Glucagon Diabetes mellitus Islet microcirculation
Glucagon Diabetes mellitus Islet microcirculation
Glucagon Diabetes mellitus Islet microcirculation
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α-cells<br />
Zinc<br />
opened K ATP channels<br />
inhibited glucose and pyruvate-stimulated<br />
glucagon secretion<br />
did not inhibit arginine-induced glucagon release<br />
… when K ATP channel activity is bypassed, Zn is unable to<br />
block hormone secretion<br />
Pancreatic ß-cell K + -ATP sensitive channel: SUR1/Kir6.2<br />
SUR1<br />
Kir6.2<br />
Transcripts encoding K ATP subunits were more<br />
abundant in α- than ß-cells (FACS-isolated)<br />
Zinc action probably results from direct activation of<br />
α-cell K ATP channels rather than inhibition of<br />
Ca 2+ channels<br />
37<br />
Site of Zn action may be located on the SUR1 subunit<br />
38<br />
Relative abundance of insulin receptor and GLP-1<br />
receptor transcripts in FACS-isolated α- and ß-cells<br />
and compared with liver<br />
Data are presented relative to ß-cells , n =3, *P < 0.05, **P < 0.01<br />
39 40<br />
Analysis of islet hormone secretion<br />
Analysis of islet hormone secretion<br />
absence<br />
Insulin antiserum<br />
presence<br />
absence<br />
presence<br />
“Zn-free”<br />
exogenous insulin<br />
absence<br />
presence<br />
exogenous insulin<br />
mean ± SE **P < 0.01<br />
41<br />
means+SE **P < 0.01<br />
42