Peter Arner

TL;DR: Evidence is provided for specific WHRadjBMI-associated loci as candidates to modulate adipocyte lipolysis and the data suggests that genetically increased central fat accumulation is unlikely to be a major cause of alteredlipolysis in abdominal adipocytes.

TL;DR: The conclusion is that insulin resistance in adipose tissue of NIDDM subjects is solely due to post-receptor defects in insulin action, which is completely off-set by conventional treatment with diet plus sulphonylurea.

TL;DR: The site variations may be involved in the development of regional forms of obesity and may raise the free fatty acid levels in the portal system and therefore impair metabolism of glucose and insulin by the liver.

TL;DR: A healthy ND is able to modify the gene expression in PBMCs after a 2-h oral glucose tolerance test (OGTT) in individuals with MetS, and significantly down-regulated the expression of toll-like receptor 4, interleukin 18, and thrombospondin receptor (CD36) mRNA transcripts and significantly up-regulated peroxisome proliferator-activated receptor delta (PPARD) mRNA transcript after the 2hOGTT compared to the CD.

TL;DR: In untreated hyperthyroidism, there was a decreased sensitivity to the antilipolytic effect of insulin, since the dose-response curve was shifted to the right; 250 microU/ml insulin were required for 50% of the maximal effect compared to 25 micro U/ml in the controls.