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  • Title: Effects of acquired obesity on endothelial function in monozygotic twins.
    Author: Pietiläinen KH, Bergholm R, Rissanen A, Kaprio J, Häkkinen AM, Sattar N, Yki-Järvinen H.
    Journal: Obesity (Silver Spring); 2006 May; 14(5):826-37. PubMed ID: 16855192.
    Abstract:
    OBJECTIVE: To determine whether acquired obesity or accompanying metabolic changes such as adiponectin deficiency, insulin resistance, dyslipidemia, or visceral fat are associated, independent of genetic influences, with endothelial dysfunction by studying young adult monozygotic (MZ) twin pairs discordant for obesity. RESEARCH METHODS AND PROCEDURES: Nine obesity-discordant (intra-pair difference in BMI, 3.8 to 10.1 kg/m(2)) and nine concordant (0 to 2.3 kg/m(2)) 24- to 27-year-old MZ twin pairs were identified from a population-based FinnTwin16-sample. Endothelial function was measured by blood flow responses to intrabrachial infusions of an endothelium-dependent (acetylcholine) and an endothelium-independent (sodium nitroprusside) vasodilator. Whole body insulin sensitivity was measured using the euglycemic insulin clamp technique, and forearm and body composition were measured with magnetic resonance imaging and DXA. In addition, serum levels of adiponectin, high-sensitivity C-reactive protein, and lipids were determined. RESULTS: The heavier co-twins of the discordant pairs had significantly lower whole body insulin sensitivity than the leaner co-twins. Blood flows/muscle volume during infusions of acetylcholine and sodium nitroprusside were not altered by obesity. However, intra-pair differences in serum adiponectin, intra-abdominal fat, and C-reactive protein were significantly correlated with those in endothelial function. Only the relationship between intra-pair differences in adiponectin and endothelial function persisted in multiple linear regression analysis. Obesity-concordant co-twins had comparable insulin sensitivity and endothelial function. DISCUSSION: In young adult MZ twins discordant for obesity, acquired adiponectin deficiency rather than obesity per se is an independent correlate of endothelial dysfunction.
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