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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

The Emerging Role of CYP17A1 in Diabetes and Related Metabolic Disorders

  • Zainab Alhalwachi1
  • Mashael Zainalabedin1
  • Daleen Alhayki1
  • Abdullah Buraq Alsultan2
  • Siham Abdullahi2
  • Kawther Ahmed Alnahwi3
  • Alexandra E. Butler1
  • Ammar Shaker Hasan1
  1. 1Department of Postgraduate Studies and Research, Royal College of Surgeons in Ireland, Medical University of Bahrain Busaiteen, Adliya P.O. Box 15503, Bahrain
  2. 2Department of Medicine, Royal College of Surgeons in Ireland, Medical University of Bahrain Busaiteen, Adliya P.O. Box 15503, Bahrain
  3. 3College of Medicine, Alfaisal University, P.O. Box 50927, Riyadh 11533, Saudi Arabia
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Abstract

CYP17A1 (cytochrome P450 17A1) is a key steroidogenic enzyme that catalyzes 17α-hydroxylase and 17,20-lyase reactions, controlling glucocorticoid and androgen production. Emerging evidence suggests that CYP17A1 is not only essential for adrenal and gonadal steroidogenesis, but could also contribute to obesity, insulin resistance, type 2 diabetes, and hypertension. Genetic studies have associated CYP17A1 variants with fasting glucose, type 2 diabetes risk, arterial stiffness, and metabolic syndrome traits. In mouse models, obesity induces hepatic CYP17A1 expression and 17-hydroxyprogesterone overproduction, which activates glucocorticoid receptor signaling, promotes hepatic gluconeogenesis, and exacerbates insulin resistance and hyperglycemia. CYP17A1 has also been linked to adipose tissue dysfunction, altered steroid signaling, and redistribution of fat from visceral to subcutaneous depots. This review summarizes CYP17A1 structure, regulation, protein interaction networks, and its roles in insulin resistance, adipose tissue biology, steroid excess, and vascular complications. It also discusses CYP17A1 genetic variation and the therapeutic potential and limitations of CYP17A1 inhibition and glucocorticoid receptor modulation in diabetes and related metabolic disorders.

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Cite

BibTeXRIS
BibTeX
@article{alhalwachi2026emerging,
  title = {{The Emerging Role of CYP17A1 in Diabetes and Related Metabolic Disorders}},
  author = {Zainab Alhalwachi and Mashael Zainalabedin and Daleen Alhayki and Abdullah Buraq Alsultan and Siham Abdullahi and Kawther Ahmed Alnahwi and Alexandra E. Butler and Ammar Shaker Hasan},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = nov,
  doi = {10.3390/ijms27219826},
  url = {https://www.mdpi.com/1422-0067/27/21/9826},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - The Emerging Role of CYP17A1 in Diabetes and Related Metabolic Disorders
AU  - Zainab Alhalwachi
AU  - Mashael Zainalabedin
AU  - Daleen Alhayki
AU  - Abdullah Buraq Alsultan
AU  - Siham Abdullahi
AU  - Kawther Ahmed Alnahwi
AU  - Alexandra E. Butler
AU  - Ammar Shaker Hasan
PY  - 2026
DA  - 2026/11/02
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219826
UR  - https://www.mdpi.com/1422-0067/27/21/9826
AB  - CYP17A1 (cytochrome P450 17A1) is a key steroidogenic enzyme that catalyzes 17α-hydroxylase and 17,20-lyase reactions, controlling glucocorticoid and androgen production. Emerging evidence suggests that CYP17A1 is not only essential for adrenal and gonadal steroidogenesis, but could also contribute to obesity, insulin resistance, type 2 diabetes, and hypertension. Genetic studies have associated CYP17A1 variants with fasting glucose, type 2 diabetes risk, arterial stiffness, and metabolic syndrome traits. In mouse models, obesity induces hepatic CYP17A1 expression and 17-hydroxyprogesterone overproduction, which activates glucocorticoid receptor signaling, promotes hepatic gluconeogenesis, and exacerbates insulin resistance and hyperglycemia. CYP17A1 has also been linked to adipose tissue dysfunction, altered steroid signaling, and redistribution of fat from visceral to subcutaneous depots. This review summarizes CYP17A1 structure, regulation, protein interaction networks, and its roles in insulin resistance, adipose tissue biology, steroid excess, and vascular complications. It also discusses CYP17A1 genetic variation and the therapeutic potential and limitations of CYP17A1 inhibition and glucocorticoid receptor modulation in diabetes and related metabolic disorders.
SN  - 1422-0067
ER  -