Association of Delta-6-Desaturase Expression with Aggressiveness of Cancer, Diabetes Mellitus, and Multiple Sclerosis: A Narrative Review

Document Type: Systematic Review and Meta-analysis

Authors

1 Department of Pathology of Anatomy, School of medicine, Baku University of Medical Sciences, Baku, Azerbaijan.

2 Cellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran.

3 Department of Toxicology, Faculty of Pharmacy, Islamic Azad University, Shahreza Branch, Shahreza, Iran.

4 Department of Social Medicine, Medical School, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

5 Department of Biochemistry, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.

Abstract

Background: The phosphatidylinositol 3-kinase/ protein kinase B /mammalian target of rapamycin (PI3K/Akt/
mTOR) signaling regulates multiple cellular processes and organizes cell proliferation, survival, and differentiation
with the available nutrients, in particular, fatty acids. Polyunsaturated fatty acids (PUFAs) are cytotoxic to cancer cells
and play a critical role in the treatment of multiple sclerosis (MS) and diabetes mellitus (DM). PUFAs are produced in
the body by desaturases and elongases from dietary essential fatty acids (EFAs), primarily involving delta-6-desaturase
(D6D). D6D is a rate-limiting enzyme for maintaining many aspects of lipid homeostasis and normal health. D6D is
important to recognize the mechanisms that regulate the expression of this enzyme in humans. A lower level of D6D was
seen in breast tumors compared to normal tissues. Interestingly, the elevated serum level of D6D was seen in MS and
DM, which explains the critical role of D6D in inflammatory diseases. Methods: We searched databases of PubMed,
Web of Science (WOS), Google Scholar, Scopus and related studies by predefined eligibility criteria. We assessed
their quality and extracted data. Results: Regarding the mTOR signaling pathway, there is remarkable contributions of
many inflammatory diseases to attention to common metabolic pathways are depicted. Of course, we need to have the
insights into each disorder and their pathological process. The first step in balancing the intake of EFAs is to prevent
the disruption of metabolism and expression of the D6D enzyme. Conclusions: The ω6 and ω3 pathways are two major
pathways in the biosynthesis of PUFAs. In both of these, D6D is a vital bifunctional enzyme desaturating linoleic acid
or alpha-linolenic acid. Therefore, if ω6 and ω3 EFAs are given together in a ratio of 2: 1, the D6D expression will be
down-regulated and normalized.

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