Cerebral Blood Flow and Glucose Metabolism Measured With Positron Emission Tomography Are Decreased in Human Type 1 Diabetes
- Larissa W. van Golen1⇑,
- Marc C. Huisman2,
- Richard G. Ijzerman1,
- Nikie J. Hoetjes2,
- Lothar A. Schwarte3,
- Adriaan A. Lammertsma2 and
- Michaela Diamant1
- 1Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, the Netherlands
- 2Department of Nuclear Medicine and Positron Emission Tomography Research, VU University Medical Center, Amsterdam, the Netherlands
- 3Department of Anesthesiology, VU University Medical Center, Amsterdam, the Netherlands
- Corresponding author: Larissa W. van Golen, .
Subclinical systemic microvascular dysfunction exists in asymptomatic patients with type 1 diabetes. We hypothesized that microangiopathy, resulting from long-standing systemic hyperglycemia and hyperinsulinemia, may be generalized to the brain, resulting in changes in cerebral blood flow (CBF) and metabolism in these patients. We performed dynamic [15O]H2O and [18F]-fluoro-2-deoxy-d-glucose brain positron emission tomography scans to measure CBF and cerebral glucose metabolism (CMRglu), respectively, in 30 type 1 diabetic patients and 12 age-matched healthy controls after an overnight fast. Regions of interest were automatically delineated on coregistered magnetic resonance images and full kinetic analysis was performed. Plasma glucose and insulin levels were higher in patients versus controls. Total gray matter CBF was 9%, whereas CMRglu was 21% lower in type 1 diabetic subjects versus control subjects. We conclude that at real-life fasting glucose and insulin levels, type 1 diabetes is associated with decreased resting cerebral glucose metabolism, which is only partially explained by the decreased CBF. These findings suggest that mechanisms other than generalized microangiopathy account for the altered CMRglu observed in well-controlled type 1 diabetes.
This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db12-1159/-/DC1.
- Received August 25, 2012.
- Accepted March 20, 2013.
- © 2013 by the American Diabetes Association.
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