Plasma cholesteryl ester transfer protein mass and phospholipid transfer protein activity are associated with leptin in type 2 diabetes mellitus
B B A - Molecular and Cell Biology of Lipids , Volume 1771 - Issue 1 p. 113- 118
Adipose tissue contributes to plasma levels of lipid transfer proteins and is also the major source of plasma adipokines. We hypothesized that plasma cholesteryl ester transfer protein (CETP) mass, phospholipid transfer protein (PLTP) activity and cholesteryl ester transfer (CET, a measure of CETP action) are determined by adipokine levels. In this study, relationships of plasma CETP mass, PLTP activity and CET with leptin, resistin and adiponectin were analyzed in type 2 diabetic patients and control subjects. Plasma PLTP activity (P < 0.001), CET (P < 0.001), leptin (P = 0.003), resistin (P < 0.001), high sensitive C-reactive protein (P = 0.005), and insulin resistance (HOMAir) (P < 0.001) were higher, whereas HDL cholesterol (P < 0.001) and plasma adiponectin (P < 0.001) were lower in 83 type 2 diabetic patients (32 females) than in 83 sex-matched control subjects. Multiple linear regression analysis demonstrated that in diabetic patients plasma leptin levels were related to plasma CETP mass (P = 0.018) and PLTP activity (P < 0.001), but not to the other adipokines measured. Plasma CET was inversely correlated with adiponectin in univariate analysis, but this association disappeared in multivariate models that included plasma lipids and CETP. In conclusion, both plasma CETP mass and PLTP activity are associated with plasma leptin in type 2 diabetes. The elevated CET in these patients is not independently related to any of the measured plasma adipokines.
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|B B A - Molecular and Cell Biology of Lipids|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Dullaart, R.P.F, de Vries, R, Dallinga-Thie, G.M, van Tol, A, & Sluiter, W. (2007). Plasma cholesteryl ester transfer protein mass and phospholipid transfer protein activity are associated with leptin in type 2 diabetes mellitus. B B A - Molecular and Cell Biology of Lipids, 1771(1), 113–118. doi:10.1016/j.bbalip.2006.11.003