http://www.byetta.com/hcp/glp-1_effe...p?reqNavId=1.4

this drug is Glucagon-like peptide-1 (GLP-1) an important incretin hormone secreted by L-cells in the small intestine and colon in response to food intake. As its name might imply, GLP-1 is structurally similar to glucagon. However, they are entirely different hormones and the function of GLP-1 is significantly different from that of glucagon.

GLP-1 acts by binding to specific receptors on the surface of the beta cell, as well as other tissues, and has a very short half-life (less than 2 minutes in the circulation). GLP-1 exerts multiple effects that contribute to the maintenance of glucose homeostasis:

Enhances glucose-dependent insulin secretion1,2
Suppresses inappropriate glucagon secretion1,2
Promotes satiety, leading to reduction of food intake1
Regulates the rate of gastric emptying, limiting postprandial glucose excursions1,2


GLP-1 enhances insulin secretion only in the presence of elevated glucose concentrations.


Insulin secretion
GLP-1 stimulates insulin secretion from beta cells in the pancreas in a glucose-dependent manner:

Stimulates secretion of insulin only when the glucose concentration is elevated
When glucose concentration returns toward normal, this effect of GLP-1 declines
The glucose-dependent nature of GLP-1 prevents too much insulin from being secreted, thus decreasing the risk of hypoglycemia.


Postprandial GLP-1 levels are reduced in patients with
type 2 diabetes.


Glucagon secretion
Glucagon is a hormone that causes the release of glucose from the liver in order to maintain normal glucose homeostasis during fasting and is an important protective mechanism against hypoglycemia. Conversely, glucagon secretion is suppressed during periods of hyperglycemia.

GLP-1 suppresses glucagon secretion from alpha cells in the pancreas in a glucose-dependent manner:

Suppresses glucagon secretion in the fed state
During hypoglycemia, glucagon suppression does not occur
In patients with type 2 diabetes, glucagon concentrations are often inappropriately elevated, resulting in increased hepatic glucose output and postprandial glucose excursions.

Satiety
The central nervous system is a critical site for regulating food intake, satiety, and body weight. GLP-1 works on the brain to trigger a feeling of satiety and reduce food intake.

Gastric emptying
The rate of gastric emptying is a key determinant of the rate of nutrient absorption, an important factor in postprandial glucose excursions. GLP-1 slows the rate of gastric emptying, which in turn slows the delivery and absorption of nutrients in the small intestine and thereby limits the rate at which carbohydrate is absorbed into the circulation. The rate of gastric emptying is often increased in patients with type 2 diabetes, causing a rapid rise in postprandial blood glucose.

1 Zander M, Madsbad S, Madsen JL, et al. Effect of 6-week course of glucagon-like peptide 1 on glycaemic control, insulin sensitivity, and beta-cell function in type 2 diabetes: a parallel-group study. Lancet. 2002;359:824-830.
2 Nauck MA, Wollschlager D, Werner J, et al. Effects of subcutaneous glucagon-like peptide 1 (GLP-1 [7-36 amide]) in patients with NIDDM. Diabetologia. 1996;39:1546-1553.