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Adaptive cellular mechanisms in response to glutamine-starvation
Maja Munk Eliasen1, Wolfgang Winkler, Veronika Jordan
1Department of Surgery, Medical University of Vienna, Vienna, Austria.
Summary
Glutamine-utilizing cells activate adaptive mechanisms to survive starvation during critical illness. However, severe glutamine deficiency overwhelms these responses, leading to cell dysfunction.
Area of Science:
- Cellular metabolism
- Biochemistry
- Critical care medicine
Background:
- Glutamine (Gln) is crucial for cellular energy and biosynthesis.
- Critical illness often leads to decreased plasma Gln levels, causing Gln-starvation in Gln-utilizing cells.
- The adaptive responses of cells to Gln-starvation remain incompletely understood.
Purpose of the Study:
- To investigate the adaptive mechanisms activated by Gln-utilizing cells under Gln-starvation.
- To determine the impact of varying Gln concentrations on cellular function and adaptation.
- To identify proteins involved in the cellular response to Gln deficiency.
Main Methods:
- Monocytic U937 cells were cultured under different Gln concentrations (0.6 mM and 0.2 mM).
- Measurements included ATP levels, intracellular free Gln, Hsp70 expression, proliferation rates, and AMP-activated kinase (AMPK) activation.
- Proteomic analysis was performed to identify differentially expressed proteins.
Main Results:
- Gln-starvation initially decreased ATP, Gln, Hsp70, and proliferation.
- Cells cultured at 0.6 mM Gln showed recovery in ATP, Hsp70, and proliferation, but not intracellular Gln.
- Severe Gln starvation (0.2 mM) resulted in sustained decreases in all measured parameters. AMPK activation initially increased then normalized at 0.6 mM Gln.
- Proteomic analysis revealed 23 affected proteins, including metabolic enzymes and stress proteins.
Conclusions:
- Gln-utilizing cells possess adaptive mechanisms to cope with moderate Gln shortage.
- These adaptive responses are insufficient to counteract severe Gln deficiency.
- Understanding these mechanisms is vital for managing metabolic dysfunction in critical illness.
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