The metabolic syndrome: metabolic changes with vascular consequences
Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor‐alpha (TNF‐α) play...
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| Vydáno v: | European journal of clinical investigation Ročník 37; číslo 1; s. 8 - 17 |
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| Hlavní autoři: | , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Oxford, UK
Blackwell Publishing Ltd
01.01.2007
Blackwell |
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| ISSN: | 0014-2972, 1365-2362 |
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| Abstract | Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor‐alpha (TNF‐α) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF‐α are produced in abundance by adipocytes, whereas the production of adiponectin, an anti‐inflammatory adipokine, is reduced. This imbalanced production of pro‐ and anti‐inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol‐binding protein (RBP)‐4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF‐α concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well. |
|---|---|
| AbstractList | Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor‐alpha (TNF‐α) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF‐α are produced in abundance by adipocytes, whereas the production of adiponectin, an anti‐inflammatory adipokine, is reduced. This imbalanced production of pro‐ and anti‐inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol‐binding protein (RBP)‐4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF‐α concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well. Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well.Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well. Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well. |
| Author | Visseren, F. L. J. Wassink, A. M. J. Olijhoek, J. K. |
| Author_xml | – sequence: 1 givenname: A. M. J. surname: Wassink fullname: Wassink, A. M. J. organization: University Medical Centre Utrecht, The Netherlands – sequence: 2 givenname: J. K. surname: Olijhoek fullname: Olijhoek, J. K. organization: University Medical Centre Utrecht, The Netherlands – sequence: 3 givenname: F. L. J. surname: Visseren fullname: Visseren, F. L. J. organization: University Medical Centre Utrecht, The Netherlands |
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| Keywords | Endocrinopathy Adipocyte adipocyte dysfunction Cytokine Metabolic diseases Cardiovascular disease free fatty acids Free fatty acid Change Insulin Adiponectin Vascular disease Medicine Target tissue resistance Dysfunction X Syndrome Blood vessel Atherosclerosis Risk factor Cardiovascular risk Insulin resistance Tumor necrosis factor α tumour necrosis factor-alpha |
