Abstract
It is suggested that hepatic uptake of orally ingested glucose depends not only on insulin secretion but also on the release of a gastrointestinal factor which mediates insulin action on the liver. In maturity-onset diabetes characterised by hyper-insulinæmia and insulin resistance, deficiency of this gastrointestinal factor may be the primary pathogenetic event leading to postprandial hyperglycæmia. Postprandial hyperglycæmia brings about an increase in insulin secretion; and hyperinsulinæmia, in turn, results in decreased binding of insulin to its receptor and in peripheral (extrahepatic) resistance to insulin.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1077-1079 |
| Number of pages | 3 |
| Journal | The Lancet |
| Volume | 312 |
| Issue number | 8099 |
| DOIs | |
| State | Published - Nov 18 1978 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES. / Defronzo, Ralph A; Wahren, John; Ferrannini, Eleuterio; Felig, Philip.
In: The Lancet, Vol. 312, No. 8099, 18.11.1978, p. 1077-1079.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES
AU - Defronzo, Ralph A
AU - Wahren, John
AU - Ferrannini, Eleuterio
AU - Felig, Philip
PY - 1978/11/18
Y1 - 1978/11/18
N2 - It is suggested that hepatic uptake of orally ingested glucose depends not only on insulin secretion but also on the release of a gastrointestinal factor which mediates insulin action on the liver. In maturity-onset diabetes characterised by hyper-insulinæmia and insulin resistance, deficiency of this gastrointestinal factor may be the primary pathogenetic event leading to postprandial hyperglycæmia. Postprandial hyperglycæmia brings about an increase in insulin secretion; and hyperinsulinæmia, in turn, results in decreased binding of insulin to its receptor and in peripheral (extrahepatic) resistance to insulin.
AB - It is suggested that hepatic uptake of orally ingested glucose depends not only on insulin secretion but also on the release of a gastrointestinal factor which mediates insulin action on the liver. In maturity-onset diabetes characterised by hyper-insulinæmia and insulin resistance, deficiency of this gastrointestinal factor may be the primary pathogenetic event leading to postprandial hyperglycæmia. Postprandial hyperglycæmia brings about an increase in insulin secretion; and hyperinsulinæmia, in turn, results in decreased binding of insulin to its receptor and in peripheral (extrahepatic) resistance to insulin.
UR - http://www.scopus.com/inward/record.url?scp=0018079375&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018079375&partnerID=8YFLogxK
U2 - 10.1016/S0140-6736(78)91807-X
DO - 10.1016/S0140-6736(78)91807-X
M3 - Article
C2 - 82091
AN - SCOPUS:0018079375
VL - 312
SP - 1077
EP - 1079
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 8099
ER -