Stimulation of Release of Insulin by an Extract of Intestinal Mucosa

Abstract

The mechanism of action of an extract of intestinal mucosa that accelerates the disposal of glucose given intravenously in normal man was investigated. The active material is biologically distinguishable from pancreozymin, and its effects cannot be attributed to insulin, insulin-like activity, glucagon or amino acids in the preparation. The extract enhances the increase in blood-insulin concentration which occurs in response to the intravenous infusion of glucose in normal man and which has been compared with that following ingestion of glucose. No response was demonstrable in insulin-treated juvenile-onset diabetes, and it is suggested that the extract acts in normal subjects by stimulating the jrelease of endogenous insulin. It is concluded that an insujln-aecretagogue, derived from the small intestine, may be concerned in the response to ingested glucose, and that such, an agent may be present in the active extract.

Discrepancies between the Doses of Cholecystokinin or Caerulein-Stimulating Exocrine and Endocrine Responses in Perfused Isolated Rat Pancreas

“…Recently, these effects ofthe endocrine pancreas previously attributed to CCK have been ascribed to contaminating gastric inhibitory polypeptide (GIP) present in impure preparations of CCK (9,10). In fact, Dupr6 and Beck (11), and other investigators (12)(13)(14) found no such effects of the hormone when highly purified CCK was used. More recently, however, synthetic COOH-terminal octapeptide of CCK has been shown to stimulate the release of insulin and glucagon both in vivo (15) and in vitro (6, 7).…”

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

“…Peptidergic signals derived from the intestine augment the insulin response induced by nutrients ("the incretin effect") (Dupre and Beck, 1966;Fehmann et al, 1995a). This functional connection between the intestine and the islets of Langerhans was termed the "incretin axis" or "entero-insular-axis" (Unger and Eisentraut, 1969;Fehmann et al, 1995a).…”

The enteral insulin-stimulation after pancreas transplantation in the pig

“…The mechanism behind this phenomenon, termed incretin [5], has received much attention, but its nature has not yet been entirely explained. The incretin effect has mainly been conceived as being of hormonal nature [6][7][8][9][10][11]. However, it might also be due to neural augmentation of the insulin response [4,[12][13][14], though until now no studies have excluded this possibility.…”