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  • 1
    Electronic Resource
    Electronic Resource
    Interleukin-1β inhibition of insulin release in rat pancreatic islets: possible involvement of G-proteins in the signal transduction pathway (1995)
    Springer
    Diabetologia 38 (1995), S. 779-784 
    Details
    ISSN: 1432-0428
    Keywords: Key words Interleukin-1β ; pertussis toxin ; cholera toxin ; pancreatic islets ; insulin secretion ; G-proteins ; nitric oxide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro exposure of rat pancreatic beta cells to interleukin-1β (IL-1β) inhibits glucose-stimulated insulin release (2140 ± 239 and 323 ± 80 pg · islet–1· h–1 at glucose levels of 16.7 mmol/l in control and IL-1β-exposed islets, respectively, n = 7, p 〈 0.001). Cholera toxin (2 μg/ml) or pertussis toxin (0.5 μg/ml) potentiated, as expected, glucose-induced insulin release in control islets, but, in addition, when added together with IL-1β, were able to prevent the IL-1β mediated inhibition of glucose-stimulated insulin secretion (2087 ± 301 and 1662 ± 173 pg · islet–1· h–1, respectively, p 〈 0.05 vs islets exposed to IL-1β alone). To investigate the mechanism by which the toxins prevent the IL-1β effect, we then measured nitrite levels, glucose oxidation and Ca2 + uptake. Nitrite levels in the culture medium were 4.2± 1.4 and 24.0 ± 5 pmol · islet–1· 24 h–1 in control islets and in IL-1β-exposed islets, respectively (n = 6, p = 0.05). In islets exposed to IL-1β and cholera or pertussis toxins, nitrite levels were 9.1 ± 3 and 12.4 ± 6 pmol · islet–1· 24 h–1, respectively (n = 6, NS vs control islets). Glucose oxidation at 16.7 mmol/l glucose was 31.1 ± 2.9 pmol · islet–1· 120 min–1 in control islets and 16.8 ± 2.7 pmol · islet–1· 120 min–1 in IL-1β-treated islets (p 〈 0.05). The addition of cholera or pertussis toxins simultaneously to IL-1β prevented the inhibition of glucose oxidation at 16.7 mmol/l glucose (32.9 ± 3.8 and 31.7 ± 3.3 pmol · islet–1· 120 min–1 in the presence of cholera or pertussis toxins, respectively). Glucose-stimulated 45Ca2 + up-take was also significantly inhibited in IL-1β-treat-ed islets when compared to control islets (7.1 ± 0.9 and 16.8 ± 3.2 pmol · islet–1· 20 min–1, respectively, p 〈 0.05). This inhibition was prevented by the presence of cholera or pertussis toxins (14.0 ± 3.8 and 11.2 ± 2.7 pmol · islet–1· 20 min–1, respectively). In conclusion, our data show that cholera and, to a lesser extent, pertussis toxins are able to partially prevent the IL-1β-induced increase in nitrite levels and block the inhibitory effects of IL-1β on different steps leading to glucose-induced insulin secretion. These findings support the possibility that in pancreatic beta cells, G-proteins may be involved or interfere with the cytokine signal transduction. [Diabetologia (1995) 38: 779–784]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050352
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Inhibition of the high-affinity glucose transporter GLUT 1 affects the sensitivity to glucose in a hamster-derived pancreatic beta cell line (HIT) (1993)
    Springer
    Diabetologia 36 (1993), S. 1204-1207 
    Details
    ISSN: 1432-0428
    Keywords: GLUT 1 ; GLUT 2 ; glucokinase ; glucose sensitivity ; insulin release ; HIT cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary HIT is a hamster-derived beta-cell line which in contrast to normal beta cells that only express the high Km GLUT-2 glucose transporter, also expresses the low Km glucose transporter GLUT 1. In HIT cells the abnormal glucose transport mechanism is associated with a marked shift to the left of the glucose-induced insulin release dose-response curve. We have used this cell model to investigate whether changes in glucose transport affect the glucose-induced insulin release. HIT cells were first incubated with a concentration of cytochalasin B (0.4 μmol/l) that selectively inhibits the GLUT-1 but not the GLUT-2 transporter. The consequences of blocking glucose phosphorylation and insulin release were studied. Exposure to 0.4 μmol/l cytochalasin B for 1 h caused a selective loss of the low Km transport: the calculated Vmax of GLUT 1 was reduced from 1726±98 to 184±14 pmol · mg protein−1 5 min−1 (mean±SEM, n=6, p〈0.005), while no major difference in the high Km (GLUT-2) transport was observed. In cytochalasin B exposed HIT cells the glucose phosphorylating activity (due to hexokinase and glucokinase) was unaffected. In these cells, however, the dose-response curve of glucose-induced insulin release was significantly shifted to the right: the 50% of maximal response (increment over baseline) was reached at an average glucose concentration of 2.9±0.2 mmol/l (vs 0.6±0.01 mmol/l in control HIT cells mean±SE, n=5, p〈0.05) and the maximal effect was reached at 11.0 mmol/l glucose (vs 2.8 mmol/l in control HIT cells p〈0.005). These results are consistent with the hypothesis that the affinity of the glucose transport system may contribute to determination of the glucose threshold concentration that triggers insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401067
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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