Nonalcoholic Fatty Liver Disease in Nonobese Subjects of African Origin Has Atypical Metabolic Characteristics

Debbie S. Thompson; Ingrid A. Tennant; Deanne P. Soares; Clive Osmond; Chris D. Byrne; Terrence E. Forrester; Michael S. Boyne


J Endo Soc. 2019;3(11):2051-2063. 

In This Article

Abstract and Introduction


Background: Nonobese nonalcoholic fatty liver disease is reported in several populations. However, because persons of African origin display unique fat accumulation, insulin resistance, and lipid profiles, we investigated fatty liver in nonobese persons of African origin.

Method: We recruited 78 urban Jamaican volunteers. CT was used to estimate liver and abdominal fat and dual-energy X-ray absorptiometry to measure body composition. Fasting blood was collected for lipids, alanine aminotransferase (ALT), adiponectin, and fetuin-A. Homeostatic model assessment of insulin resistance (HOMA-IR), whole-body insulin sensitivity index (WBISI), insulinogenic index (IGI), and oral disposition index (oDI) were calculated after a 75-g oral glucose tolerance test.

Results: Fifty-two percent of participants were male; mean (±SD) age was 28.5 ± 7.8 years, and body mass index was 22.4 ± 3.0 kg/m2. Mean liver attenuation (MLA) and liver/spleen (LS) ratio, both inversely correlated to liver fat, were 62.8 ± 4.3 HU and 1.2 ± 0.1, respectively; 3.8% of participants had liver fat >30% (LS ratio < 1). In age, sex, and BMI-adjusted correlations, MLA was negatively associated with weight (r = −0.30; P = 0.009) and height (r = −0.28; P = 0.017) and was associated with fasting glucose (r = 0.23; P = 0.05), fasting insulin (r = 0.42; P ≤ 0.001) and HOMA-IR (r = 0.35; P = 0.004). Serum lipids, ALT, adiponectin, fetuin-A, WBISI, IGI, and oDI were not associated with liver fat.

Conclusions: In nonobese Afro-Caribbean participants, greater liver fat was associated with weight and height and lower fasting insulin and hyperinsulinemia appears to be influential in the reduction of NAFLD. These findings may be influenced by ethnicity, body size, and method of estimating liver fat.


Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease in Western countries,[1] and it is rapidly becoming the most common liver disease worldwide.[2] It is also a major public health concern because of its association with cardiovascular risk factors.[3] NAFLD occurs when an imbalance between triglyceride accumulation and removal in hepatocytes results in fat accumulation >5% of liver weight without substantial alcohol intake. Although most commonly diagnosed in persons with obesity, NAFLD also occurs in lean/nonobese individuals. Nonobese NAFLD is defined as fatty liver with a body mass index (BMI) <25 kg/m2 in Asians and <30 kg/m2 in people of other races.[4] Its reported global prevalence ranges from 3% to ~30%,[5] and the prevalence in Western populations is 7% to 21%.[6–8]

Nonobese NAFLD is not well understood, and reports regarding its clinical and metabolic features are inconsistent. The third National Health and Nutrition Examination Survey (NHANES III) reported that compared with an overweight-obese NAFLD group, the lean NAFLD cohort was younger and more commonly female, with significantly lower prevalence of IR, DM, hypercholesterolemia, and hypertension.[8] Similarly, in a meta-analysis of 16 studies involving various ethnic groups, lean and obese patients with NAFLD shared altered metabolic and cardiovascular profiles with the effects in lean patients having lesser magnitude.[9] In contrast, patients from Korea with nonobese NAFLD had significantly higher prevalence rates of elevated blood pressure, impaired fasting glucose, low high-density lipoprotein cholesterol (HDL-C), and high triglyceride (TG) concentrations than patients with obesity and NAFLD, especially among women.[10]

The role of ethnicity in these conflicting findings is unknown; in addition, very little is known about nonobese NAFLD in persons of African origin. The prevalence of nonobese NAFLD (BMI < 30 kg/m2) has been reported to be 18% among Hispanic Americans, 9% among whites, and 6% among African Americans.[7] In addition, several metabolic variables commonly associated with fatty liver disease may not reliably predict liver fat in persons of African origin. Low-density lipoprotein cholesterol (LDL-C) and TG levels are associated with liver fat;[11] however, persons of African origin have normal TG and low HDL-C levels as the characteristic lipid profile of insulin resistance (i.e., the so-called triglyceride paradox).[12] Notable also is the fact that blacks have a lower prevalence of fatty liver than Hispanics with similar levels of obesity and insulin resistance.[6] This distinct metabolic response to insulin resistance reported in African Americans (i.e., the insulin resistance paradox)[13] may also be a feature of nonobese NAFLD. Finally, visceral obesity reportedly plays an important role in the pathogenesis of lean NAFLD.[14] However, African Americans may be less likely to accumulate visceral adipose tissue (VAT) than Asians and whites.[15]

These findings suggest that distinct mechanisms may underlie the pathogenesis of NAFLD in persons of African origin. This study aimed to investigate the clinical and biochemical parameters associated with liver fat in nonobese Jamaican adults using an objective measure of both hepatic and visceral fat. A secondary aim was to identify predictors of liver fat in this study population. We hypothesized that fatty liver in nonobese persons of African origin is not associated with insulin resistance or lipid level.