General Information:

Id: 3,200 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Mammalia
review
Reference: Peters A et al.(2011) The selfish brain: stress and eating behavior Front Neurosci 5: 74 [PMID: 21660101]

Interaction Information:

Comment The glucose transporter 1 (GLUT1) has been found to mediate glucose transport in a manner that depends on cytoplasmic ATP. GLUT1 are abundantly located on the luminal and abluminal side of endothelial cells forming the blood-brain barrier and on the end feet of the adjacent astrocytes which make contact to the endothelial cells. It has been shown that astrocytes enhance their GLUT1 mediated glucose uptake once they consume ATP.
Formal Description
Interaction-ID: 29422

drug/chemical compound

ATP

increases_activity of

process

glucose import

into the brain
Comment Because insulin is required for glucose uptake in the peripheral fat and muscle tissue via glucose transporter 4 (GLUT4), these postsynaptic VMH-neurons are able to limit glucose outflow the blood into the peripheral energy buffers. In this way, these allocative mechanisms are able to preserve blood glucose as a source for the insulin-independent glucose uptake via GLUT1 into the brain.
Formal Description
Interaction-ID: 29429

increases_activity of

process

glucose import

into muscle, into adipose tissue; via GLUT4 (SLC2A4)
Comment Because insulin is required for glucose uptake in the peripheral fat and muscle tissue via glucose transporter 4 (GLUT4), these postsynaptic VMH-neurons are able to limit glucose outflow the blood into the peripheral energy buffers. In this way, these allocative mechanisms are able to preserve blood glucose as a source for the insulin-independent glucose uptake via GLUT1 into the brain.
Formal Description
Interaction-ID: 29431

affects_activity of

process

glucose import

into muscle, into adipose tissue; via GLUT4 (SLC2A4)
Comment Because insulin is required for glucose uptake in the peripheral fat and muscle tissue via glucose transporter 4 (GLUT4), these postsynaptic VMH-neurons are able to limit glucose outflow the blood into the peripheral energy buffers. In this way, these allocative mechanisms are able to preserve blood glucose as a source for the insulin-independent glucose uptake via GLUT1 into the brain.
Formal Description
Interaction-ID: 29432

affects_activity of

process

glucose import

into the brain; via GLUT1 (SLC2A1)