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Zoccali 2001; 50 1997; 40 1991; 17 1991; 14 1995; 38 1993; 21 2002; 13 1997; 46 1999; 48 2002; 156 2004; 6 2003; 278 2003; 52 1998; 15 2004; 33 1994; 267 1989; 32 2004; 291 2006; 21 2000; 247 1991; 88 2006; 27 2000; 11 2004; 34 2006; 26 2006; 29 1979; 2 2002; 90 1993; 259 2003; 41 1994; 71 2003; 42 2003; 163 2004; 43 2001; 285 2005; 111 2005; 112 2001; 280 2005; 90 2004; 47 1999; 103 1998; 139 1999; 100 2001; 24 2006; 354 1996; 97 2006; 114 2004; 53 2000; 102 2002; 360 2005; 366 2000; 106 2003; 26 2000; 101 2005; 16 1994; 94 1985; 75 1994; 93 2003; 23 1996; 39 2000; 49 2002; 51 1999; 84 2005; 28 2003; 10 2001; 103 2001; 86 1998; 47 2005; 25 1990; 85 1991; 266 1993; 73 2002; 40 1997; 96 1999; 17 2002; 45 1999; 16 1987; 317 2000; 160 2003; 3 2005; 307 2002; 105 1999; 257 1996; 334 2005; 34 1983; 67 1996; 7 1995; 95 1991; 34 1995; 15 2002; 32 2004; 89 2000; 20 2005; 436 2000; 152 2001; 409 1995; 19 2005; 48 2005; 45 2003; 253 2005; 46 1993; 13 1986; 61 1986; 62 2004; 93 2005; 289 1993; 92 2002; 23 2002; 287 2002; 288 1996; 271 2005; 54 2003; 148 1996; 156 1996; 45 e_1_2_6_72_2 e_1_2_6_114_2 e_1_2_6_53_2 e_1_2_6_95_2 e_1_2_6_137_2 e_1_2_6_30_2 e_1_2_6_118_2 e_1_2_6_110_2 e_1_2_6_133_2 e_1_2_6_19_2 Eckel RH (e_1_2_6_96_2) 1995; 19 e_1_2_6_34_2 e_1_2_6_11_2 e_1_2_6_38_2 e_1_2_6_76_2 e_1_2_6_57_2 e_1_2_6_99_2 e_1_2_6_102_2 e_1_2_6_125_2 e_1_2_6_83_2 e_1_2_6_64_2 e_1_2_6_106_2 e_1_2_6_129_2 e_1_2_6_41_2 e_1_2_6_60_2 e_1_2_6_140_2 e_1_2_6_121_2 e_1_2_6_9_2 e_1_2_6_5_2 e_1_2_6_22_2 e_1_2_6_49_2 e_1_2_6_87_2 e_1_2_6_26_2 e_1_2_6_45_2 e_1_2_6_68_2 e_1_2_6_50_2 e_1_2_6_73_2 e_1_2_6_113_2 e_1_2_6_136_2 e_1_2_6_31_2 e_1_2_6_92_2 e_1_2_6_117_2 e_1_2_6_132_2 e_1_2_6_12_2 e_1_2_6_35_2 e_1_2_6_58_2 Eck SL (e_1_2_6_115_2) 1993; 13 e_1_2_6_16_2 e_1_2_6_39_2 e_1_2_6_54_2 e_1_2_6_61_2 e_1_2_6_84_2 e_1_2_6_124_2 e_1_2_6_42_2 e_1_2_6_105_2 e_1_2_6_128_2 e_1_2_6_109_2 e_1_2_6_120_2 Landsberg L (e_1_2_6_88_2) 1986; 61 e_1_2_6_101_2 e_1_2_6_6_2 e_1_2_6_23_2 e_1_2_6_69_2 e_1_2_6_2_2 e_1_2_6_65_2 e_1_2_6_27_2 e_1_2_6_46_2 e_1_2_6_51_2 e_1_2_6_97_2 e_1_2_6_135_2 e_1_2_6_74_2 e_1_2_6_116_2 e_1_2_6_93_2 e_1_2_6_139_2 e_1_2_6_70_2 Vaccaro O (e_1_2_6_80_2) 1996; 39 e_1_2_6_131_2 e_1_2_6_112_2 e_1_2_6_13_2 e_1_2_6_59_2 Balkau B (e_1_2_6_15_2) 1999; 16 e_1_2_6_32_2 e_1_2_6_17_2 e_1_2_6_55_2 e_1_2_6_36_2 e_1_2_6_78_2 e_1_2_6_62_2 e_1_2_6_104_2 e_1_2_6_127_2 e_1_2_6_85_2 e_1_2_6_20_2 e_1_2_6_108_2 e_1_2_6_81_2 e_1_2_6_100_2 e_1_2_6_123_2 e_1_2_6_7_2 e_1_2_6_3_2 e_1_2_6_24_2 e_1_2_6_47_2 e_1_2_6_28_2 e_1_2_6_43_2 e_1_2_6_66_2 e_1_2_6_89_2 e_1_2_6_52_2 e_1_2_6_75_2 e_1_2_6_94_2 e_1_2_6_138_2 e_1_2_6_71_2 e_1_2_6_90_2 e_1_2_6_119_2 e_1_2_6_130_2 e_1_2_6_111_2 e_1_2_6_134_2 e_1_2_6_18_2 e_1_2_6_10_2 e_1_2_6_33_2 e_1_2_6_14_2 e_1_2_6_37_2 e_1_2_6_56_2 e_1_2_6_79_2 e_1_2_6_98_2 e_1_2_6_103_2 e_1_2_6_63_2 e_1_2_6_86_2 e_1_2_6_126_2 e_1_2_6_107_2 e_1_2_6_40_2 e_1_2_6_82_2 Baron AD (e_1_2_6_91_2) 1994; 267 e_1_2_6_141_2 e_1_2_6_122_2 e_1_2_6_8_2 e_1_2_6_29_2 e_1_2_6_4_2 e_1_2_6_48_2 e_1_2_6_21_2 Haffner SM (e_1_2_6_77_2) 1996; 156 e_1_2_6_44_2 e_1_2_6_67_2 e_1_2_6_25_2 |
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