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Riccarda Granata, Marco Volante, Fabio Settanni, Carlotta Gauna, Corrado Ghé, Marta Annunziata, Barbara Deidda, Iacopo Gesmundo, Thierry Abribat, Aart-Jan van der Lely, Giampiero Muccioli, Ezio Ghigo and Mauro Papotti

insulin secretion and expression in human islet cells, and increases the mRNA of genes involved in β-cell function, survival, and differentiation ( Granata et al . 2008 ). AG had been reported to prevent diabetes in streptozotocin (STZ)-treated rats

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Jianling Xie, Norhan M El Sayed, Cheng Qi, Xuechan Zhao, Claire E Moore and Terence P Herbert

]-methionine/cysteine was purchased from Amersham Pharmacia Biotech. All other chemicals and reagents were purchased from Sigma–Aldrich, unless otherwise stated. Islet isolation and islet cell culture Male Wistar albino rats weighing 200–250 g were used for the isolation of

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Talitha van der Meulen and Mark O Huising

been described by which transdifferentiation of islet endocrine cells takes place, i.e., where a hormone-expressing islet cell converts into a hormone-expressing islet cell of a different type. One is direct transdifferentiation that proceeds via a

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V. Leclercq-Meyer, J. Marchand, A. Sener, F. Blachier and W. J. Malaisse

ABSTRACT

l-Leucine and 2-ketoisocaproate stimulated insulin release from perifused rat tumoral islet cells (RINm5F line). The secretory response coincided with an increase in the intracellular ATP/ADP ratio, a stimulation of 45Ca outflow from cells perifused in the presence of extracellular Ca2+, and an increase in 32P efflux from cells prelabelled with radioactive orthophosphate. In contrast to d-glucose, however, l-leucine or 2-ketoisocaproate failed to decrease 86Rb outflow, to inhibit 45Ca outflow from cells perifused in the absence of Ca2+ and to enhance the labelling of inositol-containing phospholipids in cells exposed to myo-[2-3H]inositol. These findings suggest that d-glucose, l-leucine and 2-ketoisocaproate exert dissimilar effects on the subcellular distribution of adenine nucleotides and/or 86Rb. The nonmetabolized analogue of l-leucine, 2-aminobicyclo-[2.2.1]heptane-2-carboxylic acid (BCH), also caused an initial stimulation of insulin release and 32P efflux, but this was soon followed by a severe and irreversible inhibition of insulin output, associated with a permanent enhancement of 86Rb outflow. The dual ionic and secretory response to BCH is interpreted in the light of its dual effect on the catabolism of endogenous amino and fatty acids, and raises the view that BCH could be used to interfere with the function of insulinoma cells.

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M. Welsh, D. L. Eizirik and E. Strandell

ABSTRACT

To elucidate the role of thermal stress on the function of pancreatic β cells, isolated mouse pancreatic islets were incubated for 30 min at 42°C. This resulted in decreased glucose-stimulated insulin secretion, inhibited total protein and pro-insulin synthesis and the induction of heat-shock proteins with molecular weights of 64 and 88 kDa. Six days later, the islets exposed to heat shock showed a lower DNA content, indicating islet cell death. However, the insulin secretory response and rates of oxygen consumption in the presence of glucose were normal. It is suggested that the induction of heat-shock proteins does not permanently impair β-cell function, but rather protects these cells from lasting damage.

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Inês Cebola and Lorenzo Pasquali

or developmental stages involved in the onset and progression of the disease. Enhancer clusters and pancreatic islet-cell identity Initial studies in human pancreatic islets and other tissues revealed that tissue-specific regulatory elements are not

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G A Martens, E Motté, G Kramer, G Stangé, L W Gaarn, K Hellemans, J H Nielsen, J M Aerts, Z Ling and D Pipeleers

separate viable from damaged cells prior to FACS sorting. The 10-week-old β cells are mainly discriminated from other islet cell types by their higher cell size (forward scatter (FSC)) in combination with higher FAD/FMN fluorescence ( Fig. 1C ; Van De

Open access

Gemma Tan, Andrew G Elefanty and Edouard G Stanley

for immunosuppression. However, for type 1 diabetes, the impact of immune-mediated destruction of the transplanted islet cells will still need to be addressed, even if patient iPSCs are the source. Moreover, in either case, the question of safety of

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Michael Welsh, Maria Jamalpour, Guangxiang Zang and Björn Åkerblom

2005 siRNA produced by recombinant dicer mediates efficient gene silencing in islet cells . Annals of the New York Academy of Sciences 1040 114 – 122 . ( doi:10.1196/annals.1327.014 ). Hagerkvist R Mokhtari D Lindholm C Farnebo F

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Sumaira Z Hasnain, Johannes B Prins and Michael A McGuckin

-cell degeneration, and diabetes . Cold Spring Harbor Perspectives in Medicine 2 a007666 . ( doi:10.1101/cshperspect.a007666 ). Peiris H Bonder CS Coates PT Keating DJ Jessup CF 2014 The β-cell/EC axis: how do islet cells talk to each other