scholarly journals Vescalagin from Pink Wax Apple (Syzygium samarangense (Blume) Merrill and Perry) Protects Pancreatic β-Cells against Methylglyoxal-Induced Inflammation in Rats

Plants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1448
Author(s):  
Wen-Chang Chang ◽  
James Swi-Bea Wu ◽  
Szu-Chuan Shen
Keyword(s):  
Protein Expression ◽  
Diabetic Rats ◽  
Related Factor ◽  
Advanced Glycation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Expression Levels ◽  
Enhancer Binding Protein ◽  
Glycation End Products ◽  
Mitogen Activated Protein

Methylglyoxal (MG) is the primary precursor of advanced glycation end products involved in the pathogenesis of inflammation and diabetes. A previous study in our laboratory found anti-inflammatory and anti-hyperglycemic effects of the polyphenol vescalagin (VES) in rats with MG-induced carbohydrate metabolic disorder. The present study further investigated the occurrence of inflammation in pancreatic β-cells in MG-induced diabetic rats and the mechanism by which VES prevents it. The results showed that VES downregulates the protein expression levels of advanced glycation end product receptors and CCAAT/enhancer binding protein-β and upregulates the protein expression levels of pancreatic duodenal homeobox-1, nuclear factor erythroid 2-related factor 2 and glyoxalase I from the pancreatic cells. The results also revealed that VES elevates glutathione and antioxidant enzyme contents and then downregulates c-Jun N-terminal kinase and p38 mitogen-activated protein kinases pathways to protect pancreatic β-cells in MG-administered rats.

Advanced glycation end products impair glucose-induced insulin secretion from rat pancreatic β-cells

2013 ◽  
Vol 21 (2) ◽  
pp. 134-141 ◽  
Author(s):  
Hiroyuki Hachiya ◽  
Yoshikazu Miura ◽  
Ken-ichi Inoue ◽  
Kyung Hwa Park ◽  
Masayoshi Takeuchi ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Glycation End Products ◽  
End Products

scholarly journals Long-Term Exposure of Pancreatic β-Cells to Palmitate Results in SREBP-1C-Dependent Decreases in GLP-1 Receptor Signaling via CREB and AKT and Insulin Secretory Response

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2243-2258 ◽  
Author(s):  
Annalisa Natalicchio ◽  
Giuseppina Biondi ◽  
Nicola Marrano ◽  
Rossella Labarbuta ◽  
Federica Tortosa ◽  
...  
Keyword(s):  
Protein Expression ◽  
Insulin Release ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Camp Response Element ◽  
Element Binding Protein ◽  
Viral Oncogene Homolog ◽  
Erk Kinase

The effects of prolonged exposure of pancreatic β-cells to high saturated fatty acids on glucagon-like peptide-1 (GLP-1) action were investigated. Murine islets, human pancreatic 1.1B4 cells, and rat INS-1E cells were exposed to palmitate for 24 hours. mRNA and protein expression/phosphorylation were measured by real-time RT-PCR and immunoblotting, respectively. Specific short interfering RNAs were used to knockdown expression of the GLP-1 receptor (Glp1r) and Srebf1. Insulin release was assessed with a specific ELISA. Exposure of murine islets, as well as of human and INS-1E β-cells, to palmitate reduced the ability of exendin-4 to augment insulin mRNA levels, protein content, and release. In addition, palmitate blocked exendin-4-stimulated cAMP-response element-binding protein and v-akt murine thymoma viral oncogene homolog phosphorylation, whereas phosphorylation of MAPK-ERK kinase-1/2 and ERK-1/2 was not altered. Similarly, RNA interference-mediated suppression of Glp1r expression prevented exendin-4-induced cAMP-response element-binding protein and v-akt murine thymoma viral oncogene homolog phosphorylation, but did not impair exendin-4 stimulation of MAPK-ERK kinase-1/2 and ERK-1/2. Both islets from mice fed a high fat diet and human and INS-1E β-cells exposed to palmitate showed reduced GLP-1 receptor and pancreatic duodenal homeobox-1 (PDX-1) and increased sterol regulatory element-binding protein (SREBP-1C) mRNA and protein levels. Furthermore, suppression of SREBP-1C protein expression prevented the reduction of PDX-1 and GLP-1 receptor levels and restored exendin-4 signaling and action. Finally, treatment of INS-1E cells with metformin for 24 h resulted in inhibition of SREBP-1C expression, increased PDX-1 and GLP-1 receptor levels, consequently, enhancement of exendin-4-induced insulin release. Palmitate impairs exendin-4 effects on β-cells by reducing PDX-1 and GLP-1 receptor expression and signaling in a SREBP-1C-dependent manner. Metformin counteracts the impairment of GLP-1 receptor signaling induced by palmitate.

