Stearoyl-CoA desaturase that utilizes O(2) and electrons from reduced cytochrome b5 to introduce the first double bond into saturated fatty acyl-CoA substrates. Catalyzes the insertion of a cis double bond at the Delta-9 position into fatty acyl-CoA substrates including palmitoyl-CoA and stearoyl-CoA (PubMed:11500518, PubMed:11533264, PubMed:16275639, PubMed:16443825, PubMed:26098370). Gives rise to a mixture of 16:1 and 18:1 unsaturated fatty acids (PubMed:11500518, PubMed:11533264, PubMed:16443825, PubMed:26098370). Plays an important role in lipid biosynthesis (PubMed:17127673, PubMed:10899171, PubMed:11500518, PubMed:11441127, PubMed:11533264, PubMed:12177411, PubMed:26098370). Plays an important role in regulating the expression of genes that are involved in lipogenesis and in regulating mitochondrial fatty acid oxidation (PubMed:12177411, PubMed:17127673, PubMed:24356954, PubMed:24295027). Plays an important role in body energy homeostasis (PubMed:17127673, PubMed:15210843, PubMed:24295027, PubMed:24356954). Contributes to the biosynthesis of membrane phospholipids, cholesterol esters and triglycerides (PubMed:10899171, PubMed:11500518, PubMed:11441127, PubMed:11533264, PubMed:12177411, PubMed:15210843, PubMed:26098370). Required for normal development of sebaceous glands (PubMed:17738154, PubMed:11533264). Required for the biosynthesis of normal levels of Delta-9 unsaturated fatty acids and 1-alkyl-2,3-diacylglycerol in the Harderian gland (PubMed:11500518). Required for normal production of meibum, an oily material that prevents drying of the cornea (PubMed:11533264). 2 Fe(II)-[cytochrome b5] + 2 H(+) + O2 + octadecanoyl-CoA = (9Z)-octadecenoyl-CoA + 2 Fe(III)-[cytochrome b5] + 2 H2O Expected to bind 2 Fe(2+) ions per subunit, instead of the Zn(2+) ions seen in the 3D-structure. Detected in liver (at protein level) (PubMed:10899171, PubMed:11533264). Detected in skin and liver (PubMed:10545940, PubMed:11161812, PubMed:11441127, PubMed:11533264). Detected in sebaceous gland, but not in hair follicle (PubMed:10545940). Detected in white and brown adipose tissue, eyelid, Harderian gland, and at lower levels in Meibomian gland, eyeball and adrenal gland (PubMed:11500518, PubMed:11533264). Highly expressed in liver, and detected at low levels in brain, heart, lung, stomach, skeletal muscle and kidney (PubMed:11161812, PubMed:12815040). Up-regulated during the early anagen phase of the hair cycle. Thereafter, levels decrease and are very low at telogen phase. Up-regulated by agonists that activate NR1H3 (PubMed:12815040). Up-regulated by a high-carbohydrate diet (PubMed:11441127). Up-regulated by a fat-free, high-carbohydrate diet (PubMed:12815040). Down-regulated by a high-carbohydrate diet enriched in unsaturated fatty acids (PubMed:12815040). Up-regulated by a diet containing high levels of stearate (PubMed:17127673). The histidine box domains are involved in binding the catalytic metal ions. Defects is Scd1 are the cause of asebia (ab) (PubMed:17738154, PubMed:10545940, PubMed:10854228, PubMed:10899171, PubMed:15278437). The trait is due to spontaneous autosomal recessive mutations that give rise to deletions or point mutations in Scd1. The ab trait has complete penetrance (PubMed:17738154). Ab mice are characterized by reduced body weight, extreme sebaceous gland hypoplasia leading to nearly complete absence of sebaceous glands, and thickened, scaly skin with hyperkeratosis and alopecia (PubMed:17738154, PubMed:10854228, PubMed:15278437). The hair follicles are abnormally long and extend at a sharp angle into the subcutis, probably due to abnormal persistence of inner root sheath. Frequently the hair shaft ruptures through the base of the hair follicle, giving rise to inflammation that results in scarring alopecia (PubMed:10854228, PubMed:15278437). Besides, ab mice display increased transepithelial