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Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Alterations in glucose-6-phosphatase gene expression in sepsis
S R Maitra1, S Wang, C E Brathwaite
1Department of Emergency Medicine, University Hospital and Medical Center, State University of New York, Stony Brook 11794-7400, USA.
The Journal of Trauma
|July 27, 2000
Summary
Sepsis initially increases hepatic glucose-6-phosphatase (Glu-6-Pase) expression and activity, leading to hyperglycemia, then suppresses it, causing normal glucose levels. This is mediated by corticosterone and insulin.
Area of Science:
- Biochemistry
- Endocrinology
- Physiology
Background:
- Sepsis significantly impacts glucose metabolism.
- Hepatic glucose-6-phosphatase (Glu-6-Pase) plays a crucial role in glucose homeostasis.
- The dynamic changes in Glu-6-Pase during sepsis phases are not fully understood.
Purpose of the Study:
- To investigate the influence of sepsis on hepatic Glu-6-Pase expression and activity.
- To correlate these changes with glucose levels and key hormones during early and late sepsis phases.
Main Methods:
- Sepsis was induced in rats via cecal ligation and puncture.
- Liver samples were collected at various time points (0, 0.5, 1, 1.5, and 20 hours).
- Measurements included Glu-6-Pase mRNA and activity, glucose, glucose-6-phosphate, insulin, glucagon, and corticosterone levels.
Main Results:
- Hepatic Glu-6-Pase mRNA and activity increased significantly at 0.5 and 1 hour post-sepsis, coinciding with hyperglycemia.
- Corticosterone levels rose 2.5-fold during the hyperglycemic phase.
- At 20 hours, Glu-6-Pase expression decreased drastically, glucose normalized, and insulin, glucagon, and corticosterone levels increased substantially.
Conclusions:
- The early surge in blood glucose is linked to corticosterone-induced hepatic Glu-6-Pase expression.
- Later, insulin-dependent mechanisms suppress Glu-6-Pase expression, contributing to glucose normalization.
- These findings highlight the complex hormonal regulation of glucose metabolism during sepsis.
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