Key result
Impaired glucose tolerance is linked to ~31% faster HDL apoA-I fractional catabolism.
Why the study?
The mechanisms underlying decreased HDL cholesterol and apoA-I levels in subjects with impaired glucose tolerance were not fully understood.
Case-Control (n=12)
Absolute Event Rate: 0.34% vs 0.26%
p-value: p=<0.01
May link impaired glucose tolerance to altered HDL kinetics; hypothesis-generating and should not yet change practice.
The in vivo kinetics of the HDL apolipoproteins (apo) A-I and A-II were studied in six subjects with impaired glucose tolerance (IGT) and six control subjects with normal glucose tolerance (NGT), using a stable isotope approach. During a 12-h primed constant infusion of L-[ring-13C6]-phenylalanine, tracer enrichment was determined in apoA-I and apoA-II from ultracentrifugally isolated HDL. The rates of HDL apoA-I and apoA-II production and catabolism were estimated using a one-compartment model-based analysis. Triglycerides were higher in IGT subjects (1.33 +/- 0.21 vs. 0.84 +/- 0.27 mmol/l, P < 0.05), but were within the normal range. HDL cholesterol and apoA-I levels were significantly lower in subjects with IGT (1.07 +/- 0.15 vs. 1.36 +/- 0.14 mmol/l, P < 0.05; 0.94 +/- 0.10 vs. 1.34 +/- 0.07 g/l, P < 0.01). In IGT subjects, HDL composition was significantly altered, characterized by an increase in HDL triglycerides (4.9 +/- 1.9 vs. 3.2 +/- 1.0%, P < 0.05) and HDL phospholipids (34.7 +/- 2.6 vs. 27.5 +/- 5.8%, P < 0.05) and a decrease in HDL cholesteryl esters (10.1 +/- 2.0 vs. 12.7 +/- 2.9%, P < 0.05) and HDL apoA-I (31.5 +/- 4.4 vs. 43.2 +/- 2.4%, P < 0.05). The mean fractional catabolic rate (FCR) of HDL apoA-I was significantly higher in IGT subjects (0.34 +/- 0.05 vs. 0.26 +/- 0.03 day(-1), P < 0.01), while the HDL apoA-I production rate (PR), as well as the PR and FCR of HDL apoA-II, showed no differences between the two groups. There were significant correlations between HDL apoA-I FCR and the following parameters: HDL apoA-I (r = -0.902, P < 0.001), HDL cholesterol (r = -0.797, P = 0.001), plasma triglycerides (r = 0.743, P < 0.01), HDL triglycerides (r = 0.696, P < 0.01), and cholesterol ester transfer protein activity (r = 0.646, P < 0.01). We observed a strong positive association between increased apoA-I catabolism and insulin (r = 0.765, P < 0.01) and proinsulin (r = 0.797, P < 0.01) concentrations. These data support the hypothesis that the decrease in HDL cholesterol and apoA-I levels in IGT is principally the result of an enhanced apoA-I catabolism. The latter seems to be an early metabolic finding in IGT even when other lipid parameters, especially plasma triglycerides, still appear to be not or only weakly affected.
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Pietzsch et al. (1998) conducted a case-control in Impaired glucose tolerance (n=12). Impaired glucose tolerance vs. Normal glucose tolerance was evaluated on Mean fractional catabolic rate of HDL apoA-I (day^-1) (p=<0.01). Impaired glucose tolerance was associated with a significantly higher fractional catabolic rate of HDL apoA-I compared to normal glucose tolerance (0.34 vs. 0.26 day^-1; P<0.01).
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