@article {754,
	title = {Dipeptidyl Peptidase-IV (DPP-IV) Inhibitory Activity of Parotid Exudate of Bufo melanostictus},
	journal = {Pharmacognosy Research},
	volume = {1},
	year = {2009},
	month = {January 2010 },
	pages = {98-101},
	type = {Original Article},
	chapter = {98},
	abstract = {<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>
},
	keywords = {DPP-IV, GLP-1, Parotid exudate, type 2 diabetes},
	doi = {Nil},
	author = {Allenki Venkatesham and Neerati Prasad and Devarakonda R Krishna and Yellu Narsimha Reddy}
}
