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Updated: Jun 4, 2026
09:14
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Beta-cell dysfunction and insulin resistance after subarachnoid haemorrhage
N D Kruyt1, A Musters, G J Biessels
1Department of Neurology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. ndkruyt@gmail.com
Neuroendocrinology
|February 5, 2011
Summary
Aneurysmal subarachnoid hemorrhage (SAH) causes temporary glucose metabolism issues, primarily due to pancreatic beta-cell dysfunction and insulin resistance in the first week. These disturbances in glucose regulation resolve over time in SAH patients.
Area of Science:
- Neurocritical care
- Endocrinology
- Metabolic disorders
Background:
- Hyperglycemia is common and a risk factor for poor outcomes in aneurysmal subarachnoid hemorrhage (SAH).
- Underlying mechanisms of hyperglycemia in SAH patients are not well understood, despite being often attributed to insulin resistance.
Purpose of the Study:
- To prospectively investigate temporal changes in glucose metabolism after aneurysmal SAH.
- To explore correlations between glucose metabolism disturbances and stress markers in SAH patients without prior metabolic abnormalities.
Main Methods:
- Oral glucose tolerance tests (OGTTs) and assessments of insulin resistance, pancreatic beta-cell function, free fatty acids (FFA), and cortisol were conducted.
- SAH patients without insulin therapy were compared with reference values during hospitalization and follow-up.
Main Results:
- All patients showed glucose intolerance at days 3 and 7 post-SAH.
- Elevated fasting glucose and FFA, with normal insulin levels, were observed in the first two weeks.
- Impaired pancreatic beta-cell function and insulin resistance were noted, correlating with cortisol and FFA levels.
Conclusions:
- Aneurysmal SAH patients experience transient glucose metabolism abnormalities.
- These disturbances in the first week are mainly due to temporary pancreatic beta-cell dysfunction and insulin resistance.
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