title: Influence of total vs. visceral fat on insulin action and secretion in African American and white children.
abstract: OBJECTIVE
  To examine whether total body fat (FAT) in general or visceral fat (VFAT) in particular is associated with greater metabolic risk in white and African American children.
  
  
  METHODS
  A total of 68 white and 51 African American children had measures of insulin sensitivity (Si) and acute insulin response (AIR) by a frequently sampled intravenous glucose tolerance test, total body fat by DXA and abdominal fat distribution (visceral vs. subcutaneous) by computed tomography. The influence of FAT and VFAT on insulin parameters were examined by comparing subgroups of children with high or low FAT vs. high or low VFAT and by multiple regression analysis.
  
  
  RESULTS
  In whites, fasting insulin, Si, and AIR were significantly influenced by FAT, but not VFAT (e.g., for Si, 9.8 +/- 0.8 in low FAT vs. 4.6 +/- 0.7 x 10(-4)/min/[microIU/mL[ in high FAT, p < 0.05; 6.8 +/- 0.7 in low VFAT vs. 7.5 +/- 0.8 x 10(-4)/min/[microIU/mL] in high VFAT, p > 0.1). In African Americans, fasting insulin and Si were also primarily influenced by FAT (e.g., for Si, 4.9 +/- 0.4 in low FAT vs. 2.8 +/- 0.5 x 10(-4)/min/[microIU/mL] in high FAT, p < 0.05) but not by VFAT, and there were no significant effects of either fat compartment on AIR. In multiple regression analysis, Si was significantly influenced by FAT (negative effect), ethnicity (lower in African Americans), and gender (lower in females), whereas fasting insulin was significantly influenced by VFAT (positive effect), ethnicity (higher in African Americans), and fat free mass (positive effect).
  
  
  CONCLUSIONS
  Body fat in general is the predominant factor influencing Si, but VFAT may have additional effects on fasting insulin. The lack of major effects of VFAT on Si in children may be explained by lower levels of VFAT or because VFAT affects aspects of whole body insulin action that are not measured by the minimal model.
authors.affiliation: Institute for Prevention Research, Department of Preventive Medicine, University of Southern California, Los Angeles, 90033, USA. goran@usc.edu
authors.forename: M I
authors.initials: MI
authors.lastname: Goran
authors.forename: R N
authors.initials: RN
authors.lastname: Bergman
authors.forename: B A
authors.initials: BA
authors.lastname: Gower
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology / Q000378:metabolism*; D044383:Black People; D001823:Body Composition; D002648:Child; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D008297:Male; D009765:Obesity / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D012044:Regression Analysis; D014781:Viscera; D044465:White People; D001741:Black or African American
chemical_list: D007328:Insulin