LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES

Ralph Defronzo; John Wahren; Eleuterio Ferrannini; Philip Felig

doi:10.1016/S0140-6736(78)91807-X

LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES

Ralph Defronzo, John Wahren, Eleuterio Ferrannini, Philip Felig

Research output: Contribution to journal › Article › peer-review

27 Scopus citations

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	https://doi.org/10.1016/S0140-6736(78)91807-X
State	Published - Nov 18 1978
Externally published	Yes

ASJC Scopus subject areas

General Medicine

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10.1016/S0140-6736(78)91807-X

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title = "LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES",

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-insulin{\ae}mia and insulin resistance, deficiency of this gastrointestinal factor may be the primary pathogenetic event leading to postprandial hyperglyc{\ae}mia. Postprandial hyperglyc{\ae}mia brings about an increase in insulin secretion; and hyperinsulin{\ae}mia, in turn, results in decreased binding of insulin to its receptor and in peripheral (extrahepatic) resistance to insulin.",

author = "Ralph Defronzo and John Wahren and Eleuterio Ferrannini and Philip Felig",

note = "Funding Information: We thank the animal-house staff, King{\textquoteright}s College Hospital Medical School, and the renal unit technical staff, Dulwich Hospital, for their assistance during this study. G. A. was supported by the Joint Research Committee, King{\textquoteright}s College Hospital. Requests for reprints should be addressed to M. J. W.",

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doi = "10.1016/S0140-6736(78)91807-X",

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AU - Defronzo, Ralph

AU - Wahren, John

AU - Ferrannini, Eleuterio

AU - Felig, Philip

N1 - Funding Information: We thank the animal-house staff, King’s College Hospital Medical School, and the renal unit technical staff, Dulwich Hospital, for their assistance during this study. G. A. was supported by the Joint Research Committee, King’s College Hospital. Requests for reprints should be addressed to M. J. W.

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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.

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LACK OF A GASTROINTESTINAL MEDIATOR OF INSULIN ACTION IN MATURITY-ONSET DIABETES

Abstract

ASJC Scopus subject areas

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