Adipose tissue and atherosclerosis

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 monocyt...

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Veröffentlicht in:	Physiological research 2015-01, Vol.64 (Suppl 3), p.S395-S402
Hauptverfasser:	Poledne, R, Králová Lesná, I, Čejková, S
Format:	Artikel
Sprache:	eng
Schlagworte:	Adipocytes Adipocytes - immunology Adipocytes - metabolism Adipocytes - pathology Adipose Tissue - immunology Adipose Tissue - metabolism Adipose Tissue - pathology Animals Atherosclerosis Atherosclerosis - immunology Atherosclerosis - metabolism Atherosclerosis - pathology Body fat Cardiomyopathy Cardiovascular disease Cholesterol Coronary vessels Cytokines Energy Metabolism - physiology Fasting Fatty acids Heart Homeostasis Humans Insulin Insulin resistance Insulin Resistance - physiology Lipoproteins Liver Macrophages - immunology Macrophages - metabolism Macrophages - pathology Metabolism Obesity Obesity - immunology Obesity - metabolism Obesity - pathology Oxidation Physiology Rodents Triglycerides Veins & arteries
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Beschreibung
Zusammenfassung:	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.
ISSN:	0862-8408 1802-9973
DOI:	10.33549/physiolres.933152