. "ADIPOCYTOKINY - NED\u00C1VNO OBJEVEN\u00C9 HORMONY TUKOV\u00C9 TK\u00C1N\u011A"@cs . "[434FF5ABA946]" . "ADIPOCYTOKINY - NED\u00C1VNO OBJEVEN\u00C9 HORMONY TUKOV\u00C9 TK\u00C1N\u011A" . "The number of obese and overweight individuals has risen dramatically over the last three decades. Obesity is not only associated with the development of the type 2 diabetes and hypertension but it also has negative effects on liver function, leading to diseases such as nonalcoholic fatty liver disease. Insulin resistance is the primary defect underlying the development of the type 2 diabetes and is a central component defining the metabolic syndrome. Adipose tissue produces and secretes a variety of tissue hormones ? adipocytokines and adipokines The recently described adipocyte secretory hormones contribute to the pathogenesis of impaired insulin secretion and insulin resistance, endothelial dysfunction, a pro-inflammatory state and promote progression of atherosclerosis. The present article gives an overview of the well-known adipocytokines (TNF-\u03B1, IL-6, IL-1-\u03B2, MCP-1, resistin, RBP4, PAI-1, adiponectin, leptin, visfatin, ASP, vaspin, omentin, IL-18, Pref-1, angiotensin) and their role in"@cs . "3" . . "103" . "Kontrov\u00E1, Kate\u0159ina" . "Z\u00EDdkov\u00E1, Jarmila" . . "RIV/60461373:22330/09:00022117" . "ADIPOCYTOKINY - NED\u00C1VNO OBJEVEN\u00C9 HORMONY TUKOV\u00C9 TK\u00C1N\u011A" . "Z\u00EDdek, V\u00E1clav" . . "\u0160kop, Vojt\u011Bch" . . "Adipocytokines; adipokines; obesity; fat tissue; insulin; diabetes; insulin resistance; glucose"@en . "22330" . "RIV/60461373:22330/09:00022117!RIV10-MSM-22330___" . . "000264538500003" . . "0009-2770" . "The number of obese and overweight individuals has risen dramatically over the last three decades. Obesity is not only associated with the development of the type 2 diabetes and hypertension but it also has negative effects on liver function, leading to diseases such as nonalcoholic fatty liver disease. Insulin resistance is the primary defect underlying the development of the type 2 diabetes and is a central component defining the metabolic syndrome. Adipose tissue produces and secretes a variety of tissue hormones ? adipocytokines and adipokines The recently described adipocyte secretory hormones contribute to the pathogenesis of impaired insulin secretion and insulin resistance, endothelial dysfunction, a pro-inflammatory state and promote progression of atherosclerosis. The present article gives an overview of the well-known adipocytokines (TNF-\u03B1, IL-6, IL-1-\u03B2, MCP-1, resistin, RBP4, PAI-1, adiponectin, leptin, visfatin, ASP, vaspin, omentin, IL-18, Pref-1, angiotensin) and their role in" . . . . . . . "P(IAA500110805), Z(MSM6046137305)" . "CZ - \u010Cesk\u00E1 republika" . . . . . . . "Adipocytokines ? Recently Discovered Fat Tissue Hormones"@en . "Adipocytokines ? Recently Discovered Fat Tissue Hormones"@en . "2"^^ . "Chemick\u00E9 listy" . "4"^^ . . . "5"^^ . "The number of obese and overweight individuals has risen dramatically over the last three decades. Obesity is not only associated with the development of the type 2 diabetes and hypertension but it also has negative effects on liver function, leading to diseases such as nonalcoholic fatty liver disease. Insulin resistance is the primary defect underlying the development of the type 2 diabetes and is a central component defining the metabolic syndrome. Adipose tissue produces and secretes a variety of tissue hormones ? adipocytokines and adipokines The recently described adipocyte secretory hormones contribute to the pathogenesis of impaired insulin secretion and insulin resistance, endothelial dysfunction, a pro-inflammatory state and promote progression of atherosclerosis. The present article gives an overview of the well-known adipocytokines (TNF-\u03B1, IL-6, IL-1-\u03B2, MCP-1, resistin, RBP4, PAI-1, adiponectin, leptin, visfatin, ASP, vaspin, omentin, IL-18, Pref-1, angiotensin) and their role in"@en . "301983" . . "ADIPOCYTOKINY - NED\u00C1VNO OBJEVEN\u00C9 HORMONY TUKOV\u00C9 TK\u00C1N\u011A"@cs . .