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Glucocorticoids regulate glutaminase gene expression in human intestinal epithelial cells
P Sarantos1, Z Abouhamze, E M Copeland
1Department of Surgery, University of Florida College of Medicine, Gainesville 32611.
The Journal of Surgical Research
|July 1, 1994
Summary
Glucocorticoids accelerate intestinal glutamine metabolism during critical illness. This occurs by increasing glutaminase activity and mRNA in enterocytes, potentially maintaining gut function when glutamine is scarce.
Area of Science:
- Cell Biology
- Molecular Biology
- Gastroenterology
Background:
- Glutamine is vital for intestinal function but may be limited during critical illness.
- Glucocorticoids increase during critical illness and may affect glutamine metabolism.
Purpose of the Study:
- To investigate if glucocorticoids accelerate intestinal glutamine metabolism.
- To examine the regulation of glutaminase, the key enzyme in enterocyte glutamine metabolism.
Main Methods:
- Human enterocytic Caco-2 cells were treated with dexamethasone.
- Glutaminase activity, mRNA levels, and protein synthesis were measured.
- Dose- and time-response studies were conducted, including inhibition assays.
Main Results:
- Dexamethasone increased glutaminase activity by 45% and mRNA by 40%.
- The response was dose- and time-dependent, with maximal effects at 12 hours.
- Inhibition of RNA and protein synthesis blocked the dexamethasone effect.
Conclusions:
- Glucocorticoids stimulate enterocyte glutamine metabolism by upregulating glutaminase.
- This upregulation involves increased gene transcription and de novo protein synthesis.
- This mechanism may preserve gut glutamine metabolism during critical illness.