Syndrome X in children: Influence of ethnicity and visceral fat

Academic Article


  • Syndrome X, the clustering of risk factors for cardiovascular disease, is recognized as an obesity-related health concern among adults. In particular, individuals with visceral (intra-abdominal) obesity are prone to developing syndrome X. Although extremes of visceral fat have been detected in prepubertal children, the extent to which visceral fat contributes to the development of disease risk factors in children is not known. This review addresses the occurrence of syndrome X and its antecedents in the pediatric population, as well as two specific issues regarding syndrome X in children: the roles of ethnicity and visceral fat. The central feature to emerge from most studies is that basal and post-challenge insulin are significantly higher in African-American, Mexican-American, and Pima Indian children compared to Caucasian children. Although these ethnic differences are independent of adiposity, adiposity is associated with greater insulin in all ethnic groups examined. Mexican-Americans have a higher lipid risk factor level, which is related to greater obesity, and African-Americans have lesser lipid-associated risk, independent of obesity. African-American children may be more likely to develop type 2 diabetes due to obesity-independent hyperin-sulinemia and insulin resistance, but appear less predisposed to the obesity-related clustering of risk factors associated with syndrome X. Mexican-American children may be more likely to develop syndrome X due to greater obesity-related hyperinsulinemia and dyslipidemia. Total body fat, rather than visceral fat, appears be the primary determinant of insulin resistance prior to puberty. However, visceral adipose tissue is uniquely related to both insulin and lipid risk factors in children and adolescents, and thus may contribute to the development of the early stages of syndrome X. © 1999 Wiley-Liss, Inc.
  • Published In

    Author List

  • Gower BA
  • Start Page

  • 249
  • End Page

  • 257
  • Volume

  • 11
  • Issue

  • 2