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Protein expression patterns in mice fed high fat and high sucrose diet
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-93452OAI: oai:DiVA.org:uu-93452DiVA: diva2:166928
Available from: 2005-09-16 Created: 2005-09-16 Last updated: 2010-01-13Bibliographically approved
In thesis
1. Disturbed Islet Function and Alterations in Islet Protein Expression
Open this publication in new window or tab >>Disturbed Islet Function and Alterations in Islet Protein Expression
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Pancreatic β-cells sense the concentration of glucose in the systemic circulation through metabolism of the sugar molecule. Failure to correlate the blood sugar concentration to an appropriate metabolic signal disrupts the function of the β-cell as a controller of glucose homeostasis and may contribute to the development of type 2 diabetes mellitus. Release of insulin is pulsatile and this thesis presents data that support that metabolism drives such pulsatile release. It is also found that increase in insulin release in response to elevation of the glucose concentration is only seen when the rise in glucose induces a prompt and sustained increase in mitochondrial metabolism. Such activation of mitochondrial metabolism depended on the metabolic state of the β-cell prior to the glucose challenge. In this context, prolonged periods of elevated levels of fatty acids are harmful to the pancreatic β-cell. To study the protein expression changes induced by fatty acids a protocol for islet protein profiling and identification of differently expressed proteins were developed. By using this protocol it was discovered that oleate decreased the cellular level of the chaperone peptidyl-prolyl isomerase B. The protocol was also used to study protein expression in islets obtained from mice fed a high-fat and/or a high-sucrose diet. Excess of glucocorticoids in the systemic circulation also cause a diabetic phenotype. Tissue response to glucocorticoids is regulated by the intracellular concentration of the active form of glucocorticoids, which is formed from the inactive form by the enzyme 11β-hydroxysteroid dehydrogenase type 1. It was found that pancreatic islets produce 11β-HSD1 protein in relation to substrate availability and that the amount of islet 11β-HSD1 protein was negatively correlated with insulin secretion.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 49 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 66
Cell biology, islet, glucose, oleate, corticosterone, oxygen tension, insulin release, protein profiling, Clark-like electrodes, SELDI-TOF MS, PPI-B, 11β-HSD1, Cellbiologi
National Category
Cell Biology
urn:nbn:se:uu:diva-5924 (URN)91-554-6332-0 (ISBN)
Public defence
2005-10-07, B22, Biomedical center, Husargatan 3, Uppsala, 14:00
Available from: 2005-09-16 Created: 2005-09-16Bibliographically approved

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