Ethnic Differences Found for Fatty Liver Disease and Insulin Resistance

Laurie Barclay, MD

February 28, 2009

February 28, 2009 — Ethnic differences have been found for nonalcoholic fatty liver disease (NAFLD) and insulin resistance, according to the results of the largest population-based study of this topic to date, reported in the March issue of Hepatology.

"[NAFLD] is a spectrum of disorders defined by abnormal accumulation of triglyceride in liver," write Richard Guerrero, from the University of Texas Southwestern Medical Center at Dallas, and colleagues. "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."

The goal of this study was to assess the contribution of body fat distribution to the differing prevalence of hepatic steatosis in 3 major US ethnic groups: black, Hispanic, and white. Proton magnetic resonance spectroscopy, dual-energy x-ray absorptiometry, and multislice abdominal magnetic resonance imaging were performed in a study cohort of 2170 participants.

Compared with Hispanics and whites, blacks had less intraperitoneal (IP) fat and more lower extremity fat, despite controlling for age and total adiposity. After controlling for total, abdominal subcutaneous, and lower extremity adiposity, these groups still differed in hepatic triglyceride content (HTGC). Controlling for IP fat nearly abolished the differences in HTGC, however, which suggests that IP and liver fat are closely related independent of ethnicity.

Although blacks had lower levels of IP and liver fat, prevalence of insulin resistance in this group was similar to that in Hispanics, in whom levels of IP and liver fat were highest. After controlling for IP fat, blacks had the highest insulin levels and homeostasis model assessment values and the lowest serum triglyceride levels.

"IP fat is linked to HTGC, irrespective of ethnicity," the study authors write. "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."

Study limitations include inability to determine whether visceral fat causes the development of hepatic steatosis or is simply a marker of an underlying metabolic derangement contributing to excess liver fat.

"Many of the derangements in lipid metabolism typically associated with insulin resistance were not present in African-Americans," the study authors conclude. "A possible explanation for these findings is that the insulin-resistant phenotype is: (1) a function of the organ contributing primarily to reduced insulin sensitivity and/or (2) a function of the ability to expand subcutaneous adipose tissue in response to overnutrition. Further study is needed to establish the basis for this insulin resistance paradox."

The Donald W. Reynolds Cardiovascular Clinical Research Center at Dallas, supported by the National Institutes of Health grants, supported this study. The study authors have disclosed no relevant financial relationships.

Hepatology. 2009;49:791–801.


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