The glucose-transporter protein and glucopenic brain injury

Article Abstract:

Glucose, a sugar, moves rapidly across the blood-brain barrier, and across cellular membranes to nourish neurons and glia (nerve cells and supporting tissues of the brain and spinal cord). When deprived of glucose, the brain not only ceases to function properly, but can be permanently damaged. Hypoglycemia (low blood sugar) causes mental clouding, stupor, coma, spasms, seizures, tremor, anxiety, pallor, rapid heartbeat, and a variety of metabolic abnormalities. Five specific glucose-transporter proteins have been identified. Darryl C. De Vivo and his colleagues, in the September 5, 1991 issue of The New England Journal of Medicine, present two cases of infants with seizures and developmental delays. There were no metabolic or neurologic abnormalities, except for low levels of glucose and lactate in the cerebrospinal fluid, presumably caused by a defect in the glucose-transporter protein. A ketogenic diet high in fatty acids (which do not require the glucose transporter) was initiated to provide the major source of energy for the brain. Seizures stopped soon after the diet was initiated and the children improved. It has been reported that the density of glucose-transporter protein is low in the brains of patients with Alzheimer's disease, although this may be a result rather than a cause of the disease. The density of glucose-transporter protein is high during infancy and maturation. How the functional regulation of the glucose-transporter protein works is unknown, but other research has shown that impaired cerebral glucose transport occurs in acquired as well as genetic disorders. The problem of defective glucose transport in infants may improve with maturity, so therapy may only be required temporarily. (Consumer Summary produced by Reliance Medical Information, Inc.)

Convulsions, editorial

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Defective glucose transport across the blood-brain barrier as a cause of persistent hypoglycorrhachia, seizures, and developmental delay

Article Abstract:

Glucose (d-glucose or dextrose, a sugar) is essential for the functioning of the brain and other tissues; it is carried to the brain by five glucose-transporter proteins. Certain genetic conditions impede the movement of glucose across the blood-brain barrier. Two cases involving children with hypoglycorrhachia (low levels of glucose in cerebrospinal fluid), seizures and delayed development are discussed. Both children evidently suffered from a genetic defect of the type 1 glucose transporter. In both cases, seizures began at about two months of age, mental and physical development was delayed, and microcephaly (abnormally small head circumference) was observed. Seizures were treated unsuccessfully with anticonvulsant medications. Lumbar punctures indicated low cerebrospinal fluid levels of glucose and the enzyme lactate; the former suggested a defect of in the transport of glucose to the brain. The condition was diagnosed as a partial defect of the glucose transporter. The genetic aspects of the defect, and its detection, are discussed. Both children were put on ketogenic diets, which produce ketones (compounds generated by the oxidation of fatty acids). This diet is one treatment for seizures that can not be controlled otherwise, but how it works is unknown. Apparently, the ketones provide the brain with energy necessary for the developing nervous system. Both children were free of seizures within one week of beginning the diet. From the relative performances of these two patients, it is concluded that early detection and treatment of hypoglycorrhachia and seizures with a ketogenic diet will moderate some of the ill effects of the condition. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Diet therapy, Seizures (Medicine), Cerebrospinal fluid

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A practical approach to fasting hypoglycemia

Article Abstract:

Fasting hypoglycemia, or low blood levels of glucose during fasting, may be caused by several different medical conditions. In resting adults, the central nervous system (CNS) uses two-thirds of the body's glucose supply, and other parts of the body use the remainder. During fasting, the liver maintains blood levels of glucose, but several diseases can decrease the ability of the liver to produce glucose. Blood levels of insulin that are too high or too low may cause hypoglycemia. A blood test can determine which type of hypoglycemia a patient has. Patients who produce too much insulin may have insulinoma, factitious hypoglycemia or a condition that causes the production of antibodies that bind insulin. Patients with insulinoma have benign tumors that increase the release of insulin and a substance called peptide C into the blood. Factitious hypoglycemia caused by ingestion of a sulfonylurea drug appears similar to insulinoma, but the drug can be detected in the patient's urine. Factitious hypoglycemia can also be caused by injection of insulin. Patients who produce anti-insulin antibodies have low blood levels of peptide C and high blood levels of insulin.

Editorial

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