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Glucolipotoxicity in INS-1E cells is counteracted by carnitine palmitoyltransferase 1 over-expression
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2008 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 375, no 4, 517-521 p.Article in journal (Refereed) Published
Abstract [en]

Effects of non-esterified fatty acids (FAs) are accentuated when applied together with elevated glucose through preferential use of glucose as fuel, which leads to decreased oxidation of FAs. We examined how over-expression of the mitochondrial FA transporter carnitine palmitoyltransferase 1 (CPT1) affects glucose-stimulated insulin secretion (GSIS), apoptosis and ER stress in INS-1E cells cultured in the presence of elevated levels of glucose and palmitate. INS-1E cells were infected with Tet-ON regulated adenovirus containing CPT1 and cultured for 48h in the presence of 0.5mM palmitate and 20mM glucose. Over-expressing CPT1 lowered basal insulin secretion in a dose-dependent manner thereby improving GSIS from INS-1E cells. Also, apoptosis was alleviated and ER-stress markers p-eIF2alpha and CHOP were decreased in cells over-expressing CPT1. We conclude that regulated over-expression of CPT1 is beneficial for glucolipotoxic beta-cells.

Place, publisher, year, edition, pages
2008. Vol. 375, no 4, 517-521 p.
Keyword [en]
Type 2 diabetes, Glucolipotoxicity, INS-1E, Palmitate, Carnitine palmitoyltransferase 1, ER-stress, GSIS, Apoptosis, p-eIF2 alpha, CHOP/GADD153
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-100420DOI: 10.1016/j.bbrc.2008.08.013ISI: 000259769200006PubMedID: 18706397OAI: oai:DiVA.org:uu-100420DiVA: diva2:219113
Available from: 2009-05-26 Created: 2009-03-31 Last updated: 2017-12-13Bibliographically approved

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Akusjärvi, Göran

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