2007
DOI: 10.1055/s-2007-984473
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The Relationship of Serum Lipoprotein Lipase Mass with Fasting Serum Apolipoprotein B-48 and Remnant-like Particle Triglycerides in Type 2 Diabetic Patients

Abstract: The decrease in LPL protein mass could cause an increase in serum apo B-48 and RLP-TG levels, which is related to the retardation of remnant metabolism.

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Cited by 9 publications
(6 citation statements)
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“…Decreased LPL activity accounts for a great deal of the elevation of serum TG in insulin-deficient diabetes patients [19, 20]. As the RLP-TG to TG ratio has been reported to correlate with LPL activity [21], the result of a significant and positive relationship between RBP4 and the RLP-TG to TG ratio in this study suggests that decreased LPL activity would have contributed much to the elevation of RLP-TG.…”
Section: Discussionmentioning
confidence: 56%
“…Decreased LPL activity accounts for a great deal of the elevation of serum TG in insulin-deficient diabetes patients [19, 20]. As the RLP-TG to TG ratio has been reported to correlate with LPL activity [21], the result of a significant and positive relationship between RBP4 and the RLP-TG to TG ratio in this study suggests that decreased LPL activity would have contributed much to the elevation of RLP-TG.…”
Section: Discussionmentioning
confidence: 56%
“…From the point at which cilostazol treatment does not signifi cantly change the plasma apoAI level, cholesterol effl ux from peripheral tissues via the apoAI-ABCA1 pathway may be promoted. Further studies including the effects on lipoprotein lipase protein mass and activity [33,34] are needed to clarify the mechanisms of cilostazol ' s effect on HDL-C metabolism and its relationship with the antiatherogenic effects exhibited in this study. Recently, the development of torcetrapib, a CETP inhibitor, that signifi cantly upregulated plasma HDL-C-levels was discontinued after an increase in the mortality rate was observed after administration of torcetrapib [35] .…”
Section: Resultsmentioning
confidence: 98%
“…6 From these results, we investigated if ANGPTL3 really regulates TG-rich lipoprotein metabolism through inhibiting LPL and HTGL activities in human plasma as in mice. LPL has been known to hydrolyse chylomicrons and very low-density lipoproteins (VLDL) to form their remnants in human plasma, 7,8 and HTGL has been known to hydrolyse b-VLDL or intermediate density lipoproteins (IDL) to form small, dense LDL (sd LDL). 9 HTGL is also known to hydrolyse TG in LDL and HDL, especially to hydrolyse HDL2 to form HDL3.…”
Section: Introductionmentioning
confidence: 99%