02106nas a2200217   4500008004100000245009800041210006900139260001800208300001100226490000600237520143200243653001101675653001001686653002001696653002001716100002501736700002001761700002801781700002701809856005201836       2009                        eng d00aDipeptidyl Peptidase-IV (DPP-IV) Inhibitory Activity of Parotid Exudate of Bufo melanostictus0 aDipeptidyl PeptidaseIV DPPIV Inhibitory Activity of Parotid Exud  cJanuary 2010   a98-1010 v13 a<p class="rtejustify">Type 2 diabetes arises as a result of -cell failure combined with concomitant insulin resistance. Glucagon-like peptide-1 is a gastrointestinal hormone that is released postprandially from the L cells of the gut and exerts a glucose- dependent and direct insulinotropic effect on the pancreatic  cell. Which activate adenylate cyclase and enhances insulin secretion. GLP-1 is rapidly degraded by DPP-IV to GLP-1(9-37) amide following release from gut L cells. GLP-1 directly enhances glucose-dependent insulin secretion via an increase in -cell cAMP. Dipeptidyl peptidase IV (DPP-IV) is a plasma membrane glycoprotein ectopeptidase. In mammals, DPP-IV was widely expressed on the surface of endothelial and epithelial cells and highest levels in humans have been reported to occur in the intestine, bone marrow and kidney. Inhibiting DPP-IV reduces its rapid degradation of GLP-1, increasing circulating levels of the active hormone in vivo and prolonging its beneficial effects. The IC<sub>50</sub> value of parotid exudate was found to be 9.4 2g/ml. The maximum % inhibition (61.8) was showed at a concentration of 122g/ml. Parotid exudate through inhibition of DPP-IV, improves glucose tolerance and enhances insulin secretion. DPP-IV inhibitors are a novel class of oral hypoglycemic agents with a potential to improve pancreatic beta cell function and the clinical course of type 2 diabetes.</p>
10aDPP-IV10aGLP-110aParotid exudate10atype 2 diabetes1 aVenkatesham, Allenki1 aPrasad, Neerati1 aKrishna, Devarakonda, R1 aReddy, Yellu, Narsimha  uhttps://www.phcogres.com/article/2009/1/2/nil-6