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Peter Arner

Researcher at Karolinska Institutet

Publications -  565
Citations -  56932

Peter Arner is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Adipose tissue & Lipolysis. The author has an hindex of 114, co-authored 553 publications receiving 52710 citations. Previous affiliations of Peter Arner include Karolinska University Hospital & Bristol-Myers Squibb.

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A Human-Specific Role of Cell Death-Inducing DFFA (DNA Fragmentation Factor-α)-Like Effector A (CIDEA) in Adipocyte Lipolysis and Obesity

TL;DR: An important and human-specific role is proposed for CIDEA in lipolysis regulation and metabolic complications of obesity, which is at least in part mediated by cross-talk between CideA and TNF-alpha.
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Automatic luminometric kinetic assay of glycerol for lipolysis studies.

TL;DR: The analytical performance and degree of automation of the glycerol method makes it well suited for serial studies oflipolysis in human fat cells in the presence of lipolytic or antilipolytic agents.
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Downregulation of Electron Transport Chain Genes in Visceral Adipose Tissue in Type 2 Diabetes Independent of Obesity and Possibly Involving Tumor Necrosis Factor-α

TL;DR: Type 2 diabetes is associated with a tissue- and region-specific downregulation of oxidative phosphorylation genes that is independent of obesity and at least in part mediated by TNF-α, suggesting that impaired oxidative phosphORYlation of visceral adipose tissue has pathogenic importance for development of type 2 diabetes.
Journal Article

Regulation of lipolysis in humans. Pathophysiological modulation in obesity, diabetes, and hyperlipidaemia.

TL;DR: New advances in genetic studies indicate that polymorphisms in several genes encoding for proteins that regulate the lipolysis process are important for the development of obesity and its complications.
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Different aetiologies of type 2 (non-insulin-dependent) diabetes mellitus in obese and non-obese subjects.

TL;DR: Type 2 diabetes in obese and non-obese elderly male subjects may take two forms where the cause of hyperglycaemia differs, as indicated by insulin responses to intravenous glucose infusion and glucose utilization during hyperinsulinaemic euglycaemic clamp.