Stress-induced protein dermcidin develops diabetes targeting GLUT4/insulinviaNO/cGMP inhibition.
Sarbashri BankSuman BhattacharyaAndreas KoschinskiManuela ZaccoloSmarajit MaitiAmrita BanerjeeSubrata Kumar DeGausal A KhanMadhusudan DasSantanu GuhaArjun GhoshUdayan RayAsru K SinhaPublished in: British journal of pharmacology (2021)
Molecular-docking experiments (AUTODOCK/PATCHDOCK) decisively showed high-affinity binding of DCD to GLUT-4, insulin, and its receptor (Ectodomain1/2). Synergism of all these effects resulted in the breakdown of glucose homeostasis-machinery i.e. insulin-resistance, and further dermcidin induced NO/cGMP down-regulation in individuals under a variety of stressors.
Keyphrases
- stress induced
- molecular docking
- type diabetes
- insulin resistance
- glycemic control
- nitric oxide
- molecular dynamics simulations
- protein kinase
- blood glucose
- binding protein
- high glucose
- cardiovascular disease
- adipose tissue
- high fat diet
- polycystic ovary syndrome
- skeletal muscle
- blood pressure
- amino acid
- drug induced
- oxidative stress
- drug delivery
- transcription factor
- endothelial cells