Abstract:
Incretins are hormones that are secreted by the gut upon feeding; their release alerts the pancreatic islets that nutrients will come through the gastrointestinal tract and islets start priming by vagal stimulation (Boron and Boulpaep, 2005). Glucagon-Like Peptide-1 (GLP-1) and Glucose Dependent Insulinotropic Peptide (GIP) are the major incretin hormones produced by the L cells of the ileum and colon, and K cells of the duodenum and jejunum, respectively (Xu et al., 2007). GLP-1 has numerous postprandial effects on glucose homeostasis. Upon interaction with its receptor on β-cells, GLP-1 increases the intracellular levels of cAMP and calcium, thereby releasing insulin. GLP-1 has also inhibitory effects on Glucagon secretion from the α-cells, gastric emptying and food ingestion (Drucker, 2007). In both type 1 and type 2 diabetes mellitus, there is a marked reduction in the incretin effect (Knop et al., 2007). A recent study showed that GLP-1 receptor expression is down regulated in β-cells exposed to high glucose concentrations in vitro and hyperglycemia in vivo (Xu et al., 2007). The β-cells in diabetic individuals exhibit attenuated sensitivity to GLP-1. Moreover, Type 2 diabetic patients exhibited significantly lower GLP-1 secretion in response to meal absorption (D'Alessio and Vahl, 2004). This chapter, focuses on the function of incretin hormones, specifically, GLP-1 and its analogues on glucagon homeostasis and diabetes. © 2013 by Nova Science Publishers, Inc. All rights reserved.