WFRF:(Olofsson Charlotta S 1971)
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- Collins, S. C. (författare)
Long-term exposure of mouse pancreatic islets to oleate or palmitate results in reduced glucose-induced somatostatin and oversecretion of glucagon
- Artikel/kapitelEngelska2008
Förlag, utgivningsår, omfång ...
- 2008-07-12
- Springer Science and Business Media LLC,2008
Nummerbeteckningar
- LIBRIS-ID:oai:lup.lub.lu.se:5f55f4fd-5aaa-41c3-9157-1e4b55bed481
- https://lup.lub.lu.se/record/1253466URI
- https://doi.org/10.1007/s00125-008-1082-0DOI
- https://gup.ub.gu.se/publication/97349URI
Kompletterande språkuppgifter
- Språk:engelska
- Sammanfattning på:engelska
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- SwePubSwePub
Klassifikation
Anmärkningar
- Aims/hypothesis Long-term exposure to NEFAs leads to inhibition of glucose-induced insulin secretion. We tested whether the release of somatostatin and glucagon, the two other major islet hormones, is also affected. Methods Mouse pancreatic islets were cultured for 72 h at 4.5 or 15 mmol/l glucose with or without 0.5 mmol/l oleate or palmitate. The release of glucagon and somatostatin during subsequent 1 h incubations at 1 or 20 mmol/l glucose as well as the islet content of the two hormones were determined. Lipid-induced changes in islet cell ultrastructure were assessed by electron microscopy. Results Culture at 15 mmol/l glucose increased islet glucagon content by similar to 50% relative to that observed following culture at 4.5 mmol/l glucose. Inclusion of oleate or palmitate reduced islet glucagon content by 25% (at 4.5 mmol/l glucose) to 50% (at 15 mmol/l glucose). Long-term exposure to the NEFA increased glucagon secretion at 1 mmol/l glucose by 50% (when islets had been cultured at 15 mmol/l glucose) to 100% (with 4.5 mmol/l glucose in the culture medium) and abolished the inhibitory effect of 20 mmol/l glucose on glucagon secretion. Somatostatin content was unaffected by glucose and lipids, but glucose-induced somatostatin secretion was reduced by similar to 50% following long-term exposure to either of the NEFA, regardless of whether the culture medium contained 4.5 or 15 mmol/l glucose. Ultrastructural evidence of lipid deposition was seen in < 10% of non-beta cells but in > 80% of the beta cells. Conclusions/interpretation Long-term exposure to high glucose and/or NEFA affects the release of somatostatin and glucagon. The effects on glucagon secretion are very pronounced and in type 2 diabetes in vivo may aggravate the hyperglycaemic effects due to lack of insulin.
Ämnesord och genrebeteckningar
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Endokrinologi och diabetes hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine Endocrinology and Diabetes hsv//eng
- palmitate
- oleate
- NEFA
- glucolipotoxicity
- diabetes
- glucagon
- somatostatin
- beta-cells
- secretion
- activation
- insulin
Biuppslag (personer, institutioner, konferenser, titlar ...)
- Salehi, S AlbertLund University,Lunds universitet,Islet cell physiology,Forskargrupper vid Lunds universitet,Lund University Research Groups(Swepub:lu)farm-sal (författare)
- Eliasson, LenaLund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups(Swepub:lu)mphy-lel (författare)
- Olofsson, Charlotta S,1971Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology(Swepub:gu)xoloch (författare)
- Rorsman, P. (författare)
- Islet cell physiologyForskargrupper vid Lunds universitet (creator_code:org_t)
Sammanhörande titlar
- Ingår i:Diabetologia: Springer Science and Business Media LLC51:9, s. 1689-16931432-04280012-186X
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- Salehi, S Albert
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- Rorsman, P.
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