), also known as pantothenic acid, is pivotal to the biosynthesis of CoA, which is an acyl group carrier in the β-oxidation of fatty acids and other metabolic reactions. Vitamin B5 is also an essential part of an acyl carrier protein (ACP), which is associated with the synthesis of fatty acids. The CoA is converted into acyl-CoA, which serves as a substrate for β-oxidation reactions, production of NADH and FADH2, and eventually generation of ATP (cellular energy). (Tahiliani & Beinlich, 1991) Hence, vitamin B5 is indirectly associated with providing ample acyl-CoA substrate and supplying energy for the rapidly dividing cells in the human skin. 

Another ingredient present in LipidTAC products that is associated with mitochondrial function and β-oxidation of fatty acids is safflower oil. Safflower oil is a very rich source of polyunsaturated fatty acids, accounting for 77% linoleic acid. (Singh & Nimbkar, 2016) In addition, two other LipidTAC ingredients, Avocado oil and Grape seed oil each have over 60% linoleic acid while its Rose Hips oil has between 40-50% linoleic acid. 

Conclusion

Mitochondria is an organelle present in the human cells including the cells found in the largest organ, the skin. This mitochondria organelle produces energy, mediates the redox reactions, and modulates different signaling and metabolic pathways with the help of enzymes encoded by the mitochondrial genome or mtDNA. One of the enzymes that are associated with the β-oxidation of fatty acids in mitochondria is ACAD. This enzyme catalyzes the production of NADH and FADH2, which then mediate the production of ATP (cellular energy) in the mitochondria. This ATP is the energy fuel for the skin cells to carry out a myriad of functions. Vitamin B5, safflower oil, avocado oil, grape seed oil and rose hips oil in the LipidTAC products indirectly play an important role in normal β-oxidation of fatty acids and cellular energy production.

References 

Abdenur, J. E., Chamoles, N. A., Schenone, A. B., Jorge, L., Guinle, A., Bernard, C., Levandovskiy, V., Fusta, M., & Lavorgna, S. (2001). Multiple Acyl-CoA-Dehydrogenase Deficiency (MADD): Use of Acylcarnitines and Fatty Acids to Monitor the Response to Dietary Treatment. Pediatric Research, 50(1), 61-66. https://doi.org/10.1203/00006450-200107000-00013 

Chinnery, P. F., & Schon, E. A. (2003). Mitochondria. Journal of Neurology, Neurosurgery & Psychiatry, 74(9), 1188-1199. 

Fillmore, N., Alrob, O. A., & Lopaschuk, G. D. (2011). Fatty acid beta-oxidation. AOCS Lipid library, 10. 

Lucas, T. G., Henriques, B. J., Rodrigues, J. V., Bross, P., Gregersen, N., & Gomes, C. M. (2011). Cofactors and metabolites as potential stabilizers of mitochondrial acyl-CoA dehydrogenases. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1812(12), 1658-1663. 

McBride, H. M., Neuspiel, M., & Wasiak, S. (2006). Mitochondria: more than just a powerhouse. Current biology, 16(14), R551-R560. 

Schiff, M., Haberberger, B., Xia, C., Mohsen, A.-W., Goetzman, E. S., Wang, Y., Uppala, R., Zhang, Y., Karunanidhi, A., & Prabhu, D. (2015). Complex I assembly function and fatty acid oxidation enzyme activity of ACAD9 both contribute to disease severity in ACAD9 deficiency. Human molecular genetics, 24(11), 3238-3247. 

Singh, V., & Nimbkar, N. (2016). Chapter 7 – Safflower. In S. K. Gupta (Ed.), Breeding Oilseed Crops for Sustainable Production (pp. 149-167). Academic Press. https://doi.org/https://doi.org/10.1016/B978-0-12-801309-0.00007-0 

Sreedhar, A., Aguilera-Aguirre, L., & Singh, K. K. (2020). Mitochondria in skin health, aging, and disease. Cell Death & Disease, 11(6), 444. https://doi.org/10.1038/s41419-020-2649-z 

Swigonová, Z., Mohsen, A. W., & Vockley, J. (2009). Acyl-CoA dehydrogenases: Dynamic history of protein family evolution. J Mol Evol, 69(2), 176-193. https://doi.org/10.1007/s00239-009-9263-0 

Tahiliani, A. G., & Beinlich, C. J. (1991). Pantothenic acid in health and disease. Vitam Horm, 46, 165-228. https://doi.org/10.1016/s0083-6729(08)60684-6 

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