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Effects of Insulin on Brain Glucose Metabolism in Impaired Glucose Tolerance

Posted: Sunday, February 13, 2011

Insulin stimulates brain glucose metabolism at physiological postprandial levels in patients with impaired glucose tolerance but not in healthy subjects.

Insulin stimulates brain glucose metabolism, but this effect of insulin is already maximal at fasting concentrations in healthy subjects. It is not known whether insulin is able to stimulate glucose metabolism above fasting concentrations in patients with impaired glucose tolerance.

Disturbances in brain insulin signaling in patients with impaired glucose tolerance may occur at multiple levels, including delivery of insulin in the brain across the blood-brain barrier, actions of insulin at insulin receptors, and downstream effects via second-messenger systems. Obese patients have a lower cerebrospinal fluid-to-plasma insulin ratio, which would suggest deficient delivery of insulin into the brain. However, obese patients also show decreased catabolic, but not cognitive, responses to intranasal insulin, which bypasses the blood-brain barrier, suggesting that insulin resistance in the brain occurs at multiple levels. Based on the current results, it may be speculated that some components along the insulin pathway in the brain are actually sensitized because of long-term deprivation of insulin stimulation and show exaggerated responses to high insulin levels in these patients. For example, if decreased insulin delivery across the blood-brain barrier and decreased responsiveness of insulin receptors inhibit stimulation of the insulin pathway at physiological insulin levels, despite compensatory hyperinsulinemia, we might expect to see increased responses to insulin when insulin levels are sufficiently high to overcome these deficits upstream in the signaling pathway. Unfortunately, no evidence for sensitization of any of the components in this signaling pathway exists in humans, and this hypothesis remains speculative until further data emerge.

Researchers in Finland looked at the effects of insulin on brain glucose metabolism and cerebral blood flow in 13 patients with impaired glucose tolerance and nine healthy subjects using positron emission tomography (PET). All subjects underwent PET with both [18F]fluorodeoxyglucose (for brain glucose metabolism) and [15O]H2O (for cerebral blood flow) in two separate conditions (in the fasting state and during a euglycemic-hyperinsulinemic clamp). Arterial blood samples were acquired during the PET scans to allow fully quantitative modeling.

From the results it was found that the hyperinsulinemic clamp increased brain glucose metabolism only in patients with impaired glucose tolerance (whole brain: +18%, P = 0.001) but not in healthy subjects (whole brain: +3.9%, P = 0.373). The hyperinsulinemic clamp did not alter cerebral blood flow in either group.

In conclusion they found that insulin stimulates brain glucose metabolism at physiological postprandial levels in patients with impaired glucose tolerance but not in healthy subjects. These results suggest that insulin stimulation of brain glucose metabolism is maximal at fasting concentrations in healthy subjects but not in patients with impaired glucose tolerance.

Source: http://www.diabetesincontrol.com/index.php?option=com_content&view=article&id=10494&catid=53&Itemid=8, Diabetes. 2011;60(2):443-447

 
 
 
 
 
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