water loss (PubMed:10854228). Ab mice present a narrow eye fissure and their eyes are nearly closed (PubMed:10854228, PubMed:15278437). Older mice develop blindness (PubMed:17738154). Scd1 activity is almost absent in liver, and is not compensated by expression of another family member (PubMed:10899171). Liver levels of total cholesterol esters are decreased by 87%, while plasma cholesterol levels are increased by 35% (PubMed:10899171). Likewise, skin sterol esters and diol diesters are strongly reduced (PubMed:10854228). Liver triglyceride levels are decreased by 62%, while plasma triglyceride levels are decreased by 67% (PubMed:10899171). The fatty acid composition of liver triglycerides is altered, with a decrease of about 85% in palmitoleate (C16:1) and oleate (C18:1) levels (PubMed:10899171). These defects cannot be compensated by a diet enriched in unsaturated fatty acids (PubMed:10899171, PubMed:11441127). Mice are viable and fertile (PubMed:11533264). Compared to wild-type, they consume about 25% more food, but are leaner and acumulate less white adipose tissue (PubMed:12177411, PubMed:17127673). Their liver glycogen levels are lower than wild-type, except when their diet is supplemented with high levels of triolein (PubMed:17127673). They gain weight and accumulate white adipose tissue when their diet contains high levels of triolein (PubMed:17127673). They loose weight on a diet rich in tristearin, contrary to wild-type (PubMed:17127673). Mutant mice cannot maintain their body temperature when exposed to cold; they display hypoglycemia, depleted liver glycogen levels, and die of hypothermia (PubMed:15210843). Mutant mice display increased levels of mitochondrial fatty acid oxidation and decreased expression of genes that are important for de novo lipogenesis, especially when their diet is enriched in saturated fatty acids (PubMed:12177411, PubMed:17127673). Their brown adipose tissues shows increased lipolysis and fatty acid oxidation (PubMed:15210843). They display increased metabolic rates during the day and the night (PubMed:12177411). Liver, skin and white adipose tissue from mutant mice show strongly decreased levels of palmitoleate and reduced levels of oleate, with increased levels of saturated fatty acids (PubMed:11533264). Likewise, skin and eyelids are deficient in cholesterol esters, wax esters and triglycerides (PubMed:11533264). These defects cannot be compensated by a diet enriched in unsaturated fatty acids (PubMed:11533264). Mutant mice have decreased levels of liver and plasma triglycerides (PubMed:17127673). Likewise, the levels of triglycerides, 1,2-diacylglycerol and free fatty acids are decreased in the brown adipose tissue (PubMed:15210843). Besides, brown adipose tissue, liver and plasma triglycerides are depleted in unsaturated fatty acids and are enriched in saturated fatty acids (PubMed:15210843, PubMed:17127673). A diet enriched in triolein increases liver and plasma levels of triglycerides (PubMed:17127673). Mutant mice display lower fasting insulin levels, normal fasting glucose levels, increased glucose tolerance and increased insulin sensitivity (PubMed:12177411). Mutant mice display alopecia and atrophy of sebaceous glands and Meibomian glands (PubMed:11533264). Besides, they present a narrow eye fissure and their eyes are nearly closed (PubMed:11533264). This eye phenotype is probably due to a defect in the production of meibum, the oily material that prevents drying of the cornea. Scd1 activity is almost absent in liver, and is not compensated by expression of another family member (PubMed:11533264). Strongly reduced levels of lipids containing Delta-9 unsaturated fatty acids in the Harderian gland, leading to strongly reduced levels of 1-alkyl-2,3-diacylglycerol in the Harderian gland (PubMed:11500518). Belongs to the fatty acid desaturase type 1 family.