Metabolic syndrome: from insulin resistance to adipose tissue dysfunction.

Camera A; Hopps E; Caimi G

    Risultato della ricerca: Article

    14 Citazioni (Scopus)

    Abstract

    Recently the definition, the pathophysiology and even the clinical utility of metabolic syndrome (MS) have been discussed. The risk induced by each component of the metabolic syndrome is higher than the risk induced by MS alone. MS alone is, in fact, a weaker predictor of cardiovascular disease than diabetes. New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. IGF/IGFBP system could be a link between insulin resistance and cardiovascular disease. RBP-4 can attenuate insulin signalling in skeletal muscle and induce hepatic gluconeogenesis. The belief that insulin-resistance is the main cause of MS could change in favour of the adipose tissue dysfunction. The most common cause of a reduced capacity of the adipose tissue to store fats is the increased dietary intake, also present in lipodistrophy, type 1 diabetes mellitus and polycystic ovarian syndrome. The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. The comprehension of adipose tissue dysfunction mechanisms offers new possibilities of prevention and therapy.
    Lingua originaleEnglish
    pagine (da-a)307-321
    RivistaMinerva Medica
    Volume99
    Stato di pubblicazionePublished - 2008

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    Insulin Resistance
    Adipose Tissue
    Adipokines
    Cardiovascular Diseases
    Fats
    Insulin-Like Growth Factor Binding Protein 1
    Insulin-Like Growth Factor Binding Proteins
    Gluconeogenesis
    Polycystic Ovary Syndrome
    Liver
    Plasminogen Activator Inhibitor 1
    Hyperinsulinism
    Type 1 Diabetes Mellitus
    Transforming Growth Factor beta
    Myocardial Ischemia
    Interleukin-6
    Myocardium
    Skeletal Muscle
    Tumor Necrosis Factor-alpha
    Insulin

    All Science Journal Classification (ASJC) codes

    • Medicine(all)

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    Metabolic syndrome: from insulin resistance to adipose tissue dysfunction. / Camera A; Hopps E; Caimi G.

    In: Minerva Medica, Vol. 99, 2008, pag. 307-321.

    Risultato della ricerca: Article

    Camera A; Hopps E; Caimi G 2008, 'Metabolic syndrome: from insulin resistance to adipose tissue dysfunction.', Minerva Medica, vol. 99, pagg. 307-321.
    Camera A; Hopps E; Caimi G. / Metabolic syndrome: from insulin resistance to adipose tissue dysfunction. In: Minerva Medica. 2008 ; Vol. 99. pagg. 307-321.
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    abstract = "Recently the definition, the pathophysiology and even the clinical utility of metabolic syndrome (MS) have been discussed. The risk induced by each component of the metabolic syndrome is higher than the risk induced by MS alone. MS alone is, in fact, a weaker predictor of cardiovascular disease than diabetes. New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. IGF/IGFBP system could be a link between insulin resistance and cardiovascular disease. RBP-4 can attenuate insulin signalling in skeletal muscle and induce hepatic gluconeogenesis. The belief that insulin-resistance is the main cause of MS could change in favour of the adipose tissue dysfunction. The most common cause of a reduced capacity of the adipose tissue to store fats is the increased dietary intake, also present in lipodistrophy, type 1 diabetes mellitus and polycystic ovarian syndrome. The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. The comprehension of adipose tissue dysfunction mechanisms offers new possibilities of prevention and therapy.",
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    AU - Hopps, Eugenia

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    AB - Recently the definition, the pathophysiology and even the clinical utility of metabolic syndrome (MS) have been discussed. The risk induced by each component of the metabolic syndrome is higher than the risk induced by MS alone. MS alone is, in fact, a weaker predictor of cardiovascular disease than diabetes. New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. IGF/IGFBP system could be a link between insulin resistance and cardiovascular disease. RBP-4 can attenuate insulin signalling in skeletal muscle and induce hepatic gluconeogenesis. The belief that insulin-resistance is the main cause of MS could change in favour of the adipose tissue dysfunction. The most common cause of a reduced capacity of the adipose tissue to store fats is the increased dietary intake, also present in lipodistrophy, type 1 diabetes mellitus and polycystic ovarian syndrome. The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. The comprehension of adipose tissue dysfunction mechanisms offers new possibilities of prevention and therapy.

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