| 1. |
- Pereverzev, A, et al.
(författare)
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The ablation of the Ca(v)2.3/E-type voltage-gated Ca2+ channel causes a mild phenotype despite an altered glucose induced glucagon response in isolated islets of Langerhans
- 2005
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 1879-0712 .- 0014-2999. ; 511:1, s. 65-72
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Tidskriftsartikel (refereegranskat)abstract
- Glucagon release upon hypoglycemia is an important homeostatic mechanism utilized by vertebrates to restore blood glucose to normal. Glucagon secretion itself is triggered by Ca2+ influx through voltage-gated ion channels, and the gene inactivation of R-type Ca2+ channels, with Ca(v)2.3 as the ion conducting subunit, has been shown to disturb glucose homeostasis. To understand how glucagon release may be affected in Ca(v)2.3-deficient mice, carbachol, insulin and glucose induced glucagon response was investigated. While the rise of insulin and glucose induced by carbachol is normal, mutant mice show an impaired glucagon-response. Further, the effect of insulin injection on glucagon levels was altered by the loss of the Ca(v)2.3 subunit. Ca(v)2.3-deficientmice are characterized by an impaired glucose suppression of glucagon release. This was most obvious at the level of isolated islets suggesting that Ca(v)2.3 containing R-type voltage-gated Ca2+ channels are involved in the glucose-mediated signalling to glucagon release in mice.
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| 2. |
- Beheshti, Hoosang M., et al.
(författare)
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E-business diffusion in large Swedish firms
- 2008
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Ingår i: Estableciendo puentes en una economía global.
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Konferensbidrag (refereegranskat)abstract
- Advances in e-business are potentially the most important development for both large manufacturing and service organizations around the globe. E-business technology affords the company to move from a traditional business model to a model that promotes shared activities, desicion making, and problem solving as well as strengthening the management of inter- and intra-organizationl processes.
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| 3. |
- Beheshti, Hoosang M., et al.
(författare)
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The strategic and organizational impact of electronic business on large firms
- 2008
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Ingår i: Journal of International Business Disciplines. - Frostburg, Maryland, USA : Frostburg State University. - 1934-1822. ; 2:3, s. 48-61
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Tidskriftsartikel (refereegranskat)abstract
- This research examines the impact of and the benefits derived from e-business integration in large manufacturing and service organizations in Sweden. Business managers are increasingly under pressure to improve the financial performance and the profitability of their companies. The Internet-based electronic business can provide opportunities for business ti improve the efficiency and the effectiveness of their business operations, to form partnership with suppliers, improve customer service, and to manage better their supply chain. The results show that large Swedish firms are benefiting from e-business implementation in many key areas of their business.
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| 4. |
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| 5. |
- Johansson, Stina M., et al.
(författare)
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A(1) receptor deficiency causes increased insulin and glucagon secretion in mice
- 2007
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Ingår i: Biochemical Pharmacology. - : Elsevier BV. - 0006-2952 .- 1356-1839. ; 74:11, s. 1628-1635
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Tidskriftsartikel (refereegranskat)abstract
- Adenosine influences metabolism and the adenosine receptor antagonist caffeine decreases the risk of type 2 diabetes. In this study the metabolic role of one adenosine receptor subtype, the adenosine A(1)R, was evaluated in mice lacking this receptor [A(1)R (-/-)]. The HbA1c levels and body weight were not significantly different between wild type [A(1)R (+/+)] and A(1)R (-/-) mice (3-4 months) fed normal lab chow. At rest, plasma levels of glucose, insulin and glucagon were similar in both genotypes. Following glucose injection, glucose tolerance was not appreciably altered in A(1)R (-/-) mice. Glucose injection induced sustained increases in plasma insulin and glucagon levels in A(1)R (-/-) mice, whereas A(1)R (+/+) control mice reacted with the expected transient increase in insulin and decrease in glucagon levels. Pancreas perfusion experiments showed that A(1)R (-/-) mice had a slightly higher basal insulin secretion than A(1)R (+/+) mice. The first phase insulin secretion (initiated with 16.7 mM glucose) was of the same magnitude in both genotypes, but the second phase was significantly enhanced in the A(1)R (-/-) pancreata compared with A(1)R (+/+). Insulin- and contraction-mediated glucose uptake in skeletal muscle were not significantly different between in A(1)R (-/-) and A(1)R (+/+) mice. All adenosine receptors were expressed at mRNA level in skeletal muscle in A(1)R (+/+) mice and the mRNA A(2A)R, A(2B)R and A(3)R levels were similar in A(1)R (-/-) and A(1)R (+/+) mice. In conclusion, the A(1)R minimally affects muscle glucose uptake, but is important in regulating pancreatic islet function.
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| 7. |
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| 8. |
- Zhang, Quan, et al.
(författare)
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R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion
- 2007
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Ingår i: Nature Cell Biology. - : Springer Science and Business Media LLC. - 1465-7392 .- 1476-4679. ; 9:4, s. 171-453
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Tidskriftsartikel (refereegranskat)abstract
- Pancreatic islets have a central role in blood glucose homeostasis. In addition to insulin-producing beta-cells and glucagon-secreting alpha-cells, the islets contain somatostatin-releasing delta-cells(1). Somatostatin is a powerful inhibitor of insulin and glucagon secretion(2). It is normally secreted in response to glucose(3) and there is evidence suggesting its release becomes perturbed in diabetes(4). Little is known about the control of somatostatin release. Closure of ATP-regulated K+-channels (K-ATP-channels)(5) and a depolarization-evoked increase in cytoplasmic free Ca2+ concentration ([Ca2+](i))(6-8) have been proposed to be essential. Here, we report that somatostatin release evoked by high glucose (>= 10 mM) is unaffected by the K-ATP-channel activator diazoxide and proceeds normally in K-ATP-channel-deficient islets. Glucose-induced somatostatin secretion is instead primarily dependent on Ca2+-induced Ca2+-release (CICR). This constitutes a novel mechanism for K-ATP-channel-independent metabolic control of pancreatic hormone secretion.
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