title: Ethnic differences in hepatic steatosis: an insulin resistance paradox?
abstract: Nonalcoholic fatty liver disease is a burgeoning problem. We have previously shown that Hispanics were at greater risk for nonalcoholic fatty liver disease than were African-Americans despite a similar prevalence of risk factors between these groups. We have performed the largest, population-based study to date (n = 2170) utilizing proton magnetic resonance (MR) spectroscopy, dual-energy x-ray absorptiometry, and multislice abdominal MR imaging to determine the contribution of body fat distribution to the differing prevalence of hepatic steatosis in the three major U.S. ethnic groups (African-American, Hispanic, Caucasian). Despite controlling for age and total adiposity, African-Americans had less intraperitoneal (IP) fat and more lower extremity fat than their Hispanic and Caucasian counterparts. The differences in hepatic triglyceride content (HTGC) between these groups remained after controlling for total, abdominal subcutaneous, and lower extremity adiposity; however, controlling for IP fat nearly abolished the differences in HTGC, indicating a close association between IP and liver fat regardless of ethnicity. Despite the lower levels of IP and liver fat in African-Americans, their prevalence of insulin resistance was similar to Hispanics, who had the highest levels of IP and liver fat. Furthermore, insulin levels and homeostasis model assessment values were highest and serum triglyceride levels were lowest among African-Americans after controlling for IP fat.
  
  
  CONCLUSIONS
  IP fat is linked to HTGC, irrespective of ethnicity. The differing prevalence of hepatic steatosis between these groups was associated with similar differences in visceral adiposity. The metabolic response to obesity and insulin resistance differs in African-Americans when compared to either Hispanics or Caucasians: African-Americans appear to be more resistant to both the accretion of triglyceride in the abdominal visceral compartment (adipose tissue and liver) and hypertriglyceridemia associated with insulin resistance.
authors.affiliation: Department of Internal Medicine, Dallas, TX, USA.
authors.forename: Richard
authors.initials: R
authors.lastname: Guerrero
authors.forename: Gloria L
authors.initials: GL
authors.lastname: Vega
authors.forename: Scott M
authors.initials: SM
authors.lastname: Grundy
authors.forename: Jeffrey D
authors.initials: JD
authors.lastname: Browning
mesh_terms: D015502:Absorptiometry, Photon; D050154:Adiposity / Q000208:ethnology / Q000502:physiology; D000328:Adult; D044383:Black People / Q000208:ethnology*; D005234:Fatty Liver / Q000097:blood / Q000208:ethnology* / Q000503:physiopathology*; D005260:Female; D006630:Hispanic or Latino / Q000208:ethnology*; D006801:Humans; D007333:Insulin Resistance / Q000208:ethnology* / Q000502:physiology; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology; D050356:Lipid Metabolism / Q000502:physiology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D050151:Subcutaneous Fat / Q000378:metabolism / Q000473:pathology; D014280:Triglycerides / Q000378:metabolism; D044465:White People / Q000208:ethnology*; D001741:Black or African American
chemical_list: D014280:Triglycerides