Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice

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...

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Autores: Martin, Franz, Andreu, Etelvina, Rovira, Juan Manuel, Pertusa, Jose A. G., Raurell, Mercè, Ripoll, Cristina, Sanchez-Andres, Juan Vicente, Montanya Mias, Eduard, Soria, Bernat
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:1999
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/135008
Acceso en línea:https://hdl.handle.net/2445/135008
Access Level:acceso abierto
Palabra clave:Glucosa
Fisiologia
Illots de Langerhans
Ratolins (Animals de laboratori)
Cèl·lules B
Glucose
Physiology
Islands of Langerhans
Mice (Laboratory animals)
B cells
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spelling Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized miceMartin, FranzAndreu, EtelvinaRovira, Juan ManuelPertusa, Jose A. G.Raurell, MercèRipoll, CristinaSanchez-Andres, Juan VicenteMontanya Mias, EduardSoria, BernatGlucosaFisiologiaIllots de LangerhansRatolins (Animals de laboratori)Cèl·lules BGlucosePhysiologyIslands of LangerhansMice (Laboratory animals)B cellsIncreased 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.American Diabetes Association1999info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/135008Articles publicats en revistes (Ciències Clíniques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.2337/diabetes.48.10.1954Diabetes, 1999, vol. 48, num. 10, p. 1954-1961https://doi.org/10.2337/diabetes.48.10.1954cc-by-nc-nd (c) American Diabetes Association, 1999http://creativecommons.org/licenses/by-nc-nd/3.0/esinfo:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1350082026-05-27T06:46:51Z
dc.title.none.fl_str_mv Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
title Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
spellingShingle Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
Martin, Franz
Glucosa
Fisiologia
Illots de Langerhans
Ratolins (Animals de laboratori)
Cèl·lules B
Glucose
Physiology
Islands of Langerhans
Mice (Laboratory animals)
B cells
title_short Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
title_full Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
title_fullStr Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
title_full_unstemmed Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
title_sort Mechanisms of glucosa hypersensitivity in ß-cells from normoglycemic, partially pancreatectomized mice
dc.creator.none.fl_str_mv Martin, Franz
Andreu, Etelvina
Rovira, Juan Manuel
Pertusa, Jose A. G.
Raurell, Mercè
Ripoll, Cristina
Sanchez-Andres, Juan Vicente
Montanya Mias, Eduard
Soria, Bernat
author Martin, Franz
author_facet Martin, Franz
Andreu, Etelvina
Rovira, Juan Manuel
Pertusa, Jose A. G.
Raurell, Mercè
Ripoll, Cristina
Sanchez-Andres, Juan Vicente
Montanya Mias, Eduard
Soria, Bernat
author_role author
author2 Andreu, Etelvina
Rovira, Juan Manuel
Pertusa, Jose A. G.
Raurell, Mercè
Ripoll, Cristina
Sanchez-Andres, Juan Vicente
Montanya Mias, Eduard
Soria, Bernat
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Glucosa
Fisiologia
Illots de Langerhans
Ratolins (Animals de laboratori)
Cèl·lules B
Glucose
Physiology
Islands of Langerhans
Mice (Laboratory animals)
B cells
topic Glucosa
Fisiologia
Illots de Langerhans
Ratolins (Animals de laboratori)
Cèl·lules B
Glucose
Physiology
Islands of Langerhans
Mice (Laboratory animals)
B cells
description 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.
publishDate 1999
dc.date.none.fl_str_mv 1999
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/135008
url https://hdl.handle.net/2445/135008
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.2337/diabetes.48.10.1954
Diabetes, 1999, vol. 48, num. 10, p. 1954-1961
https://doi.org/10.2337/diabetes.48.10.1954
dc.rights.none.fl_str_mv cc-by-nc-nd (c) American Diabetes Association, 1999
http://creativecommons.org/licenses/by-nc-nd/3.0/es
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by-nc-nd (c) American Diabetes Association, 1999
http://creativecommons.org/licenses/by-nc-nd/3.0/es
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Diabetes Association
publisher.none.fl_str_mv American Diabetes Association
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Clíniques)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300719

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