Abstract
ObjectivePrevious studies demonstrated that a phenylpropenoic acid glucoside (PPAG) from rooibos (Aspalathus linearis) extract had anti-hyperglycemic activity and significant protective effects on the pancreatic beta cell mass in a chronic diet-induced diabetes model. The present study evaluated the cytoprotective effect of the phytochemical on beta cells exposed to acute cell stress.MethodsSynthetically prepared PPAG was administered orally in mice treated with a single dose of streptozotocin to acutely induce beta cell death and hyperglycemia. Its effect was assessed on beta cell mass, proliferation and apoptotic cell death. Its cytoprotective effect was also studied in vitro on INS-1E beta cells and on human pancreatic islet cells.ResultsTreatment with the phytochemical PPAG protected beta cells during the first days after the insult against apoptotic cell death, as evidenced by TUNEL staining, and prevented loss of expression of anti-apoptotic protein BCL2 in vivo. In vitro, PPAG protected INS-1E beta cells from streptozotocin-induced apoptosis and necrosis in a BCL2-dependent and independent way, respectively, depending on glucose concentration. PPAG also protected human pancreatic islet cells against the cytotoxic action of the fatty acid palmitate.ConclusionsThese findings show the potential use of PPAG as phytomedicine which protects the beta cell mass exposed to acute diabetogenic stress.
Highlights
Regulation of the blood glucose level after a meal depends on the pancreatic insulin-producing beta cells
phenylpropenoic acid glucoside (PPAG) protected human pancreatic islet cells against the cytotoxic action of the fatty acid palmitate. These findings show the potential use of PPAG as phytomedicine which protects the beta cell mass exposed to acute diabetogenic stress
The aim of this study was to examine whether the phytochemical PPAG has a beta cell protective effect in a model of acute damage for which we used a high dose of STZ
Summary
Regulation of the blood glucose level after a meal depends on the pancreatic insulin-producing beta cells. High-caloric western diets rich in saturated fats and sugars lead to obesity and insulin resistance which increases the secretory demand on beta cells. Beta cells need to compensate for the increasing insulin demands by raising insulin synthesis and secretion. Failure to compensate leads to a vicious circle of increased metabolic stress and decreased beta-cell number which underlies the pathogenesis and progression of type 2 diabetes [1]. There is an urgent need to find new anti-diabetic drugs that decrease glycemia and preserve beta cell mass and thereby would be disease-modifying [2]. There is interest in the potential use of dietary supplements or nutraceuticals that promote preservation of the beta cell mass in pre-diabetic or at risk individuals [3]
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