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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

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