<p>(A) INS-1 cells were stimulated by exenatide at 11.1 mM glucose for insulin secretion. (B) Serum-deprived INS-1 cells were treated 0.3 μM thapsigargin in the absence or presence of various concentrations of exenatide for 6 h. At the end of experiment, cellular viability was assessed by determining intracellular ATP levels. (C) After 6 h treatment, cellular caspase-3/7 activity was determined as a sensitive apoptotic marker. (D) Caspase-3/7 activity was determined according to the treatment time of 0.3 μM thapsigargin in the absence or presence of 10 nM exenatide. ***<i>p</i>< 0.001 vs. untreated control by Bonferroni’s t-test. Each experiment was run in triplicate.</p
Glucagon-like peptide 1 (GLP1) agonists are promising therapeutic agents in the treatment of diabete...
ObjectivesThis study sought to examine whether exenatide is capable of reducing myocardial infarct s...
Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct ...
<p>Serum-deprived INS-1 cells were treated 0.3 μM thapsigargin in the absence or presence of 10 nM e...
<p>(A) INS-1 cells, serum-starved overnight, were pre- and post-treated with each drug with or witho...
Beta cell death caused by endoplasmic reticulum (ER) stress is a key factor aggravating type 2 diabe...
<div><p>Beta cell death caused by endoplasmic reticulum (ER) stress is a key factor aggravating type...
<p>(A) In Tg-induced cell death, INS-1 cells were pretreated with 10 µM of various kinase inhibitors...
<p>A) INS1E control cells were cultured at 11 mM glucose and treated with 1 µM of thapsigargin for 8...
<p>(A, C, D) In Tg-induced cell death, INS-1 cells were harvested 1 h (for pAkt and Akt) and 3 h (fo...
<p><b>A</b>: INS-1E cells were cultured in 10 mM glucose medium for 48 hours with increasing concent...
Agonists of glucagon-like peptide-1 receptor (GLP-1R) and glucokinase activators (GKA) act as antidi...
Background: Agonists of glucagon-like peptide-1 receptor (GLP-1R) and glucokinase activators (GKA) a...
<p>ERS was induced by exposure cells to thapsigargin (TG, 0.1μmol/L), tunicamycin (TM, 2.5μg/mL) or ...
This study assessed whether glucose-dependent insulin secretion and overall counterregulatory respon...
Glucagon-like peptide 1 (GLP1) agonists are promising therapeutic agents in the treatment of diabete...
ObjectivesThis study sought to examine whether exenatide is capable of reducing myocardial infarct s...
Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct ...
<p>Serum-deprived INS-1 cells were treated 0.3 μM thapsigargin in the absence or presence of 10 nM e...
<p>(A) INS-1 cells, serum-starved overnight, were pre- and post-treated with each drug with or witho...
Beta cell death caused by endoplasmic reticulum (ER) stress is a key factor aggravating type 2 diabe...
<div><p>Beta cell death caused by endoplasmic reticulum (ER) stress is a key factor aggravating type...
<p>(A) In Tg-induced cell death, INS-1 cells were pretreated with 10 µM of various kinase inhibitors...
<p>A) INS1E control cells were cultured at 11 mM glucose and treated with 1 µM of thapsigargin for 8...
<p>(A, C, D) In Tg-induced cell death, INS-1 cells were harvested 1 h (for pAkt and Akt) and 3 h (fo...
<p><b>A</b>: INS-1E cells were cultured in 10 mM glucose medium for 48 hours with increasing concent...
Agonists of glucagon-like peptide-1 receptor (GLP-1R) and glucokinase activators (GKA) act as antidi...
Background: Agonists of glucagon-like peptide-1 receptor (GLP-1R) and glucokinase activators (GKA) a...
<p>ERS was induced by exposure cells to thapsigargin (TG, 0.1μmol/L), tunicamycin (TM, 2.5μg/mL) or ...
This study assessed whether glucose-dependent insulin secretion and overall counterregulatory respon...
Glucagon-like peptide 1 (GLP1) agonists are promising therapeutic agents in the treatment of diabete...
ObjectivesThis study sought to examine whether exenatide is capable of reducing myocardial infarct s...
Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct ...