[Physiology and pathology of the entero-insular axis].
In the entero-insular axis, humoral factors predominate over neural factors. Gastric inhibitory polypeptide (GIP) is the most important incretin candidate. Release of GIP depends on nutrient absorption, and therefore secondary disturbances of GIP secretion occur in a number of gastrointestinal and metabolic diseases. Alterations of GIP secretion are not necessarily followed by alterations of insulin secretion. Disturbances of the entero-insular axis are best evaluated by estimating the incretin effect (i.e. comparing the insulin response to oral glucose with the insulin response to an isoglycaemic i.v. glucose infusion). From the poor correlation between disturbances of the entero-insular axis and GIP abnormalities it can even be concluded that other intestinal factors with incretin activity exist. The extent of the incretin effect may be overestimated if only serum insulin levels are measured. Unknown gut factors seem to exist which inhibit hepatic insulin extraction and thus alter serum insulin levels without stimulating insulin secretion.
D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D004386:Duodenum / Q000502:physiology*; D005749:Gastric Inhibitory Polypeptide / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000502:physiology*; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide
Physiologie und Pathologie der entero-insulären Achse.