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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003660naa a2200385 4500
001oai:lup.lub.lu.se:256a8c84-f6a5-47b0-a7d1-5f5c82d70d70
003SwePub
008200507s2020 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/256a8c84-f6a5-47b0-a7d1-5f5c82d70d702 URI
024a https://doi.org/10.1210/jendso/bvz0362 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Ahrén, Bou Lund University,Lunds universitet,Medicin/akutsjukvård, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Diabetes,Forskargrupper vid Lunds universitet,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups4 aut0 (Swepub:lu)med-bah
2451 0a The incretin effect in female mice with double deletion of GLP-1 and GIP receptors
264 c 2019-12-23
264 1b The Endocrine Society,c 2020
520 a To establish the contribution of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) for the incretin effect after oral glucose, studies were undertaken in female mice with genetic deletion of receptors for GIP and GLP-1 (double incretin receptor knockout [DIRKO] mice) and their wild-type (WT) counterparts. Insulin secretion was explored after oral glucose (doses ranging from 0 to 100 mg), after intravenous glucose (doses ranging from 0 to 0.75 g/kg), and after oral and intravenous glucose at matching circulating glucose. DIRKO mice had glucose intolerance after oral glucose challenges in association with impaired beta-cell function. Suprabasal area under the curve for C-peptide (AUCC-peptide) correlated linearly with suprabasal AUCglucose both in WT (r = 0.942, P = .017) and DIRKO mice (r = 0.972, P = .006). The slope of this regression was lower in DIRKO than in WT mice (0.012 ± 0.006 vs 0.031 ± 0.006 nmol C-peptide/mmol glucose, P = .042). In contrast, there was no difference in the insulin response to intravenous glucose between WT and DIRKO mice. Furthermore, oral and intravenous glucose administration at matching glucose levels showed that the augmentation of insulin secretion after oral glucose (the incretin effect) in WT mice (11.8 ± 2.3 nmol/L min) was entirely absent in DIRKO mice (3.3 ± 1.2 nmol/L min). We conclude that GIP and GLP-1 are required for normal glucose tolerance and beta-cell function after oral glucose in mice, that they are the sole incretin hormones after oral glucose at higher dose levels, and that they contribute by 65% to insulin secretion after oral glucose.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
653 a Animal models
653 a Glucose tolerance
653 a Incretin effect
653 a Incretin hormones
653 a Insulin secretion
700a Yamada, Yuichirou Aichi Cancer Center Research Institute4 aut
700a Seino, Yutakau Kansai Electric Power Hospital4 aut
710a Medicin/akutsjukvård, Lundb Sektion II4 org
773t Journal of the Endocrine Societyd : The Endocrine Societyg 4:2q 4:2x 2472-1972
856u http://dx.doi.org/10.1210/jendso/bvz036x freey FULLTEXT
856u https://academic.oup.com/jes/article-pdf/4/2/bvz036/33564676/bvz036.pdf
8564 8u https://lup.lub.lu.se/record/256a8c84-f6a5-47b0-a7d1-5f5c82d70d70
8564 8u https://doi.org/10.1210/jendso/bvz036

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Ahrén, Bo
Yamada, Yuichiro
Seino, Yutaka
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MEDICIN OCH HÄLSOVETENSKAP
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och Klinisk medicin
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Lunds universitet

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