Scd1

Official Full Name

stearoyl-Coenzyme A desaturase 1

Organism

Mus musculus

GeneID

20249

Background

Enables metal ion binding activity; palmitoyl-CoA 9-desaturase activity; and stearoyl-CoA 9-desaturase activity. Involved in several processes, including positive regulation of cold-induced thermogenesis; sterol homeostasis; and tarsal gland development. Acts upstream of or within several processes, including brown fat cell differentiation; monounsaturated fatty acid biosynthetic process; and white fat cell differentiation. Located in endoplasmic reticulum membrane. Is expressed in several structures, including adipose tissue; central nervous system; cranium; integumental system; and liver. Orthologous to human SCD (stearoyl-CoA desaturase). [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

Scd1; ab; Scd; Scd-1;

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Detailed Information

The SCD1 gene encodes stearoyl-CoA desaturase 1, located on human chromosome 10q24.31. It belongs to the fatty acid desaturase family and produces an integral endoplasmic reticulum membrane protein whose catalytic activity relies on the electron transfer chain composed of cytochrome b5 reductase and cytochrome b5. Two major transcript isoforms of SCD1 exist, approximately 3.9 kb and 5.2 kb in length, resulting from alternative polyadenylation, although both encode identical protein sequences. The human genome also contains a related enzyme gene, SCD5, on chromosome 4 and an SCD1 pseudogene on chromosome 17, suggesting evolutionary gene duplication events. SCD1 expression is tightly regulated transcriptionally and post-transcriptionally, with promoter elements responsive to sterol regulatory element-binding proteins (SREBPs) and liver X receptors (LXRs), linking nutrient status to gene expression. Hormones such as insulin and leptin, as well as dietary components, also significantly modulate SCD1 levels, highlighting its central role in systemic energy homeostasis.

Biological Significance

SCD1 functions as a rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids (MUFAs). It catalyzes the introduction of the first cis double bond at the 螖9 position of saturated fatty acyl-CoA substrates, primarily palmitoyl-CoA and stearoyl-CoA, producing palmitoleic acid and oleic acid. These MUFAs are essential building blocks for complex lipids. The ratio of MUFAs to saturated fatty acids is a key determinant of membrane fluidity, cellular signaling, and numerous metabolic processes. SCD1-derived MUFAs serve as precursors for phospholipids, cholesterol esters, and triglycerides, crucial for lipid droplet formation, membrane synthesis, and intracellular signaling.

Figure 1. Desaturation of fatty acids by SCD. (Ascenzi F, et al., 2021)

Beyond catalysis, SCD1 influences systemic energy homeostasis. Elevated hepatic SCD1 activity promotes triglyceride synthesis and lipid accumulation, contributing to metabolic-associated steatotic liver disease (MASLD). Conversely, SCD1 deficiency enhances mitochondrial fatty acid 尾-oxidation and energy expenditure. SCD1 also regulates ER stress and inflammation by modulating lipid species that act as TLR ligands or influence membrane properties. Its activity correlates with insulin sensitivity; moderate SCD1 activity is necessary for normal insulin signaling, whereas excessive activity can lead to lipotoxicity and insulin resistance.

Clinical Relevance

SCD1 is a promising target for metabolic disease and cancer therapy. In MASLD, hepatic SCD1 upregulation drives triglyceride accumulation and disease progression, making SCD1 inhibition a strategy to reduce pathogenic lipid synthesis. In obesity and type 2 diabetes models, tissue-specific or systemic SCD1 inhibition improves insulin sensitivity, increases energy expenditure, and reduces body weight. In oncology, many tumors upregulate SCD1 to meet membrane lipid demands; inhibition induces ER stress and lipid peroxidation, selectively suppressing tumor growth.

Clinical translation faces challenges: systemic SCD1 inhibition may impair skin barrier function or cause ocular dryness due to essential lipid requirements in specific tissues. Therefore, tissue-specific delivery or targeting downstream effectors is under investigation. Identifying patient populations likely to benefit from SCD1 inhibition based on lipidomic profiles or genetic variants is critical for precision medicine. Several small-molecule SCD1 inhibitors are in preclinical or early clinical development for MASLD, cancer, and dermatologic conditions such as acne.

References

Miyazaki M, Dobrzyn A, Sampath H, et al. Reduced adiposity and liver steatosis by stearoyl-CoA desaturase deficiency are independent of peroxisome proliferator-activated receptor-alpha. J Biol Chem. 2004;279(33):35017-35024.
Ascenzi F, De Vitis C, Maugeri-Sacc脿 M, et al. SCD1, autophagy and cancer: implications for therapy. J Exp Clin Cancer Res. 2021 Aug 24;40(1):265.
Ntambi JM, Miyazaki M, Dobrzyn A. Regulation of stearoyl-CoA desaturase expression. Lipids. 2004;39(11):1061-1065.

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