Abstract
Glucagon-like peptide 1 (GLP-1) is a hormone, inducing glucose-dependent stimulation of insulin secretion from beta cells. Liraglutide acts as a GLP-1 receptor agonist. To assess the effect of liraglutide on the beta cell function, we performed oral glucose tolerance tests in 7 subjects with type 2 diabetes before and after treatment of liraglutide. Moreover, we performed same study again in 4 subjects at 6 months after induction. Liraglutide significantly increased area under the Curve (AUC) of plasma insulin level after glucose loading and significantly decreased AUC of plasma glucose level, compared with before induction. HOMA-beta was significantly increased, whereas insulinogenic index was not changed. HOMA-R was not affected but Matsuda index was significantly decreased after induction of liraglutide. Disposition index was not altered significantly, but tendency of improvement was observed. Glucose tolerance tests revealed that those effects of liraglutide were continued for 6 months after induction. These results showed that treatment of liraglutide could improve insulin secretion but early phase of insulin secretion was not improved. The results suggest that liraglutide is likely to improve beta-cell function, but this effect is still inadequate by six-month treatment.
Highlights
Since incretin mimetic drugs were available for the treatment of type 2 diabetes these drugs were widely used because of its hypoglycemic effect and safety
glucagon-like peptide-1 (GLP-1) is secreted from L cells in the lower small intestine in response to ingested nutrients and stimulates insulin secretion from pancreatic β cells depending on the blood glucose concentration [1]
In our 7 patients with type 2 diabetes without depletion of endogenous insulin secretion, liraglutide was newly introduced after improving glycemic control
Summary
Since incretin mimetic drugs were available for the treatment of type 2 diabetes these drugs were widely used because of its hypoglycemic effect and safety. The effect of these drugs is considered to mainly result from the actions of glucagon-like peptide-1 (GLP-1). Liraglutide, which is a GLP-1 receptor agonist resistant to DPP-4, was developed using one amino acid substitution and fatty acid addition and found to produce a sufficient therapeutic effect with only one injection per day [4]. The GLP-1 receptor agonist improves blood glucose, and was suggested to restore β cell function by relieving oxidation stress on β cells in diabetic mice [5]. There was slightly evidence for the restoration of β cell function by the GLP-1 receptor agonist in human [6]
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