The Role of Insulin in Human Brain Glucose Metabolism: An 18Fluoro-Deoxyglucose Positron Emission Tomography Study -- Bingham et al. 51 (12): 3384 -- Diabetes
The Role of Insulin in Human Brain Glucose Metabolism: An 18Fluoro-Deoxyglucose Positron Emission Tomography Study -- Bingham et al. 51 (12): 3384 -- Diabetes
Our study results challenge the accepted view that human brain glucose uptake is an entirely insulin-independent process. Instead, our data suggest that there is a significant element of brain glucose uptake that is insulin sensitive, with a dose-response curve that is shifted well to the left of dose-response curves for other insulin-sensitive tissues, such as muscle or liver. Previous studies have demonstrated no change in rate of brain glucose metabolism in response to elevations of circulating insulin above the basal (fasting) range (19,22). Our data, examining the effect of basal insulin replacement during somatostatin infusion, show that brain glucose uptake is however partially insulin sensitive, as there was a significant reduction in global brain glucose uptake when circulating insulin levels were reduced below this. Coupled with the published data showing no effect of increasing circulating insulin above fasting levels, we can infer that brain glucose metabolism is maximally stimulated at these fasting insulin concentrations. The magnitude of the effect may not seem large, but this is because it is superimposed on a background of insulin-independent brain glucose uptake. A 15% increase in brain glucose uptake secondary to insulin stimulation may have clinical significance.
It would follow then that insulin insensitivity caused by lots of carbs would block the flow of glucose to your brain as well as your body.
Our study results challenge the accepted view that human brain glucose uptake is an entirely insulin-independent process. Instead, our data suggest that there is a significant element of brain glucose uptake that is insulin sensitive, with a dose-response curve that is shifted well to the left of dose-response curves for other insulin-sensitive tissues, such as muscle or liver. Previous studies have demonstrated no change in rate of brain glucose metabolism in response to elevations of circulating insulin above the basal (fasting) range (19,22). Our data, examining the effect of basal insulin replacement during somatostatin infusion, show that brain glucose uptake is however partially insulin sensitive, as there was a significant reduction in global brain glucose uptake when circulating insulin levels were reduced below this. Coupled with the published data showing no effect of increasing circulating insulin above fasting levels, we can infer that brain glucose metabolism is maximally stimulated at these fasting insulin concentrations. The magnitude of the effect may not seem large, but this is because it is superimposed on a background of insulin-independent brain glucose uptake. A 15% increase in brain glucose uptake secondary to insulin stimulation may have clinical significance.
It would follow then that insulin insensitivity caused by lots of carbs would block the flow of glucose to your brain as well as your body.
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