GLUT1: Difference between revisions
From Proteopedia
Jump to navigationJump to search
No edit summary |
No edit summary |
||
| Line 40: | Line 40: | ||
GLUT1 has been found to be upregulated in retinal tissue of diabetic mice. Studies on mice show that GLUT1 overexpression plays a key role in development of diabetic retinopathy.<ref>PMID:33622781</ref> While it has been proven that hyperglycemia causes diabetic retinopathy in humans, at this point more research is necessary to determine if GLUT1 plays a direct role in diabetic retinopathy. | GLUT1 has been found to be upregulated in retinal tissue of diabetic mice. Studies on mice show that GLUT1 overexpression plays a key role in development of diabetic retinopathy.<ref>PMID:33622781</ref> While it has been proven that hyperglycemia causes diabetic retinopathy in humans, at this point more research is necessary to determine if GLUT1 plays a direct role in diabetic retinopathy. | ||
===Alzheimer's Disease=== | |||
A handful of glucose transporters, including GLUT1, have been shown to be downregulated in Alzheimer's disease.<ref>PMID:29235507</ref> Potential therapeutic solutions to glucose transporter deficiency in conditions such as Alzheimer's include [https://en.wikipedia.org/wiki/Glucagon-like_peptide-1 glucagon-like peptide 1 (GLP-1)] analog treatment. Although GLP-1 agonists have been proven to increase insulin secretion by the pancreas in type II diabetes mellitus<ref>PMID:26177483</ref>, it is unclear how they affect glucose transporter kinetics in the brain. | A handful of glucose transporters, including GLUT1, have been shown to be downregulated in Alzheimer's disease.<ref>PMID:29235507</ref> Potential therapeutic solutions to glucose transporter deficiency in conditions such as Alzheimer's include [https://en.wikipedia.org/wiki/Glucagon-like_peptide-1 glucagon-like peptide 1 (GLP-1)] analog treatment. Although GLP-1 agonists have been proven to increase insulin secretion by the pancreas in type II diabetes mellitus<ref>PMID:26177483</ref>, it is unclear how they affect glucose transporter kinetics in the brain. | ||