EC Number   |
General Information |
Reference |
|---|
    1.14.19.1 | evolution |
isozymes SCD1 and SCD3 share 89% primary sequence identity, but they yield remarkably different total fatty acid profiles in the recombinant yeast host cells, likely reflecting differences in their preferences for reaction with 16:0 and 18:0 substrates |
745883 |
| 1.14.19.1 | malfunction |
alterations in expression reported in several prevalent metabolic diseases, such as diabetes, obesity and atherosclerosis |
714663 |
| 1.14.19.1 | malfunction |
chemical SCD1 inhibition in the presence of stearic acid results in a significant induction of apoptosis in cumulus cells of matured cumulus-oocyte complexes. SCD1 inhibition does not affect the levels of palmitic acid and its desaturated form, palmitoleic acid |
744461 |
| 1.14.19.1 | malfunction |
dysregulation of stearoyl-CoA desaturase 1 likely contributes to obesity associated metabolic disturbances. Effect of genetic ablation of SCD1 in 3T3-L1 adipocytes on membrane microdomain lipid composition at the species-specific level, overview. 90% reduction in scd1 mRNA expression, caused by siRNA expression, leads to altered cellular lipid composition, SCD1 knockout modifies the acyl chain composition of lipids, as well as the lipid composition per se of membrane microdomains in 3T3-L1 adipocytes.The effects of SCD1 knockout are not limited to alterations in 16:0 and 18:0 fatty acids. Cholesterol content is unchanged although decreases in other lipids result in cholesterol accounting for a higher proportion of lipid in the membranes. This is associated with decreased membrane lateral diffusion. An increased ratio of 24:0 to 24:1 in ceramide, mono- and dihexosylceramide, and sphingomyelin likely also contributes to this decrease in lateral diffusion. Lipidomic profiling is targeted to specific membrane microdomains, overview. A decrease in phospholipids containing arachidonic acid is observed. Given the high degree of structural flexibility of this acyl chain this will influence membrane lateral diffusion, and is likely responsible for the transcriptional activation of Lands' cycle enzymes lpcat3 and mboat7 |
746212 |
| 1.14.19.1 | malfunction |
enzyme inhibition by genetic and chemical tools is detrimental for parasite development. The partial ablation of the enzyme inhibits drastically the parasite growth |
-, 726861 |
| 1.14.19.1 | malfunction |
inhibition of SCD1 activity represents a potential novel approach for the treatment of metabolic diseases such as obesity, type 2 diabetes and dyslipidemia, as well as skin diseases, acne and cancer |
744487 |
| 1.14.19.1 | malfunction |
loss of SCD-1 activity induces complex changes in the fatty acid composition of membrane lipids which are not restricted to the MUFA/SFA ratio. SCD-1 deficiency induces insulin signaling in peripheral tissues, namely phosphorylation of insulin receptor and insulin receptor substrates (IRS)1 and 2. Association of IRS isoforms with the regulatory subunit of phosphatidylinositol-3-kinase (PI3K) promotes the synthesis of phosphatidylinositol-3,4,5-trisphoshates (PIP3) as membrane anchor sites for the serine/threonine kinase Akt. SCD-1 inhibition suppressed starvation-induced autophagy in mouse embryonic fibroblasts and palmitate-induced autophagy in rat pancreatic beta-cells apparently by disturbing autophagosome-lysosome fusion |
744416 |
| 1.14.19.1 | malfunction |
loss of SCD-1 activity induces complex changes in the fatty acid scomposition of membrane lipids which are not restricted to the MUFA/SFA ratio. SCD-1 deficiency induces insulin signaling in peripheral tissues, namely phosphorylation of insulin receptor and insulin receptor substrates (IRS)1 and 2. Association of IRS isoforms with the regulatory subunit of phosphatidylinositol-3-kinase (PI3K) promotes the synthesis of phosphatidylinositol-3,4,5-trisphoshates (PIP3) as membrane anchor sites for the serine/threonine kinase Akt |
744416 |
| 1.14.19.1 | malfunction |
reduced SCD1 activity in the liver causes endoplasmic reticulum stress that is only normalized by exogenous or endogenous oleate but not palmitoleate. SCD1 deficiency-mediated glucose uptake in skeletal muscle and brown adipose tissue feeds toward glycogen synthesis. Localized and systemic SCD1 deficiency increases glucose uptake in white adipose tissue through apparently different mechanisms involving GLUT1 and GLUT4, respectively |
746542 |
| 1.14.19.1 | malfunction |
reduced SCD1 activity in the liver causes endoplasmic reticulum stress that is only normalized by exogenous or endogenous oleate but not palmitoleate. SCD1 deficiency-mediated glucose uptake in skeletal muscle and brown adipose tissue feeds toward glycogen synthesis. Localized and systemic SCD1 deficiency increases glucose uptake in white adipose tissue through apparently different mechanisms involving GLUT1 and GLUT4, respectively. Liver-specific SCD1 KO mice exhibit different phenotypes compared to skin-specific SCD1 KO mice, suggesting that SCD1 products, monounsaturated fatty acids, carry out different functions in different tissues. Global SCD1 KO mice are protected against high carbohydrate diet and high fat diet-induced adiposity and hepatic steatosis. Liver-specific SCD1 knockout mice fed high-fat diet show a significant reduction of white adipose tissue weights compared with control mice. Hepatic SCD1 deficiency causes a significant reduction in hepatic lipogenic gene expression and reduced de novo lipogenesis associated with reduced hepatic triglyceride secretion. Skin-specific knockout mice show protection against high-fat diet-induced adiposity along with increased energy expenditure expected to be sufficient to counter increased calorie intake associated with feeding high-fat diet. In addition, similar to SCD1 global KO mice, skin-specific KO mice are hyperphagic and maintain lean phenotype accompanied by protection against extended high-fat diet feeding-induced insulin resistance. Skin-specific KO mice exhibit increased cold sensitivity and died within 3 h of cold exposure due to hypoglycemia. SCD1 isozyme-specific knockout phenotypes with respect to the other isozymes, detailed overview |
746542 |
