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Christian X. Andersson

Researcher at University of Gothenburg

Publications -  27
Citations -  1337

Christian X. Andersson is an academic researcher from University of Gothenburg. The author has contributed to research in topics: Adipose tissue & Insulin resistance. The author has an hindex of 15, co-authored 26 publications receiving 1228 citations. Previous affiliations of Christian X. Andersson include Sahlgrenska University Hospital.

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Inflamed Adipose Tissue A Culprit Underlying the Metabolic Syndrome and Atherosclerosis

TL;DR: The metabolic syndrome is associated with a dysregulated adipose tissue; in part a consequence of adipose cell enlargement and the associated infiltration of macrophages, which leads to a proinflammatory state in the cells with reduced secretion of adiponectin and with increased secretion of several cytokines and chemokines.
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Overexpression of Il6 leads to hyperinsulinaemia, liver inflammation and reduced body weight in mice

TL;DR: Chronically elevated IL-6 levels lead to inappropriate hyperinsulinaemia, reduced body weight, impaired insulin-stimulated glucose uptake by the skeletal muscles and marked inflammation in the liver, despite the fact that weight reduction may be expected.
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The effect of PPARγ ligands on the adipose tissue in insulin resistance

TL;DR: Treatment with PPARgamma and its ligands, the thiazolidinediones (TZD), result in improved insulin signaling and adipocyte differentiation, increased adipose tissue influx of free fatty acids and inhibition of cytokine expression and action.
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Inflamed adipose tissue, insulin resistance and vascular injury.

TL;DR: Of major concern is the two‐ to fourfold increase in cardiovascular morbidity and mortality in this group compared to a nondiabetic population.
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AMP-activated protein kinase inhibits IL-6-stimulated inflammatory response in human liver cells by suppressing phosphorylation of signal transducer and activator of transcription 3 (STAT3).

TL;DR: Evidence is provided for a key function of AMPK in suppression of the acute-phase response caused by the action of IL-6 in liver, suggesting that AMPK may act as an intracellular link between chronic low-grade inflammation and metabolic regulation in peripheral metabolic tissues.