title: Adipose tissue and atherosclerosis.
abstract: High-energy intake which exceeds energy expenditure leads to the accumulation of triglycerides in adipose tissue, predominantly in large-size adipocytes. This metabolic shift, which drives the liver to produce atherogenic dyslipidemia, is well documented. In addition, an increasing amount of monocytes/macrophages, predominantly the proinflammatory M1-type, cumulates in ectopic adipose tissue. The mechanism of this process, the turnover of macrophages in adipose tissue and their direct atherogenic effects all remain to be analyzed.
authors.affiliation: Laboratory for Atherosclerosis Research, Centre of Experimental Medicine, Institute for Clinical and Experimental Medicine (IKEM), Prague, Czech Republic. rudolf.poledne@ikem.cz.
authors.forename: R
authors.initials: R
authors.lastname: Poledne
authors.forename: I
authors.initials: I
authors.lastname: Králová Lesná
authors.forename: S
authors.initials: S
authors.lastname: Čejková
mesh_terms: D017667:Adipocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004734:Energy Metabolism / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000276:immunology / Q000378:metabolism / Q000473:pathology