scholarly journals Regulation of Insulin Gene Transcription by the Immediate-Early Growth Response Gene Egr-1

Endocrinology ◽  
2006 ◽  
Vol 147 (6) ◽  
pp. 2923-2935 ◽  
Author(s):  
Kazuhiro Eto ◽  
Varinderpal Kaur ◽  
Melissa K. Thomas
Keyword(s):  
Transcriptional Activation ◽  
Growth Response ◽  
Insulin Gene ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Expression Levels ◽  
Promoter Sequences ◽  
Early Growth Response ◽  
Insulin Promoter ◽  
Insulin Gene Expression

Abstract Changes in extracellular glucose levels regulate the expression of the immediate-early response gene and zinc finger transcription factor early growth response-1 (Egr-1) in insulin-producing pancreatic β-cells, but key target genes of Egr-1 in the endocrine pancreas have not been identified. We found that overexpression of Egr-1 in clonal (INS-1) β-cells increased transcriptional activation of the rat insulin I promoter. In contrast, reductions in Egr-1 expression levels or function with the introduction of either small interfering RNA targeted to Egr-1 (siEgr-1) or a dominant-negative form of Egr-1 decreased insulin promoter activation, and siEgr-1 suppressed insulin gene expression. Egr-1 did not directly interact with insulin promoter sequences, and mutagenesis of a potential G box recognition sequence for Egr-1 did not impair the Egr-1 responsiveness of the insulin promoter, suggesting that regulation of insulin gene expression by Egr-1 is probably mediated through additional transcription factors. Overexpression of Egr-1 increased, and reduction of Egr-1 expression decreased, transcriptional activation of the glucose-responsive FarFlat minienhancer within the rat insulin I promoter despite the absence of demonstrable Egr-1-binding activity to FarFlat sequences. Notably, augmenting Egr-1 expression levels in insulin-producing cells increased the mRNA and protein expression levels of pancreas duodenum homeobox-1 (PDX-1), a major transcriptional regulator of glucose-responsive activation of the insulin gene. Increasing Egr-1 expression levels enhanced PDX-1 binding to insulin promoter sequences, whereas mutagenesis of PDX-1-binding sites reduced the capacity of Egr-1 to activate the insulin promoter. We propose that changes in Egr-1 expression levels in response to extracellular signals, including glucose, can regulate PDX-1 expression and insulin production in pancreatic β-cells.

Protective and therapeutic effects of Phoenix dactylifera leaf extract on pancreatic β-cells and diabetic parameters in streptozotocin-induced diabetic rats

2020 ◽  
Vol 29 (4) ◽  
pp. 847-854 ◽  
Author(s):  
Ebrahim Esfandiari ◽  
Aliasghar Dorali ◽  
Mostafa Ghanadian ◽  
Bahman Rashidi ◽  
Fatemeh Sadat Mostafavi
Keyword(s):  
Leaf Extract ◽  
Phoenix Dactylifera ◽  
Diabetic Rats ◽  
Therapeutic Effects ◽  
Β Cells ◽  
Pancreatic Β Cells
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