TY - JOUR

T1 - Incretin hormones--an update

AU - Holst, J J

AU - Orskov, C

PY - 2001

Y1 - 2001

N2 - Incretin hormones are insulinotropic hormones from the intestinal mucosa, which after being released in response to ingestion of a meal, enhance insulin secretion in excess of that elicited by the absorbed nutrients (glucose. amino acids etc) themselves. To day it is well established that the most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP, previously known as gastric inhibitory polypeptide) and glucagon-like peptide-1 (GLP-1) from the upper and lower small intestinal mucosa, respectively. It has been shown that interference with the incretin function causes glucose intolerance and it has also been shown that the incretin function is greatly impaired in type 2 diabetes mellitus. The reason for this seems to be twofold: an impaired secretion of GLP-1 and a severely impaired insulinotropic effect of GIP in these patients. In agreement with this, administration of the active incretin, GLP-1, to patients with type 2 diabetes may nearly normalise their fasting and postprandial hyperglycaemia. In addition to its insulinotropic effects, GLP-1 has been shown to stimulate the formation of new beta cells in rodents, partly by enhanced beta cell proliferation and partly by enhancing differentiation of duct progenitor cells to mature beta cells. GLP-1 also inhibits glucagon secretion, inhibits gastric emptying and reduces appetite and food intake. During the last years, therefore, several most promising attempts have been made to develop GLP-1 into a clinically useful therapeutic agent for the treatment of type 2 diabetes.

AB - Incretin hormones are insulinotropic hormones from the intestinal mucosa, which after being released in response to ingestion of a meal, enhance insulin secretion in excess of that elicited by the absorbed nutrients (glucose. amino acids etc) themselves. To day it is well established that the most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP, previously known as gastric inhibitory polypeptide) and glucagon-like peptide-1 (GLP-1) from the upper and lower small intestinal mucosa, respectively. It has been shown that interference with the incretin function causes glucose intolerance and it has also been shown that the incretin function is greatly impaired in type 2 diabetes mellitus. The reason for this seems to be twofold: an impaired secretion of GLP-1 and a severely impaired insulinotropic effect of GIP in these patients. In agreement with this, administration of the active incretin, GLP-1, to patients with type 2 diabetes may nearly normalise their fasting and postprandial hyperglycaemia. In addition to its insulinotropic effects, GLP-1 has been shown to stimulate the formation of new beta cells in rodents, partly by enhanced beta cell proliferation and partly by enhancing differentiation of duct progenitor cells to mature beta cells. GLP-1 also inhibits glucagon secretion, inhibits gastric emptying and reduces appetite and food intake. During the last years, therefore, several most promising attempts have been made to develop GLP-1 into a clinically useful therapeutic agent for the treatment of type 2 diabetes.

KW - Animals

KW - Diabetes Mellitus, Type 2/drug therapy

KW - Gastric Inhibitory Polypeptide/physiology

KW - Glucagon/physiology

KW - Glucagon-Like Peptide 1

KW - Glucagon-Like Peptides

KW - Glucose/administration & dosage

KW - Humans

KW - Insulin/secretion

KW - Intestinal Mucosa/physiology

KW - Peptide Fragments/physiology

KW - Protein Precursors/physiology

M3 - Review

C2 - 11713984

VL - 234

SP - 75

EP - 85

JO - Scandinavian Journal of Clinical & Laboratory Investigation

JF - Scandinavian Journal of Clinical & Laboratory Investigation

SN - 0036-5513

ER -