Abstract
In summary, this article briefly reviews the evidence that three separate autonomic inputs to the islet are capable of stimulating glucagon secretion and that each is activated during IIH. We have reviewed our evidence that these autonomic inputs mediate the glucagon response to IIH, both in non-diabetic animals and humans. Finally, we outline our new preliminary data suggesting an eSIN in an autoimmune animal model of T1DM. We conclude that the glucagon response to IIH is autonomically mediated in non-diabetic animals and humans. We further suggest that at least one of these autonomic inputs, the sympathetic innervation of the islet, is diminished in autoimmune T1DM. These data raise the novel possibility that an autonomic defect contributes to the loss of the glucagon response to IIH in T1DM.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 318-323 |
| Number of pages | 6 |
| Journal | Diabetes, Nutrition and Metabolism - Clinical and Experimental |
| Volume | 15 |
| Issue number | 5 |
| State | Published - Oct 2002 |
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Keywords
- Parasympathetic
- Sympathetic
- Type 1 diabetes
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Internal Medicine
- Endocrinology
- Food Science
- Endocrinology, Diabetes and Metabolism
Cite this
Autonomic mechanism and defects in the glucagon response to insulin-induced hypoglycaemia. / Taborsky, Gerald J.; Ahren, B.; Mundinger, T. O.; Mei, Q.; Havel, Peter J.
In: Diabetes, Nutrition and Metabolism - Clinical and Experimental, Vol. 15, No. 5, 10.2002, p. 318-323.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Autonomic mechanism and defects in the glucagon response to insulin-induced hypoglycaemia
AU - Taborsky, Gerald J.
AU - Ahren, B.
AU - Mundinger, T. O.
AU - Mei, Q.
AU - Havel, Peter J
PY - 2002/10
Y1 - 2002/10
N2 - In summary, this article briefly reviews the evidence that three separate autonomic inputs to the islet are capable of stimulating glucagon secretion and that each is activated during IIH. We have reviewed our evidence that these autonomic inputs mediate the glucagon response to IIH, both in non-diabetic animals and humans. Finally, we outline our new preliminary data suggesting an eSIN in an autoimmune animal model of T1DM. We conclude that the glucagon response to IIH is autonomically mediated in non-diabetic animals and humans. We further suggest that at least one of these autonomic inputs, the sympathetic innervation of the islet, is diminished in autoimmune T1DM. These data raise the novel possibility that an autonomic defect contributes to the loss of the glucagon response to IIH in T1DM.
AB - In summary, this article briefly reviews the evidence that three separate autonomic inputs to the islet are capable of stimulating glucagon secretion and that each is activated during IIH. We have reviewed our evidence that these autonomic inputs mediate the glucagon response to IIH, both in non-diabetic animals and humans. Finally, we outline our new preliminary data suggesting an eSIN in an autoimmune animal model of T1DM. We conclude that the glucagon response to IIH is autonomically mediated in non-diabetic animals and humans. We further suggest that at least one of these autonomic inputs, the sympathetic innervation of the islet, is diminished in autoimmune T1DM. These data raise the novel possibility that an autonomic defect contributes to the loss of the glucagon response to IIH in T1DM.
KW - Parasympathetic
KW - Sympathetic
KW - Type 1 diabetes
UR - http://www.scopus.com/inward/record.url?scp=0344838670&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0344838670&partnerID=8YFLogxK
M3 - Article
C2 - 12625478
AN - SCOPUS:0344838670
VL - 15
SP - 318
EP - 323
JO - Diabetes, Nutrition and Metabolism - Clinical and Experimental
JF - Diabetes, Nutrition and Metabolism - Clinical and Experimental
SN - 0394-3402
IS - 5
ER -