Insulin increases glucose transfer across the blood-brain barrier in man.

Hertz, Marianne M.; Paulson, Olaf B.; Barry, David I.; Christiansen, John; Svendsen, P.

doi:10.1172/jci110073

Cited by 117 publications

(33 citation statements)

References 42 publications

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“…, 1989). The calculated rate of influx of glucose across the BBB observed is also in agreement with the measurements by Hertz et al (1981) showing that only 50--60% of the glucose transported into the tissue is metabolized and the rest is transported back again into the bloodstream. To study unidirec- C p ' Ca, and Cy, glucose concentration in arterial plasma, arterial blood, and venous blood, respectively; CMR gl c(Fick), CBF .…”

Section: Resultssupporting

confidence: 88%

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Blomqvist

Stone‐Elander

Halldin

et al. 1990

J Cereb Blood Flow Metab

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Summary: Regional CMR g lc was measured in seven healthy volunteers with positron emission tomography using [I-IIC]D-glucose. Regional CBF was measured us· ing [IIC]fluoromethane. The arteriovenous differences of unlabeled glucose and oxygen together with IIC metabo lites were also measured. In addition to the loss of [llC]COZ' a loss of acidic IIC metabolites was also de tected. A three-compartment model was applied to the tracer data in the time interval 0-24 min. After correction for the loss of IIC metabolites, the tracer method gave an

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Section: Resultssupporting

confidence: 88%

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Blomqvist

Stone‐Elander

Halldin

et al. 1990

J Cereb Blood Flow Metab

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“…The effect of insulin on blood-to-brain transport of glucose remains unclear [66,[69][70][71]. Elucidation of the effect of insulin (if any) on the Michaelis-Menten constants will have to await further experimentation.…”

Section: Biological Issuesmentioning

confidence: 99%

Cerebral transport and metabolism of 1‐¹¹C‐D‐glucose during stepped hypoglycemia

Powers

Dagogo‐Jack

Markham

et al. 1995

Annals of Neurology

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Attempts to measure blood-to-brain glucose transport and cerebral glucose metabolism with 11C-glucose have been hampered by methods that require jugular venous sampling or do not adequately account for the efflux of labeled metabolites from the brain. We performed eight positron emission tomography studies with 1-11C-D-glucose in macaques at arterial plasma glucose concentrations of 8.43 to 1.51 mumol ml-1 (152-27 mg dl-1) using a model that includes a fourth rate constant to account for regional egress of all 11C-metabolites. Values for blood-to-brain glucose influx, cerebral glucose metabolism, and brain free glucose concentration agreed closely with values obtained in mammals by other investigators. Values for net extraction fraction corresponded closely to simultaneously measured arteriovenous values. We demonstrated that utilization of a model that includes a fourth rate constant to account for regional egress of all 11C-metabolites with positron emission tomography and 1-11C-D-glucose provides accurate measurements of blood-to-brain glucose transport and cerebral glucose metabolism in vivo without need for jugular venous sampling, even under conditions of severe hypoglycemia.

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“…At the level of the BBB, there is a tight relationship between the presence of insulin receptors and the topographic expression of glucose transporters particularly abundant in medial temporal lobe and diencephalic structures, which notably are related to neurocognitive functions (White 2002;Zhou et al 2001), suggesting an important role of insulin in modulation of glucose uptake and utilization (Banks 2004;Baker et al 2011;Craft et al 2012;Hertz et al 1981). Insulin stimulation of glucose transporter-4 (GLUT4) seems to be critical to the regulation of neuronal metabolism and the generation of energy needed for memory and other neurocognitive functions.…”

Section: Glycemic Controlmentioning

confidence: 99%

The diabetic brain and cognition

et al. 2017

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The prevalence of both Alzheimer's disease (AD) and vascular dementia (VaD) is increasing with the aging of the population. Studies from the last several years have shown that people with diabetes have an increased risk for dementia and cognitive impairment. Therefore, the authors of this consensus review tried to elaborate on the role of diabetes, especially diabetes type 2 (T2DM) in both AD and VaD. Based on the clinical and experimental work of scientists from 18 countries participating in the International Congress on Vascular Disorders and on literature search using PUBMED, it can be concluded that T2DM is a risk factor for both, AD and VaD, based on a pathology of glucose utilization. This pathology is the consequence of a disturbance of insulin-related mechanisms leading to brain insulin resistance. Although the underlying pathological mechanisms for AD and VaD are different in many aspects, the contribution of T2DM and insulin resistant brain state (IRBS) to cerebrovascular disturbances in both disorders

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Insulin increases glucose transfer across the blood-brain barrier in man.

Cited by 117 publications

References 42 publications

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Cerebral transport and metabolism of 1‐¹¹C‐D‐glucose during stepped hypoglycemia

The diabetic brain and cognition

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Insulin increases glucose transfer across the blood-brain barrier in man.

Cited by 117 publications

References 42 publications

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-11C]D-Glucose

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-11C]D-Glucose

Cerebral transport and metabolism of 1‐11C‐D‐glucose during stepped hypoglycemia

The diabetic brain and cognition

Contact Info

Product

Resources

About

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Cerebral transport and metabolism of 1‐¹¹C‐D‐glucose during stepped hypoglycemia