A simplified model of glucose-sensing mechanisms present in the brain.

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Presentation transcript:

A simplified model of glucose-sensing mechanisms present in the brain. A simplified model of glucose-sensing mechanisms present in the brain. Glucose from the arterial supply is transported either directly into neurons via GLUT-3 (possibly GLUT-2) or indirectly as lactate generated through glycolysis in astrocytes. Glucose is phosphorylated by GK, a key regulatory step in glucose sensing, before undergoing oxidative-phosphorylation to generate ATP. ATP closes the SUR-1–selective KATP, leading to membrane depolarization, calcium influx, and release of neurotransmitters and/or neuropeptides. In addition, AMP-to-ATP ratios are monitored by AMPK, activation that during hypoglycemia stimulates the production of nitric oxide and may act via the KATP channel or directly to stimulate neurotransmitter release. Additional mechanisms that may modulate this basic glucose-sensing mechanism include: 1) SGLTs, 2) GABAergic inhibition (or modulation by other neurotransmitters such as norepinephrine), and 3) the actions of hormones such as insulin and leptin and neuropeptides such as urocortin 3. CI−, chloride; Ins, insulin; MCT, monocarboxylate transporters; NOS, nitric oxide synthase; UCN3, urocortin 3. Rory J. McCrimmon, and Robert S. Sherwin Diabetes 2010;59:2333-2339 ©2010 by American Diabetes Association