Effect of secretin on basal- and glucose-stimulated insulin secretion in man

Abstract

Plasma immunoreactive secretin and insulin concentrations were measured in fasting normal humans after intraduodenal infusions of hydrochloric acid, isotonic or hypertonic glucose. The effect of intraduodenal acidification or intravenous bolus injections of secretin on plasma insulin concentrations during infusions of glucose was also examined. The intraduodenal glucose load did not cause an increase in plasma secretin concentrations. Secretin concentrations rose after acid both in the fasting state and during infusions of glucose. A concomitant rise in insulin levels was however only observed during infusions of glucose. Intravenous injection of secretin in a dose which mimicked the response to intraduodenal acidification was without effect on the glucose-stimulated insulin release, while a 30 times higher dose caused a highly significant augmentation of the insulin release. The insulin response pattern to this high dose of secretin differed completely from that observed after intraduodenal infusion of acid. It is concluded and confirmed that the stimulating effect of secretin on insulin secretion is pharmacological and that secretin plays no significant role in the entero-insular axis.

Role of incretin hormones in the regulation of insulin secretion in diabetic and nondiabetic humans

“…Secretin itself is a good example. Secretin powerfully stimulates insulin secretion in healthy subjects as well as in patients with type 2 diabetes (8,20). The plasma concentrations of secretin required to influence insulin secretion are in the upper range of those normally observed but comparable to those elicited by intraduodenal acidification.…”

“…The plasma concentrations of secretin required to influence insulin secretion are in the upper range of those normally observed but comparable to those elicited by intraduodenal acidification. Secretin is not released by intraduodenal or oral glucose and therefore does not qualify as an incretin in the strict sense (20) but may contribute in the more complex setting of mixed-meal ingestion. Among the peptides that actually are released in response to oral glucose, two additional members of the same peptide family, namely glucose-dependent insulinotropic polypeptide (GIP, formerly known as gastric inhibitory polypeptide) and glucagon-like peptide 1 (GLP-1) have attracted the most attention.…”

Loss of Incretin Effect Is a Specific, Important, and Early Characteristic of Type 2 Diabetes

“…No other gut hormones fulfill all criteria to act as incretin hormones, i.e., being secreted during glucose ingestion and being capable of stimulating insulin secretion during similar glycemic levels and in those concentrations that are reached during glucose ingestion (9,10). The concentrations of GIP have been reported to be both elevated, decreased, and unchanged in patients with type 2 diabetes (11), but many of the early results were obtained with assays that cross-react with substances in plasma that are unrelated to GIP (12).…”

Effects of vasoactive intestinal polypeptide (VIP), secretin and gastrin on insulin secretion in the mouse

“…Secretin seems to stimulate insulin secretion in high doses in man [1,2,[21][22][23] and while augmenting glucose-induced insulin release it had no influence on the effect of other secretagogues [22]. In doses that reproduce the level of circulating secretin, however, there was no effect on glucose-induced insulin release [24].…”