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Official Full Name
ELOVL fatty acid elongase 6
Fatty acid elongases (EC, such as ELOVL6, use malonyl-CoA as a 2-carbon donor in the first and rate-limiting step of fatty acid elongation (Moon et al., 2001 [PubMed 11567032]).[supplied by OMIM, Mar 2008]
ELOVL6; ELOVL fatty acid elongase 6; FAE; LCE; FACE; elongation of very long chain fatty acids protein 6; hELO2; ELOVL FA elongase 6; fatty acid elongase 2; fatty acyl-CoA elongase; long-chain fatty-acyl elongase; 3-keto acyl-CoA synthase ELOVL6; very-long-chain 3-oxoacyl-CoA synthase 6; ELOVL family member 6, elongation of long chain fatty acids (FEN1/Elo2, SUR4/Elo3-like, yeast); elongation of very long chain fatty acids family member protein 6; EL; cb618; zgc:73089; ELOVL family m

The ELOVL6 gene is the sixth member of the long-chain fatty acid elongase (ELOVLs) family. Its expression is mainly regulated by transcription factors and some hormones. It is one of the key expression-regulating genes for fatty acid metabolism in animals. It is also a kind of rate-limiting enzyme for long-chain fatty acid elongation and synthesis reactions, whose main function is to catalyze the extension of saturated and unsaturated fatty acids. For example it can catalyze the conversion of C16 to C18. The ELOVL6 gene is highly expressed in tissues or organs with high lipid content, such as liver, adipose tissue, and adrenal gland.

Brown adipose tissue (BAT) is responsible for the production of heat, which is due to the uncoupling of electron transport in ATP synthesis by uncoupling protein 1. ELOVL6 causes a decrease in the expression of mitochondrial electron transport chain components and a decrease in BAT heat production capacity. Tan et al. showed that ELOVL6 is a thermoregulatory gene in BAT, and ELOVL6 is essential for the complete heat generation of brown adipose tissue.

Figure 1. Brown adipose tissue thermogenic capacity is regulated by elovl6. (Tan, et al. 2015)

ELOVL6 gene and fatty acid metabolism

Ma et al. studied the regulation mechanism of miRNA on ELOVL6 gene expression, and found that it is widely expressed in many tissues, especially in kidney and liver tissues. They also found that the chicken ELOVL6 gene is affected by miR-22-3P to control chicken liver lipid metabolism. Some scholars knocked out the mouse ELOVL6 gene and found that the fatty acid desaturation index in fat cells decreased significantly, and the content of linoleic acid in the liver and lung of mice also decreased significantly, indicating that knocking out the mouse ELOVL6 gene results in the uptake of exogenous long-chain fatty acids and a significant reduction in linoleic acid in adipocytes.

ELOVL6 gene and nonalcoholic steatohepatitis (NASH)

Free fatty acids (FFA) are key factors in the induction of fatty acid degeneration and lipid toxicity, and are closely related to NASH. The ELOVL6 gene is a metabolite of FFA. Some scholars have studied the enhancement of liver regenerative factor (ALR) and found that reducing ELOVL6 gene can promote lipid reduction and anti-apoptosis, and ALR can increase mitochondrial β-oxidation by increasing mitochondrial free fatty acid transporter CPT1a. In patients with NASH, the expression of ELOVL6 gene in the liver is positively correlated with the degree of liver degeneration. The overexpression of ELOVL6 gene can aggravate steatohepatitis and liver damage, which is caused by NASH.

ELOVL6 gene and insulin resistance

The ELOVL6 gene can exert its role in obesity-induced insulin resistance by modifying monounsaturated fatty acids. Zhao et al. found that β-cells in mice are significantly increased, apoptosis is reduced, insulin adaptability is increased, and glycemic control is improved by ELOVL6 gene knockout in leptin receptor-deficient mice, indicating that the ELOVL6 gene is a key factor in the association of abnormalities in lipid metabolism with beta cell dysfunction, insulin inflammation, and beta cell apoptosis. High-energy diets were given to mice that knocked out the ELOVL6 gene. It was found that although mice showed obesity and liver fat deposition, they could prevent insulin resistance. The main reason is that the knockout of the ELOVL6 gene causes a decrease in the expression of the peroxidase-activated receptor and the sterol regulatory element binding protein 1c in the body, resulting in a decrease in fatty acid synthesis. Moreover, decreased expression of the sterol regulatory element binding protein 1c is a major factor leading to an increase in the amount of insulin receptor substrate and phosphorylation.


  1. Tan, C. Y., Virtue, S., Bidault, G., Dale, M., Hagen, R., & Griffin, J. L., et al. (2015). Brown adipose tissue thermogenic capacity is regulated by elovl6. Cell Reports, 13(10), 2039-2047.
  2. Ma, Z., Li, H., Zheng, H., Jiang, K., Yan, F., & Tian, Y., et al. (2017). Hepatic elovl6 mrna is regulated by the gga-mir-22-3p in egg-laying hen. Gene, 623.
  3. Zhao, H., Matsuzaka, T., Nakano, Y., Motomura, K., Tang, N., & Yokoo, T., et al. (2017). Elovl6 deficiency improves glycemic control in diabetic db/db mice by expanding β-cell mass and increasing insulin secretory capacity. Diabetes, 66(7), db161277.