Microphysiological Analysis Platform of Pancreatic Islet β-Cell Spheroids

2017 ◽  
Vol 7 (2) ◽  
pp. 1701111 ◽  
Author(s):  
Sang Hun Lee ◽  
SoonGweon Hong ◽  
Jihwan Song ◽  
Byungrae Cho ◽  
Esther J. Han ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Β Cell ◽  
Cell Spheroids ◽  
Analysis Platform

scholarly journals Prolonged Exposure to Insulin Inactivates Akt and Erk1/2 and Increases Pancreatic Islet and INS1E β-Cell Apoptosis

2018 ◽  
Vol 3 (1) ◽  
pp. 69-90 ◽  
Author(s):  
Nadia Rachdaoui ◽  
Luis Polo-Parada ◽  
Faramarz Ismail-Beigi
Keyword(s):  
Pancreatic Islet ◽  
Cell Apoptosis ◽  
Prolonged Exposure ◽  
Β Cell

EVIDENCE FOR THE INVOLVEMENT OF cGMP IN NITRIC OXIDE-INDUCED APOPTOSIS IN THE PANCREATIC ISLET β-CELL LINE, HIT-T15

1996 ◽  
Vol 24 (4) ◽  
pp. 595S-595S
Author(s):  
A.C. Loweth ◽  
J.H. Scarpello ◽  
N.G. Morgan
Keyword(s):  
Nitric Oxide ◽  
Cell Line ◽  
Pancreatic Islet ◽  
Β Cell ◽  
Induced Apoptosis

scholarly journals 1H NMR Based Serum Metabolic Profiles Associated with Pathological Progression of Pancreatic Islet β Cell Tumor in Rip1-Tag2 Mice

2015 ◽  
Vol 11 (5) ◽  
pp. 595-603 ◽  
Author(s):  
Yongxia Yang ◽  
Ying Liu ◽  
Lingyun Zheng ◽  
Qianqian Zhang ◽  
Quliang Gu ◽  
...  
Keyword(s):  
1H Nmr ◽  
Pancreatic Islet ◽  
Cell Tumor ◽  
Metabolic Profiles ◽  
Β Cell

scholarly journals An AP-3-dependent mechanism drives synaptic-like microvesicle biogenesis in pancreatic islet β-cells

2010 ◽  
Vol 299 (1) ◽  
pp. E23-E32 ◽  
Author(s):  
Arthur T. Suckow ◽  
Branch Craige ◽  
Victor Faundez ◽  
William J. Cain ◽  
Steven D. Chessler
Keyword(s):  
Synaptic Vesicle ◽  
Pancreatic Islet ◽  
Membrane Trafficking ◽  
Protein Complexes ◽  
Brefeldin A ◽  
Adaptor Protein ◽  
Β Cells ◽  
Β Cell ◽  
Subunit Expression ◽  
Bona Fide

Pancreatic islet β-cells contain synaptic-like microvesicles (SLMVs). The origin, trafficking, and role of these SLMVs are poorly understood. In neurons, synaptic vesicle (SV) biogenesis is mediated by two different cytosolic adaptor protein complexes, a ubiquitous AP-2 complex and the neuron-specific AP-3B complex. Mice lacking AP-3B subunits exhibit impaired GABAergic (inhibitory) neurotransmission and reduced neuronal vesicular GABA transporter (VGAT) content. Since β-cell maturation and exocytotic function seem to parallel that of the inhibitory synapse, we predicted that AP-3B-associated vesicles would be present in β-cells. Here, we test the hypothesis that AP-3B is expressed in islets and mediates β-cell SLMV biogenesis. A secondary aim was to test whether the sedimentation properties of INS-1 β-cell microvesicles are identical to those of bona fide SLMVs isolated from PC12 cells. Our results show that the two neuron-specific AP-3 subunits β3B and μ3B are expressed in β-cells, the first time these proteins have been found to be expressed outside the nervous system. We found that β-cell SLMVs share the same sedimentation properties as PC12 SLMVs and contain SV proteins that sort specifically to AP-3B-associated vesicles in the brain. Brefeldin A, a drug that interferes with AP-3-mediated SV biogenesis, inhibits the delivery of AP-3 cargoes to β-cell SLMVs. Consistent with a role for AP-3 in the biogenesis of GABAergic SLMV in β-cells, INS-1 cell VGAT content decreases upon inhibition of AP-3 δ-subunit expression. Our findings suggest that β-cells and neurons share molecules and mechanisms important for mediating the neuron-specific membrane trafficking pathways that underlie synaptic vesicle formation.

Pancreatic Islet β-Cell Failure in Obesity

2010 ◽  
pp. 199-217
Author(s):  
Tomoaki Morioka ◽  
Rohit N. Kulkarni
Keyword(s):  
Pancreatic Islet ◽  
Β Cell

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.

Enhancement of Subcutaneously Transplanted β Cell Survival Using 3D Stem Cell Spheroids with Proangiogenic and Prosurvival Potential

2020 ◽  
Vol 4 (3) ◽  
pp. 1900254 ◽  
Author(s):  
Chih‐Ping Yu ◽  
Jyuhn‐Huarng Juang ◽  
Yu‐Jie Lin ◽  
Ching‐Wen Kuo ◽  
Li‐Hung Hsieh ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Survival ◽  
Β Cell ◽  
Cell Spheroids

scholarly journals Pancreas-specific Gsα deficiency has divergent effects on pancreatic α- and β-cell proliferation

2010 ◽  
Vol 206 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Tao Xie ◽  
Min Chen ◽  
Lee S Weinstein
Keyword(s):  
Cell Proliferation ◽  
Pancreatic Islet ◽  
Exocrine Pancreas ◽  
Morphological Changes ◽  
Camp Signaling ◽  
Intracellular Camp ◽  
Β Cell ◽  
Pancreatic Islet Cell ◽  
Α Subunit ◽  
Transgenic Mouse Line

The ubiquitously expressed G protein α-subunit Gsα mediates the intracellular cAMP response to glucagon-like peptide 1 (GLP1) and other incretin hormones in pancreatic islet cells. We have shown previously that mice with β-cell-specific Gsα deficiency (βGsKO) develop severe early-onset insulin-deficient diabetes with a severe defect in β-cell proliferation. We have now generated mice with Gsα deficiency throughout the whole pancreas by mating Gsα-floxed mice with Pdx1-cre transgenic mice (PGsKO). PGsKO mice also developed severe insulin-deficient diabetes at a young age, confirming the important role of Gsα signaling in β-cell growth and function. Unlike in βGsKO mice, islets in PGsKO mice had a relatively greater proportion of α-cells, which were spread throughout the interior of the islet. Similar findings were observed in mice with pancreatic islet cell-specific Gsα deficiency using a neurogenin 3 promoter-cre recombinase transgenic mouse line. Studies in the α-cell line αTC1 confirmed that reduced cAMP signaling increased cell proliferation while increasing cAMP produced the opposite effect. Therefore, it appears that Gsα/cAMP signaling has opposite effects on pancreatic α- and β-cell proliferation, and that impaired GLP1 action in α- and β-cells via Gsα signaling may be an important contributor to the reciprocal effects on insulin and glucagon observed in type 2 diabetics. In addition, PGsKO mice show morphological changes in exocrine pancreas and evidence for malnutrition and dehydration, indicating an important role for Gsα in the exocrine pancreas as well.

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