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1.
J Pediatr ; 155(4): 572-7, 2009 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-19595365

RESUMEN

OBJECTIVES: To test the hypothesis that long-term survivors of low-risk Kawasaki disease (KD) have ongoing vascular inflammation and dysfunction and a higher risk of accelerated atherosclerosis than healthy control subjects. STUDY DESIGN: Twenty-eight patients with KD (7-20 years after acute illness) and 27 age-matched healthy control subjects were examined for medical and dietary history, serum markers of atherosclerotic risk and inflammation, carotid intimal-medial thickness (CIMT) with vascular ultrasound scanning and arterial stiffness with applanation tonometry. RESULTS: Patients and control subjects were similar in age, sex, body mass index, waist-to-hip ratio, blood pressure, cigarette smoking, family history, diet, high-density lipoprotein cholesterol level, lipoprotein (a) level, homocysteine level, glucose level, insulin level, CIMT, arterial stiffness, C-reactive protein level, and inflammatory cytokine level. Levels of total cholesterol and apolipoprotein B were significantly higher in patients with KD than in control subjects. CONCLUSIONS: There was no evidence of increased atherosclerosis. Small but significant differences in cholesterol and apolipoprotein B levels could suggest increased future risk for atherosclerosis and warrant further study.


Asunto(s)
Aterosclerosis/epidemiología , Síndrome Mucocutáneo Linfonodular/metabolismo , Síndrome Mucocutáneo Linfonodular/patología , Proteínas de Fase Aguda/metabolismo , Adolescente , Adulto , Aterosclerosis/diagnóstico , Biomarcadores/metabolismo , Arterias Carótidas/patología , Estudios de Casos y Controles , Citocinas/sangre , Femenino , Humanos , Mediadores de Inflamación/sangre , Lípidos/sangre , Masculino , Síndrome Mucocutáneo Linfonodular/complicaciones , Factores de Riesgo , Adulto Joven
2.
J Nutr Biochem ; 19(4): 237-45, 2008 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-17618104

RESUMEN

BACKGROUND: Hepatic de novo lipogenesis (DNL) is markedly stimulated in humans by low-fat diets enriched in simple sugars. However, the dietary responsiveness of the key enzyme controlling DNL in human adipose tissue, fatty acid synthase (FAS), is uncertain. HYPOTHESIS: Adipose tissue mRNA for FAS is increased in lean and obese subjects when hepatic DNL is elevated by a eucaloric, low-fat, high-sugar diet. DESIGN: Twelve lean and seven obese volunteers were given two eucaloric diets (10% vs. 30% fat; 75% vs. 55% carbohydrate; sugar/starch 60/40) each for 2 weeks by a random-order cross-over design. FAS mRNA in abdominal and gluteal adipose tissues was compared to hepatic DNL measured in serum by isotopic and nonisotopic methods. Adipose tissue mRNA for tumor necrosis factor-alpha and IL-6, which are inflammatory cytokines that modulate DNL, was also assayed. RESULTS: The low-fat high-sugar diet induced a 4-fold increase in maximum hepatic DNL (P<.001) but only a 1.3-fold increase in adipose tissue FAS mRNA (P=.029) and no change in cytokine mRNA. There was a borderline significant positive correlation between changes in FAS mRNA and hepatic DNL (P=.039). Compared to lean subjects, obese subjects had lower levels of FAS mRNA and higher levels of cytokine mRNA (P<.001). CONCLUSIONS: The results suggest that key elements of human adipose tissue DNL are less responsive to dietary carbohydrate than is hepatic DNL and may be regulated by diet-independent factors. Irrespective of diet, there is reduced expression of the FAS gene and increased expression of cytokine genes in adipose tissues of obese subjects.


Asunto(s)
Tejido Adiposo/metabolismo , Citocinas/genética , Carbohidratos de la Dieta/farmacología , Ácido Graso Sintasas/genética , Obesidad/metabolismo , Delgadez/metabolismo , Glucemia/metabolismo , Peso Corporal/efectos de los fármacos , Citocinas/metabolismo , Ácido Graso Sintasas/metabolismo , Femenino , Humanos , Inflamación/metabolismo , Insulina/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Lipogénesis/genética , Masculino , Delgadez/genética , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismo
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