While hypertriglyceridemia frequently coexists with insulin resistance and glucose intolerance, these conditions do not appear to be of direct pathogenetic importance for hypertriglyceridemia when accounting for BMI and apoB levels.
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Association between lower insulin sensitivity and HTG attenuated after BMI/apoB adjustment; challenges direct pathogenetic role and leaves mechanisms open for study.
Hypertriglyceridaemia, insulin resistance and glucose intolerance are conditions associated with an increased risk of coronary heart disease. In this study we have examined randomly selected nondiabetic hypertriglyceridaemic (HTG) males, 40-50 years (n = 65) and age-matched normotriglyceridaemic (NTG) controls (n = 61). The (mean +/- SD) insulin sensitivity index, as assessed by the Minimal Model method, was significantly lower in the HTG compared with the NTG group (3.69 +/- 2.96 vs. 6.29 +/- 3.38 x 10(-4) min-1 per mUL-1; P < 0.001). Thirty-eight per cent of the HTG group was glucose intolerant, compared with 8% in the NTG group (X2 = 13.16; P < 0.001). The glucose intolerant HTG sub-group had, when compared with the glucose tolerant one, significantly higher serum concentrations of apoB (1318 +/- 284 vs. 1094 +/- 312 mg L-1; P < 0.01) and glycerol (84 +/- 26 vs. 65 +/- 22 nmol L-1; P < 0.01). Serum FFA concentrations were, irrespective of glucose tolerance/intolerance, higher in the HTG than in the NTG group. By logistic regression analysis with the HTG/NTG state as the dichotomous variable, it was found that neither a low insulin sensitivity, nor glucose intolerance were independently linked with the HTG state. Instead, the lower insulin sensitivity of the HTG group was related to their higher body mass index. The higher frequency of glucose intolerance in the HTG group was explained by their higher mean serum apoB concentration, when compared with the NTG group. In conclusion, this study of a randomly selected of HTG group has confirmed the frequent coexistance of HTG, insulin resistance and glucose intolerance. The new important finding was that neither of these two latter conditions appear to be of direct pathogenetic importance for HTG.
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A. Asplund‐Carlson (1995) studied this question.
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