Geniposide protects pancreatic β cells from high glucose-mediated injury by activation of AMP-activated protein kinase

2017 ◽  
Vol 41 (5) ◽  
pp. 544-554 ◽  
Author(s):  
Chunyan Liu ◽  
Yanan Hao ◽  
Fei Yin ◽  
Yonglan Zhang ◽  
Jianhui Liu
Keyword(s):  
Protein Kinase ◽  
High Glucose ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Amp Activated Protein Kinase

Activation of autophagy through modulation of 5′-AMP-activated protein kinase protects pancreatic β-cells from high glucose

2010 ◽  
Vol 425 (3) ◽  
pp. 541-551 ◽  
Author(s):  
Diana Han ◽  
Byungho Yang ◽  
L. Karl Olson ◽  
Alexander Greenstein ◽  
Seung-Hoon Baek ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Survival ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Β Cell Function ◽  
Amp Activated Protein Kinase

Chronic hyperglycaemia is detrimental to pancreatic β-cells by causing impaired insulin secretion and diminished β-cell function through glucotoxicity. Understanding the mechanisms underlying β-cell survival is crucial for the prevention of β-cell failure associated with glucotoxicity. Autophagy is a dynamic lysosomal degradation process that protects organisms against metabolic stress. To date, little is known about the physiological function of autophagy in the pathogenesis of diabetes. In the present study, we explored the roles of autophagy in the survival of pancreatic β-cells exposed to high glucose using pharmacological and genetic manipulation of autophagy. We demonstrated that chronic high glucose increases autophagy in rat INS-1 (832/13) cells and pancreatic islets, and that this increase is enhanced by inhibition of 5′-AMP-activated protein kinase. Our results also indicate that stimulation of autophagy rescues pancreatic β-cells from high-glucose-induced cell death and inhibition of autophagy augments caspase-3 activation, suggesting that autophagy plays a protective role in the survival of pancreatic β-cells. Greater knowledge of the molecular mechanisms linking autophagy and β-cell survival may unveil novel therapeutic targets needed to preserve β-cell function.

scholarly journals Hypoxia reduces HNF4α/MODY1 protein expression in pancreatic β-cells by activating AMP-activated protein kinase

2017 ◽  
Vol 292 (21) ◽  
pp. 8716-8728 ◽  
Author(s):  
Yoshifumi Sato ◽  
Tomonori Tsuyama ◽  
Chinami Sato ◽  
Md. Fazlul Karim ◽  
Tatsuya Yoshizawa ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Expression ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Amp Activated Protein Kinase

scholarly journals AMP-activated protein kinase as regulator of P2Y6 receptor-induced insulin secretion in mouse pancreatic β-cells

2013 ◽  
Vol 85 (7) ◽  
pp. 991-998 ◽  
Author(s):  
Ramachandran Balasubramanian ◽  
Hiroshi Maruoka ◽  
P. Suresh Jayasekara ◽  
Zhan-Guo Gao ◽  
Kenneth A. Jacobson
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
P2y6 Receptor ◽  
Amp Activated Protein Kinase

scholarly journals Glucose Deprivation Regulates KATPChannel Trafficking via AMP-Activated Protein Kinase in Pancreatic β-Cells

Diabetes ◽  
2009 ◽  
Vol 58 (12) ◽  
pp. 2813-2819 ◽  
Author(s):  
Ajin Lim ◽  
Sun-Hyun Park ◽  
Jong-Woo Sohn ◽  
Ju-Hong Jeon ◽  
Jae-Hyung Park ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Glucose Deprivation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Amp Activated Protein Kinase

scholarly journals Involvement of Protein Kinase C β2 in c-mycInduction by High Glucose in Pancreatic β-Cells

2001 ◽  
Vol 277 (5) ◽  
pp. 3680-3685 ◽  
Author(s):  
Hideaki Kaneto ◽  
Kiyoshi Suzuma ◽  
Arun Sharma ◽  
Susan Bonner-Weir ◽  
George L. King ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
High Glucose ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C

Role of AMP-activated protein kinase in the regulation of gene transcription

2002 ◽  
Vol 30 (2) ◽  
pp. 307-311 ◽  
Author(s):  
I. Leclerc ◽  
B. Viollet ◽  
G. da Silva Xavier ◽  
A. Kahn ◽  
G. A. Rutter
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Regulation Of Gene Expression ◽  
Energy Status ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Intermediate Metabolism ◽  
Energy Consuming ◽  
Amp Activated Protein Kinase

AMP-activated protein kinase (AMPK) is a regulator of cellular metabolism in response to changes in the energy status of the cells. AMPK was known to shut down energy-consuming pathways in response to a fall in the ATP/AMP ratio by phosphorylating key enzymes of intermediate metabolism. Here we will discuss the recent evidence implicating AMPK in the regulation of gene expression in mammals, mainly in the liver and in the pancreatic β-cells.

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