Steady‐State Cerebral Glucose Concentrations and Transport in the Human Brain

Gruetter, Rolf; Uğurbil, Kâmil; Seaquist, Elizabeth R.

doi:10.1046/j.1471-4159.1998.70010397.x

Cited by 233 publications

(320 citation statements)

References 58 publications

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“…More recently Gruetter and coworkers 52 have used 1 H MRS at 4 T to analyze the relationship between plasma and brain steady-state glucose concentration over a very wide range of glucose concentration. In this study the brain glucose concentration was found above normal levels to be in a constant ratio of concentration with plasma glucose.…”

Section: In Vivo Mrs Studies To Test Models Of Glucose Transportmentioning

confidence: 99%

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Rothman

2001

NMR in Biomedicine

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Organs consist of several types of cells with specialized functions. This cellular localization of function is often referred to as compartmentation. Due to the intrinsic low sensitivity of MR methods it is generally not possible in vivo to obtain images or spectra of single cells. Instead the MRS signal is the sum of the signal from millions of cells and multiple cell types. A major challenge in using MRS to study biological processes such as metabolism and transport is to devise measurements that provide cell-specific information from this mix. Fortunately nature has helped the MR scientist by in several cases nearly completely localizing metabolic pathways and their associated metabolites in specific cell types. The chemical specificity of MRS allows the concentrations and synthesis rates of these metabolites to be measured, providing information about the compartmentation of metabolism and function. In this review examples are presented from MRS studies of metabolic trafficking between neurons and astrocytes in the brain, brain glucose transport, and the role of muscle glucose transport in insulin resistance and diabetes. The concepts and approaches used in these studies are generally applicable for studying cellular metabolic compartmentation in a wide range of systems.

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Section: In Vivo Mrs Studies To Test Models Of Glucose Transportmentioning

confidence: 99%

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Rothman

2001

NMR in Biomedicine

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“…Plasma glucose concentrations of <3 mM lead to impaired cognitive function [3,4], and limitations of glycolysis [17,18].…”

Section: Comparison Of In Vitro Glucose Ambient Levels and In Vivo CLmentioning

confidence: 99%

Effects of relative hypoglycemia on LTP and NADH imaging in rat hippocampal slices

2007

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Cognitive and neuronal impairment in diabetes may be associated with iatrogenic hypoglycemia, particularly at low serum glucose levels (< 3 mM). To evaluate cellular impairment, we assessed acute hippocampal slice functioning during decreased ambient glucose, by monitoring evoked field excitatory post-synaptic potentials (fEPSP), and slice nicotinamide adenine dinucleotide (NADH) fluorescence. The effects of lowered glucose levels (60 min) were analyzed by examining the induction and maintenance of long-term potentiation (LTP), and NADH metabolic imaging in the CA1 region. The basal fEPSP response was reduced by lowered ambient glucose, an effect that was reversible in 2.5 mM glucose, partially reversible in 1.25 mM glucose and irreversible in 0 mM glucose, after 25 min recovery. LTP induction and maintenance declined during glucose restriction, demonstrating reversibly failed maintenance in 5 mM and 2.5 mM ambient glucose, and absent induction in 1.25 mM glucose. Peak NADH levels observed during train-induced biphasic transients were significantly reduced during 1.25 mM and 2.5 mM glucose. Significant functional compromise in our slice model occurred at 2.5 mM ambient glucose, equivalent to <1mM tissue glucose in the slice center, due to diffusion limitations and active glucose utilization. This tissue glucose level correlates with human observations of a serum threshold of <3mM for cognitive impairment, since brain tissue glucose is approximately one third of serum levels. The physiological effects of hypoglycemia in our slice model, assessed through fEPSP, LTP, and NADH responses, replicate closely the in vivo situation, confirming the usefulness of this model in assessing consequences of relative hypoglycemia.

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“…S was assumed to be 0.77 ml/g [29]. The mean value of K t =4.05, as collated by Gruetter et al, was used [39].…”

Section: Biochemical Analysesmentioning

confidence: 99%

Differential changes in brain glucose metabolism during hypoglycaemia accompany loss of hypoglycaemia awareness in men with type 1 diabetes mellitus. An [11C]-3-O-methyl-d-glucose PET study

et al. 2005

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Differential changes in brain glucose metabolism during hypoglycaemia accompany loss of hypoglycaemia awareness in men with type 1 diabetes mellitus. An Abstract Aims/hypothesis: Hypoglycaemia unawareness in type 1 diabetes increases the risk of severe hypoglycaemia and impairs quality of life for people with diabetes. To explore the central mechanisms of hypoglycaemia awareness, we used [ 11 C]-3-O-methyl-D-glucose (CMG) positron emission tomography (PET) to measure changes in global and regional brain glucose metabolism between euglycaemia and hypoglycaemia in aware and unaware diabetic subjects. Materials and methods: Twelve men with type 1 diabetes, of whom six were characterised as aware and six as unaware of hypoglycaemia, underwent two CMG-PET brain scans while plasma glucose was controlled by insulin and glucose infusion either at euglycaemia (5 mmol/l) or at hypoglycaemia (2.6 mmol/l) in random order. Results: With hypoglycaemia, symptoms and sweating occurred only in the aware group. Brain glucose content fell in both groups (p=0.0002; aware, 1.18± 0.45 to 0.02±0.2 mmol/l; unaware, 1.07±0.46 to 0.19±0.23 mmol/l), with a relative increase in tracer uptake in prefrontal cortical regions, including the anterior cingulate. No detectable differences were found between groups in global brain glucose transport parameters (K 1 , k 2 ). The cerebral metabolic rate for glucose (CMRglc) showed a relative rise in the aware subjects (11.839±2.432 to 13.958± 2.372) and a fall in the unaware subjects (from 12.457± 1.938 to 10.16±0.801 μmol 100 g −1 min −1 , p=0.043). Conclusions/interpretation: Hypoglycaemia is associated with reduced brain glucose content in aware and unaware subjects, with a relative preservation of metabolism in areas associated with sympathetic activation. The relative rise in global glucose metabolic rate seen in aware subjects during hypoglycaemia contrasted with the relative fall in the unaware subjects and suggests that cortical neuronal activation is a necessary correlate of the state of hypoglycaemia awareness.

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Steady‐State Cerebral Glucose Concentrations and Transport in the Human Brain

Cited by 233 publications

References 58 publications

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Studies of metabolic compartmentation and glucose transport using in vivo MRS

Effects of relative hypoglycemia on LTP and NADH imaging in rat hippocampal slices

Differential changes in brain glucose metabolism during hypoglycaemia accompany loss of hypoglycaemia awareness in men with type 1 diabetes mellitus. An [11C]-3-O-methyl-d-glucose PET study

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