Long-term culture of pancreatic islet cells with special reference to the β-cell function

In Vitro ◽  
1979 ◽  
Vol 15 (2) ◽  
pp. 95-102 ◽  
Author(s):  
Junko Ono ◽  
Ryosaburo Takaki ◽  
Hiromitsu Okano ◽  
Michio Fukuma
Keyword(s):  
Special Reference ◽  
Pancreatic Islet ◽  
Cell Function ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Β Cell ◽  
Long Term Culture ◽  
Β Cell Function

scholarly journals Systematic prevention of bubble formation and accumulation for long-term culture of pancreatic islet cells in microfluidic device

2012 ◽  
Vol 14 (2) ◽  
pp. 419-426 ◽  
Author(s):  
Yong Wang ◽  
Dongyoung Lee ◽  
Lisa Zhang ◽  
Hyojin Jeon ◽  
Joshua E. Mendoza-Elias ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Microfluidic Device ◽  
Islet Cells ◽  
Bubble Formation ◽  
Pancreatic Islet Cells ◽  
Long Term Culture

Long-Term Culture of Isolated Pancreatic Islet Cells

1975 ◽  
Vol 149 (2) ◽  
pp. 402-406 ◽  
Author(s):  
R. Takaki ◽  
J. Ono ◽  
M. Fukuma ◽  
T. Ikegami
Keyword(s):  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Long Term Culture

scholarly journals VEGF-B ablation in pancreatic β-cells upregulates insulin expression without affecting glucose homeostasis or islet lipid uptake

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Frank Chenfei Ning ◽  
Nina Jensen ◽  
Jiarui Mi ◽  
William Lindström ◽  
Mirela Balan ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Glucose Homeostasis ◽  
Lipid Accumulation ◽  
Cell Function ◽  
Lipid Uptake ◽  
Β Cells ◽  
Β Cell ◽  
Peripheral Tissues ◽  
Β Cell Function ◽  
Triglyceride Content

AbstractType 2 diabetes mellitus (T2DM) affects millions of people and is linked with obesity and lipid accumulation in peripheral tissues. Increased lipid handling and lipotoxicity in insulin producing β-cells may contribute to β-cell dysfunction in T2DM. The vascular endothelial growth factor (VEGF)-B regulates uptake and transcytosis of long-chain fatty acids over the endothelium to tissues such as heart and skeletal muscle. Systemic inhibition of VEGF-B signaling prevents tissue lipid accumulation, improves insulin sensitivity and glucose tolerance, as well as reduces pancreatic islet triglyceride content, under T2DM conditions. To date, the role of local VEGF-B signaling in pancreatic islet physiology and in the regulation of fatty acid trans-endothelial transport in pancreatic islet is unknown. To address these questions, we have generated a mouse strain where VEGF-B is selectively depleted in β-cells, and assessed glucose homeostasis, β-cell function and islet lipid content under both normal and high-fat diet feeding conditions. We found that Vegfb was ubiquitously expressed throughout the pancreas, and that β-cell Vegfb deletion resulted in increased insulin gene expression. However, glucose homeostasis and islet lipid uptake remained unaffected by β-cell VEGF-B deficiency.

scholarly journals A Physiological Pattern of Oxygenation Using Perfluorocarbon-Based Culture Devices Maximizes Pancreatic Islet Viability and Enhances β-Cell Function

2013 ◽  
Vol 22 (9) ◽  
pp. 1723-1733 ◽  
Author(s):  
Chris A. Fraker ◽  
Sirlene Cechin ◽  
Silvia Álvarez-Cubela ◽  
Felipe Echeverri ◽  
Andrés Bernal ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function

Long-term treatment with EXf, a peptide analog of Exendin-4, improves β-cell function and survival in diabetic KKAy mice

Peptides ◽  
2013 ◽  
Vol 40 ◽  
pp. 123-132 ◽  
Author(s):  
Guo-jiang Hou ◽  
Cai-na Li ◽  
Shuai-nan Liu ◽  
Yi Huan ◽  
Quan Liu ◽  
...  
Keyword(s):  
Cell Function ◽  
Term Treatment ◽  
Β Cell ◽  
Peptide Analog ◽  
Kkay Mice ◽  
Long Term Treatment ◽  
Β Cell Function

scholarly journals Long-Term Effects of Central Leptin and Resistin on Body Weight, Insulin Resistance, and β-Cell Function and Mass by the Modulation of Hypothalamic Leptin and Insulin Signaling

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 445-454 ◽  
Author(s):  
Sunmin Park ◽  
Sang Mee Hong ◽  
So Ra Sung ◽  
Hye Kyung Jung
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Insulin Signaling ◽  
Cell Function ◽  
Cell Mass ◽  
Diabetic Rats ◽  
Β Cell ◽  
Serum Leptin ◽  
Β Cell Function

To determine the long-term effect of central leptin and resistin on energy homeostasis, peripheral insulin resistance, and β-cell function and mass, intracerebroventricular (ICV) infusion of leptin (3 ng/h), resistin (80 ng/h), leptin plus resistin, and cerebrospinal fluid (control) was conducted by means of an osmotic pump for 4 wk on normal rats and 90% pancreatectomized diabetic rats fed 40% fat-energy diets. Overall, the effects were greater in diabetic rats than normal rats. Leptin infusion, causing a significant reduction in food intake, decreased body weight and epididymal fat. However, resistin and leptin plus resistin reduced epididymal fat with decreased serum leptin levels in comparison with the control. Unlike serum leptin, only resistin infusion lowered serum resistin levels. Central leptin increased glucose infusion rates during euglycemic hyperinsulinemic clamp and suppressed hepatic glucose production in the hyperinsulinemic state in comparison with the control. However, central leptin did not affect glucose-stimulated insulin secretion and β-cell mass. Central resistin infusion also increased peripheral insulin sensitivity, but not as much as leptin. Unlike leptin, resistin significantly increased first-phase insulin secretion during hyperglycemic clamp and β-cell mass by augmenting β-cell proliferation. These metabolic changes were associated with hypothalamic leptin and insulin signaling. ICV infusion of leptin potentiated signal transducer and activator of transcription 3 phosphorylation and attenuated AMP kinase in the hypothalamus, but resistin had less potent effects than leptin. Leptin enhanced insulin signaling by potentiating IRS2→Akt pathways, whereas resistin activated Akt without augmenting insulin receptor substrate 2 phosphorylation. In conclusion, long-term ICV infusion of leptin and resistin independently improved energy and glucose homeostasis by modulating in different ways hypothalamic leptin and insulin signaling.

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