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A beta cell-specifi...
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Fex, MalinLund University,Lunds universitet,Celiaki och diabetes,Forskargrupper vid Lunds universitet,Celiac Disease and Diabetes Unit,Lund University Research Groups
(author)
A beta cell-specific knockout of hormone-sensitive lipase in mice results in hyperglycaemia and disruption of exocytosis.
- Article/chapterEnglish2009
Publisher, publication year, extent ...
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2008-11-21
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Springer Science and Business Media LLC,2009
Numbers
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LIBRIS-ID:oai:lup.lub.lu.se:e98bfc04-6dfd-435c-899e-55a164ca29f0
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https://lup.lub.lu.se/record/1271230URI
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https://doi.org/10.1007/s00125-008-1191-9DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:art swepub-publicationtype
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Subject category:ref swepub-contenttype
Notes
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AIMS/HYPOTHESIS: The enzyme hormone-sensitive lipase (HSL) is produced and is active in pancreatic beta cells. Because lipids are known to play a crucial role in normal control of insulin release and in the deterioration of beta cell function, as observed in type 2 diabetes, actions of HSL in beta cells may be critical. This notion has been addressed in different lines of HSL knockout mice with contradictory results. METHODS: To resolve this, we created a transgenic mouse lacking HSL specifically in beta cells, and characterised this model with regard to glucose metabolism and insulin secretion, using both in vivo and in vitro methods. RESULTS: We found that fasting basal plasma glucose levels were significantly elevated in mice lacking HSL in beta cells. An IVGTT at 12 weeks revealed a blunting of the initial insulin response to glucose with delayed elimination of the sugar. Additionally, arginine-stimulated insulin secretion was markedly diminished in vivo. Investigation of the exocytotic response in single HSL-deficient beta cells showed an impaired response to depolarisation of the plasma membrane. Beta cell mass and islet insulin content were increased, suggesting a compensatory mechanism, by which beta cells lacking HSL strive to maintain normoglycaemia. CONCLUSIONS/INTERPRETATION: Based on these results, we suggest that HSL, which is located in close proximity of the secretory granules, may serve as provider of a lipid-derived signal essential for normal insulin secretion.
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Haemmerle, G
(author)
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Wierup, NilsLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine(Swepub:lu)mphy-nwi
(author)
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Dekker Nitert, MarloesLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Translationell Muskel Forskning,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Translational Muscle Research,Lund University Research Groups(Swepub:lu)medk-mad
(author)
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Rehn, M
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Ristow, M
(author)
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Zechner, R
(author)
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Sundler, FrankLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine(Swepub:lu)mphy-fsu
(author)
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Holm, CeciliaLund University,Lunds universitet,Molekylär endokrinologi,Forskargrupper vid Lunds universitet,Molecular Endocrinology,Lund University Research Groups(Swepub:lu)medk-cho
(author)
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Eliasson, L
(author)
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Mulder, HindrikLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine(Swepub:lu)medk-hmu
(author)
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Celiaki och diabetesForskargrupper vid Lunds universitet
(creator_code:org_t)
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In:Diabetologia: Springer Science and Business Media LLC52, s. 271-2801432-04280012-186X
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Fex, Malin
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Haemmerle, G
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Wierup, Nils
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Dekker Nitert, M ...
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Rehn, M
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Ristow, M
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Zechner, R
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Sundler, Frank
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Holm, Cecilia
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Eliasson, L
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Mulder, Hindrik
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Diabetologia
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Lund University