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Sökning: WFRF:(Lin Jian) > (2000-2004) > Islet insulin secre...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003926nam a2200577 4500
001oai:DiVA.org:uu-2989
003SwePub
008021121s2002 | |||||||||||000 ||eng|
020 a 9155454674q print
024a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-29892 URI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a vet2 swepub-contenttype
072 7a dok2 swepub-publicationtype
100a Lin, Jian-Man,d 1961-u Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut
2451 0a Islet insulin secretory patterns in diabetes and the role of UCP2
264 1a Uppsala :b Acta Universitatis Upsaliensis,c 2002
300 a 37 s.
338 a electronic2 rdacarrier
490a Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,x 0282-7476 ;v 1207
520 a During development of type 1 and type 2 diabetes plasma insulin patterns are altered. Since the islet insulin release pattern has been implicated in this development, insulin secretion from single islets was studied and linked to the islet protein levels of uncoupling protein-2 (UCP2). Islets were isolated from NOD- and KKAy- mice, GK- and GK-derived congenic rats, which are animal models of diabetes, and three human subjects with type 2 diabetes. At basal glucose (3 mM), insulin release from such islets was pulsatile and the amount released was comparable to that of control islets. When the glucose concentration was raised to 11 mM insulin release was essentially unchanged in islets isolated from older NOD- and KKAy- mice, GK- and Niddm1i congenic rats, and NIDDM persons. In islets from Niddm1f congenic rats, younger NOD- and KKAy-mice, control animals and normal human donors the secretion rate increased 2-9 fold when the glucose concentration was raised. This rise in secretion was manifested as increase of the amplitude of the insulin oscillations without affecting their frequency. Impaired glucose-induced insulin release was associated with reduction in glucose oxidation measured in NOD-islets, unaffected respiration measured in GK-islets and higher protein level of UCP2 measured in KKAy-islets. When the UCP2 amounts in KKAy-islets were reduced by culture to those of control islets, glucose-induced insulin secretion was essentially normalized. Our studies suggest that the deranged plasma insulin patterns observed in diabetes are related to decrease in the amplitude of insulin oscillations from the islets rather than loss of the oscillatory activity. This reduction of pulse amplitude may be related to impaired glucose metabolism and/or increased mitochondrial uncoupling.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng
653 a Cell biology
653 a type 1 diabetes
653 a type 2 diabetes
653 a NOD
653 a GK
653 a congenes
653 a KKAy
653 a human
653 a islet
653 a glucose
653 a insulin release
653 a oscillation
653 a frequency
653 a amplitude
653 a oxidation
653 a respiration
653 a UCP2
653 a western blot
653 a Cellbiologi
653 a Cell biology
653 a Cellbiologi
653 a medicinsk cellbiologi
653 a Medical Cell Biology
700a Grill, Valdemar,c professoru Dept of Medicine,Section Endocrinology,University Hospital of Trondheim, Trondheim4 opn
710a Uppsala universitetb Institutionen för medicinsk cellbiologi4 org
856u https://uu.diva-portal.org/smash/get/diva2:162180/FULLTEXT01.pdfx primaryx Raw objecty fulltext
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2989

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