J
Jonas Burén
Researcher at Umeå University
Publications - 36
Citations - 1446
Jonas Burén is an academic researcher from Umeå University. The author has contributed to research in topics: Insulin resistance & Adipose tissue. The author has an hindex of 21, co-authored 34 publications receiving 1317 citations.
Papers
More filters
Journal ArticleDOI
Glucocorticoids Down-Regulate Glucose Uptake Capacity and Insulin-Signaling Proteins in Omental But Not Subcutaneous Human Adipocytes
TL;DR: Human omental adipocytes display approximately 2-fold higher glucose uptake rate compared with s.c. adipocytes, which could be explained by a higher GLUT4 expression, and the interaction between endogenous glucocorticoids and visceral fat in the development of insulin resistance.
Journal ArticleDOI
Dexamethasone impairs insulin signalling and glucose transport by depletion of insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase B in primary cultured rat adipocytes.
TL;DR: It is suggested that glucocorticoids, independently of the surrounding glucose and insulin concentration, impair glucose transport capacity in fat cells.
Journal ArticleDOI
The human visceral fat depot has a unique inflammatory profile.
TL;DR: The human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots, and it is hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT.
Journal ArticleDOI
Insulin action and signalling in fat and muscle from dexamethasone-treated rats.
TL;DR: Dexamethasone treatment decreases PKB expression and insulin-stimulated phosphorylation in both muscles and adipocytes, and increases GS phosphorylated (reduces GS fractional activity) in muscles and decreases GS expression in adipocytes.
Journal ArticleDOI
High glucose and insulin in combination cause insulin receptor substrate-1 and -2 depletion and protein kinase B desensitisation in primary cultured rat adipocytes: possible implications for insulin resistance in type 2 diabetes
TL;DR: Treatment with high insulin downregulates insulin binding capacity and, when combined with high glucose, it produces a marked depletion of IRS-1 and -2 content together with an impaired sensitivity to insulin stimulation of PKB activity.