It was reported that GPR is expressed
It was reported that GPR120 is expressed on macrophages in adipose tissue (Oh et al., 2010). Whether GPR120-positive 25-hydroxyvitamin d3 in human and rat pancreas belongs to macrophages was studied. CD68 is a transmembrane glycoprotein that is highly expressed by human monocytes and tissue macrophages (Horikawa et al., 2006, Makitie et al., 2001, van der Kooij et al., 1997). It was found that CD68 was specifically expressed on a few cells in pancreas and CD68-positive cells were distributed mainly in the connective tissue of pancreas. In addition, it was found that almost all CD68-positive cells were stained with GPR120. This result demonstrated that there are infiltrated macrophages in normal pancreas and these macrophages express GPR120, which is similar to that in adipose tissue. On the other hand, Only about 15% of GPR120-positive cells were CD68-positive, and most GPR120-positive cells were not double stained with CD68, which indicates other types of cells in pancreas express GPR120. Considering the embryonic origin of pancreas from the endoderm of duodenum (Grapin-Botton et al., 2001, Slack, 1995), we tried the markers of interstitial cells of gastrointestinal tract, CD34 and CD117. CD34 and CD117 are expressed in the interstitial cells of gastrointestinal tract (Becheanu et al., 2008, Cheuk et al., 2000, Sarlomo-Rikala et al., 1998, Vanderwinden et al., 2000), and they are used to identify the cells originated from interstitial tissues of gastrointestinal tract (Hirota and Isozaki, 2006, Lorincz et al., 2008, Streutker et al., 2007). We found that CD117 and CD34 expressed in human and rat pancreas and they both colocalized with GPR120. Above 80% of GPR120-positive cells were positive to CD117, showing that CD117-positive interstitial cells are the primary GPR120-expressing cells in human and rat pancreas. Finally, after we double stained using GPR120 with CD68, CD34 and CD117 simultaneously. the GPR120-positive cells were fully double-stained by the mixture of CD68, CD34 and CD117. It indicates that GPR120-positive cells in pancreas belong to two types of cells, which are CD68-positive macrophages and CD117 and CD34-positive interstitial cells.
Conflict of interest statement
Acknowledgements This study was supported by the grant from National Natural Science Foundation of China (No. 30971078) and the scientific research foundation from State Education Ministration of China (No. HG3501).
Introduction Free fatty acids are not only an essential source of energy for the body, but are also involved in numerous metabolic processes. Some researchers have suggested that the presence of increased numbers of unesterified free fatty acids play a role in the development of insulin resistance (Kahn et al., 2006, Cavaghan et al., 2000, Boden and Shulman, 2002). Although the precise cause of insulin resistance remains unclear, the glucose-fatty acid cycle of Randle suggests that insulin insensitivity occurs when the oxidation of free fatty acids is favored rather than the oxidation of glucose. Newer evidence has revealed that a serine kinase cascade caused by the build-up of ceramides, diacylglycerol, or acyl-CoA in muscle and liver tissue could also lead to insulin resistance (Delarue and Magnan, 2007). Recent studies have shown that free fatty acids of varying chain length can act as ligands for “orphan” GPCR(G-protein coupled) receptors. In an effort to disclose the identities of several new orphan GPCR's, Fredriksson and his research team mined the human NCBI and Celera genome databases. Their search revealed 7 new GPCR sequences, one of which was named GPR120 (G-protein receptor), located on chromosome 10 (23.33) (Fredriksson et al., 2003). The GPR120 receptor binds long-chain fatty acids with lengths of C14–C18 (saturated) and fatty acids with lengths of C16–C22 (unsaturated) (Hirasawa et al., 2005, Briscoe et al., 2006). The receptor has been found to be localized in mouse lung, intestine, adipose tissue (Miyauchi et al. 2009) and on cells in the rat tongue (Matsumura et al., 2007). Activation of the GPR120 receptor on the surface of intestinal endothelial L-cells causes the release of glucagon-like peptide (GLP-1) from the L- cell through activation of the PKC pathway following intracellular calcium release. In animal studies, mice administered the long-chain unsaturated fatty acid linolenic acid showed increased plasma levels of GLP-1 and insulin (Hirasawa et al., 2005).