Abstract
The development of type 2 diabetes requires impaired β cell function. Hyperglycemia itself causes further decreases in glucose-stimulated insulin secretion. A new study demonstrates that hyperglycemia-induced mitochondrial superoxide production activates uncoupling protein 2, which decreases the ATP/ADP ratio and thus reduces the insulin-secretory response (see the related article beginning on page 1831). These data suggest that pharmacologic inhibition of mitochondrial superoxide overproduction in β cells exposed to hyperglycemia could prevent a positive feed-forward loop of glucotoxicity that drives impaired glucose tolerance toward frank type 2 diabetes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1788-1790 |
| Number of pages | 3 |
| Journal | Journal of Clinical Investigation |
| Volume | 112 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 2003 |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
A radical explanation for glucose-induced β cell dysfunction. / Brownlee, Michael.
In: Journal of Clinical Investigation, Vol. 112, No. 12, 12.2003, p. 1788-1790.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - A radical explanation for glucose-induced β cell dysfunction
AU - Brownlee, Michael
PY - 2003/12
Y1 - 2003/12
N2 - The development of type 2 diabetes requires impaired β cell function. Hyperglycemia itself causes further decreases in glucose-stimulated insulin secretion. A new study demonstrates that hyperglycemia-induced mitochondrial superoxide production activates uncoupling protein 2, which decreases the ATP/ADP ratio and thus reduces the insulin-secretory response (see the related article beginning on page 1831). These data suggest that pharmacologic inhibition of mitochondrial superoxide overproduction in β cells exposed to hyperglycemia could prevent a positive feed-forward loop of glucotoxicity that drives impaired glucose tolerance toward frank type 2 diabetes.
AB - The development of type 2 diabetes requires impaired β cell function. Hyperglycemia itself causes further decreases in glucose-stimulated insulin secretion. A new study demonstrates that hyperglycemia-induced mitochondrial superoxide production activates uncoupling protein 2, which decreases the ATP/ADP ratio and thus reduces the insulin-secretory response (see the related article beginning on page 1831). These data suggest that pharmacologic inhibition of mitochondrial superoxide overproduction in β cells exposed to hyperglycemia could prevent a positive feed-forward loop of glucotoxicity that drives impaired glucose tolerance toward frank type 2 diabetes.
UR - http://www.scopus.com/inward/record.url?scp=0346093889&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0346093889&partnerID=8YFLogxK
U2 - 10.1172/JCI200320501
DO - 10.1172/JCI200320501
M3 - Article
C2 - 14679173
AN - SCOPUS:0346093889
VL - 112
SP - 1788
EP - 1790
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
SN - 0021-9738
IS - 12
ER -