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Title: Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
Author: Martin, Franz
Andreu, Etelvina
Rovira, Juan Manuel
Pertusa, Jose A. G.
Raurell, Mercè
Ripoll, Cristina
Sanchez-Andres, Juan Vicente
Montanya Mias, Eduard
Soria, Bernat
Keywords: Glucosa
Illots de Langerhans
Ratolins (Animals de laboratori)
Cèl·lules B
Islands of Langerhans
Mice (Laboratory animals)
B cells
Issue Date: Oct-1999
Publisher: American Diabetes Association
Abstract: Increased beta-cell sensitivity to glucose precedes the loss of glucose-induced insulin secretion in diabetic animals. Changes at the level of beta-cell glucose sensor have been described in these situations, but it is not clear whether they fully account for the increased insulin secretion. Using a euglycemic-normolipidemic 60% pancreatectomized (60%-Px) mouse model, we have studied the ionic mechanisms responsible for increased beta-cell glucose sensitivity. Two weeks after Px (Px14 group), Px mice maintained normoglycemia with a reduced beta-cell mass (0.88 +/- 0.18 mg) compared with control mice (1.41 +/- 0.21 mg). At this stage, the dose-response curve for glucose-induced insulin release showed a significant displacement to the left (P < 0.001). Islets from the Px14 group showed oscillatory electrical activity and cytosolic Ca2+ ([Ca2+]i) oscillations in response to glucose concentrations of 5.6 mmol/l compared with islets from the control group at 11.1 mmol/l. All the above changes were fully reversible both in vitro (after 48-h culture of islets from the Px14 group) and in vivo (after regeneration of beta-cell mass in islets studied 60 days after Px). No significant differences in the input resistance and ATP inhibition of ATP-sensitive K+ (K(ATP)) channels were found between beta-cells from the Px14 and control groups. The dose-response curve for glucose-induced MTT (C,N-diphenyl-N''-4,5-dimethyl thiazol 2 yl tetrazolium bromide) reduction showed a significant displacement to the left in islets from the Px14 group (P < 0.001). These results indicate that increased glucose sensitivity in terms of insulin secretion and Ca2+ signaling was not due to intrinsic modifications of K(ATP) channel properties, and suggest that the changes are most likely to be found in the glucose metabolism.
Note: Reproducció del document publicat a:
It is part of: Diabetes, 1999, vol. 48, num. 10, p. 1954-1961
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ISSN: 0012-1797
Appears in Collections:Articles publicats en revistes (Ciències Clíniques)

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