Is GLUT2 insulin independent?

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Cundiff1080

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In FA 2013, it says, GLUT1 (insulin independent glucose uptake), GLUT2 (bidirectional), GLUT4(insulin dependent). Then the BRICK L mnemonic includes the liver and intestine as insulin-independent glucose uptake, but not the beta islet cells. So does that mean GLUT2 is insulin independent as well?

Thanks.
 
GLUT 2 has to be insulin dependent independent since unless glucose enters beta cells via GLUT 2 it won't be able to make the ATP required to close the K+ channel which is required to depolarize the membrane for Ca+ channels to open and Ca+ to enter the cell to bring about insulin release.
 
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GLUT 2 has to be insulin dependent since unless glucose enters beta cells via GLUT 2 it won't be able to make the ATP required to close the K+ channel which is required to depolarize the membrane for Ca+ channels to open and Ca+ to enter the cell to bring about insulin release.
Are you saying the beta cells require insulin for glucose uptake to produce more insulin?
 
Are you saying the beta cells require insulin for glucose uptake to produce more insulin?
My apologies. It was a typo.
It should read: GLUT 2 has to be insulin independent since unless glucose enters beta cells via GLUT 2 it won't be able to make the ATP required to close the K+ channel which is required to depolarize the membrane for Ca+ channels to open and Ca+ to enter the cell to bring about insulin release.
 
Glut 2 km in beta islet is HIGH -->low affinity. This is so that normal glucose levels don't trigger insulin release.

Just to add on to this; it's my understanding that GLUT 2, the receptor found in hepatocytes and B-islet cells, has a high Km (low affinity) because hepatocytes use glucose primarily for storage - and it makes no sense to store glucose unless you've just eaten a big meal and your glucose levels are high enough to bind with this low affinity receptor) - whereas muscle and adipose respond to glucose in peripheral blood with GLUT 4 (and GLUT 1? not sure about this) and have a much lower Km (higher affinity) because they require a relatively constant supply of glucose so even in times of fasting they pull in glucose from the blood. I think it's true that GLUT 2 transporters and glucokinase serve as insulin sensors for glucose release from islet cells in the pancreas, it's just not the first thing that comes to mind when justifying their affinity.
 
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