GPR119 expressed on certain enteroendocrine cells (L and K cells) in the small intestine and by -cells within the islets of Langerhans of the pancreas is a lipid-responsive class A (rhodopsin-type) receptor. The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion from pancreatic -cells and increased release of the gut peptides GLP-1 (glucagon like peptide 1), GIP (glucose-dependent insulinotropic peptide) and PYY (polypeptide YY). Additionally, GLP-1 and GIP can both interact with their cognate receptors on the -cell to elicit insulin secretion. Thus, GPR119 agonists lead to a rise in insulin release by both direct mechanisms. Since GLP-1 (and probably GIP) also promotes -cell viability, it is possible that orally acting GPR119 agonists may influence both the secretory activity and the viability of -cells, leading to improved glucose tolerance in patients with T2DM. Preclinical and clinical studies with GPR119 agonists in type 2 diabetes support that GPR119 agonists have been proposed as a novel therapeutic strategy for diabetes. The initial data shows the WT-GPR119 performs very unstable state. We tried many ways to help stable the protein like truncation of N- and C-terminus, mutations and different fusion proteins. Since the expression level is very low at this stage, we add a GFP at C-terminus to detect the protein directly. And the protein shows the lower aggregation and more monomer now. It seems that we are in the right direction.