Normal triglyceride levels despite insulin resistance in African Americans: role of lipoprotein lipase.

Abstract Lipoprotein lipase (LPL), the enzyme responsible for hydrolyzing triglyceride (TG) in plasma lipoproteins, is a key regulator of plasma TG levels. In Caucasians, postheparin-LPL (PH-LPL) activity is impaired in the presence of insulin resistance and leads to elevated TG levels. However, African Americans are often both insulin-resistant and normotriglyceridemic. But in African Americans, the effect of insulin resistance on PH-LPL activity has not been studied. In African Americans, if insulin resistance is not associated with a decrease in PH-LPL activity, this could account for the simultaneous presence of insulin resistance and normotriglyceridemia. Therefore, our goal was to determine in African Americans the relationship between insulin resistance and PH-LPL activity. In a cross-sectional study of 107 nondiabetic African Americans (57 men and 50 women; age mean +/- SD, 35 +/- 8 years, range 22-50 years; body mass index 31.6 +/- 7.9 kg/m 2 , range 18.5-54.7 kg/m 2 ), fasting TG levels and PH-LPL activity were determined. Visceral adipose tissue was measured by abdominal computed tomographic scan. Insulin resistance was determined by the insulin sensitivity index ( S I ). Subjects were divided into tertiles by S I . The range of S I in each tertile was 12.75 to 3.99, 3.87 to 2.20, 2.06 to 0.17 mU . L -1 . min -1 . Insulin resistance was defined as being in the third tertile. TG levels in the men and women were 82.2 +/- 35.5 versus 56.4 +/- 30.1 mg/dL, P < .001. There were no sex difference in PH-LPL activity (8.9 +/- 2.5 vs 9.6 +/- 3.2 mmol/h per liter, P = .30) or S I (3.65 +/- 2.59 vs 3.23 +/- 1.89 L . mU -1 . min -1 , P = .49). Although 47% of the subjects were obese, only 4% of subjects had hypertriglyceridemia (TG > or =150 mg/dL). By 2 separate analyses, PH-LPL was a major determinant of TG levels. First, there was a significant inverse correlation between PH-LPL activity and TG levels (men: r = -0.46, P < .001; women: r = -0.28, P = .046). Second, in the multiple regression analysis with TG as the dependent variable and PH-LPL, age, sex, S I , and visceral adipose tissue as independent variables, adjusted R 2 was 54% and the effect of PH-LPL on TG levels was highly significant( P < .001). However, insulin resistance did not appear to influence PH-LPL activity. This is demonstrated in 3 ways: first, PH-LPL activity was not different in the S I tertiles (9.10 +/- 2.75, 9.52 +/- 2.91, 9.13 +/- 2.89 mmol/h per liter, P = .78); the correlation between PH-LPL and S I was not significant (men: r = 0.09, P = .51; women: r = -0.03, P = .78), and a multiple regression with PH-LPL as the dependent variable and age, S I , body mass index, and sex as independent variables, adjusted R 2 was <2% and the contribution of S I was not significant ( P = .53). Hence, in African Americans, increased PH-LPL activity is associated with a decrease in TG levels. The lack of an effect of insulin resistance on PH-LPL could allow LPL to clear TG even in the presence of insulin resistance and explain the coexistence of insulin resistance and normotriglyceridemia in African Americans.

Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans.

BACKGROUND: The "lipid criteria" consist of a triglyceride (TG) level of 130 mg/dL (1.47 mmol/L) or greater and a ratio of TG to high-density lipoprotein cholesterol (HDL-C) of 3 or greater. In Caucasians, the lipid criteria predict insulin resistance in individuals with a body mass index (BMI) of 25 kg/m(2) or greater. Our goal was to determine whether TG levels or TG-HDL-C ratio predicted insulin resistance in African Americans with a BMI of 25 kg/m(2) or more. METHODS: Of 125 African Americans, the 98 with a BMI of 25 kg/m(2) or more participated. All subjects had frequently sampled intravenous glucose tolerance tests with insulin resistance determined by the insulin sensitivity index. Subjects were divided into the following tertiles by insulin sensitivity: 12.8 to 4.3, 4.2 to 2.3, and 2.2 to 0.2 mU/L per minute. Insulin resistance was defined as being in the third tertile. Across tertiles, the distribution of variables was compared by 1-way analysis of variance. Areas under the receiver operating characteristic curve were determined to identify variables that predicted insulin resistance. RESULTS: Fasting insulin level, BMI, and waist circumference increased across tertiles (all P<.01), but TG levels and TG-HDL-C ratio did not (all P>/=.3). The mean +/- SE areas under the curves for fasting insulin, BMI, and waist circumference were 0.85 +/- 0.04, 0.72 +/- 0.05, and 0.71 +/- 0.05, respectively. For TG level and TG-HDL-C ratio, the areas under the curves were 0.55 +/- 0.06 and 0.56 +/- 0.06, respectively, meaning that the true-positive rate was nearly equal to the false-positive rate. Therefore, they could not be used as markers of insulin resistance. Furthermore, 17 subjects met the lipid criteria but only 7 were in the insulin-resistant tertile, making the sensitivity of these criteria to identify insulin resistance only 17%. CONCLUSION: In African Americans, TG levels and TG-HDL-C ratio are not reliable markers of insulin resistance.

Both subcutaneous and visceral adipose tissue correlate highly with insulin resistance in african americans.

OBJECTIVE: The contribution of visceral adipose tissue (VAT) to insulin resistance is well-established; however, the role of subcutaneous abdominal adipose tissue (SAT) in insulin resistance remains controversial. Sex may determine which of these two components of abdominal obesity is more strongly related to insulin resistance and its consequences. The aim of this study was to determine whether both VAT and SAT contribute to insulin resistance in African Americans and to examine the effects of sex on this relationship. RESEARCH METHODS AND PROCEDURES: This was a cross-sectional study of 78 nondiabetic African-American volunteers (44 men, 35 women; age 33.8 +/- 7.3 years; BMI 30.9 +/- 7.4 kg/m2). VAT and SAT volumes were measured using serial computerized tomography slices from the dome of the diaphragm to the iliac crest. The insulin sensitivity index (SI) was determined from the minimal model using data obtained from the frequently sampled intravenous glucose tolerance test. RESULTS: In men, both VAT and SAT were negatively correlated with SI (r for both correlations = -0.57; p < 0.01). In women, the correlation coefficient between VAT and SI was -0.50 (p < 0.01) and between SAT and SI was -0.67 (p < 0.01). In women, the correlation coefficient for SI with SAT was significantly greater than the correlation coefficient with VAT (p = 0.02). DISCUSSION: Both SAT and VAT are strongly correlated with insulin resistance in African Americans. For African-American women, SAT may have a greater effect than VAT on insulin resistance.