The metabolism of triglyceride-rich lipoproteins revisited: New players, new insight

Dallinga‐Thie, Geesje M.; Franssen, Remco; Mooij, Hans L.; Visser, M.; Hassing, H. Carlijne; Peelman, Frank; Kastelein, John J.P.; Péterfy, Miklós; Nieuwdorp, Max

doi:10.1016/j.atherosclerosis.2009.12.027

Cited by 156 publications

(106 citation statements)

References 76 publications

(100 reference statements)

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“…The lipase maturation factor 1 (LMF1) plays an essential role in the formation of catalytically active LPL from newly synthesized polypeptides. The glycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1 (GPIHBP1) is critically involved in LPL-mediated hydrolysis of TG rich lipoproteins [77]. GPIHBP1 provides an important platform for LPL-mediated hydrolysis of chylomicron triglycerides.…”

Section: Lipoprotein Lipase and Chylomicron Metabolismmentioning

confidence: 99%

Recent advances in physiological lipoprotein metabolism

Ramasamy

2014

Clinical Chemistry and Laboratory Medicine (CCLM)

184

159

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Abstract:Research into lipoprotein metabolism has developed because understanding lipoprotein metabolism has important clinical indications. Lipoproteins are risk factors for cardiovascular disease. Recent advances include the identification of factors in the synthesis and secretion of triglyceride rich lipoproteins, chylomicrons (CM) and very low density lipoproteins (VLDL). These included the identification of microsomal transfer protein, the cotranslational targeting of apoproteinB (apoB) for degradation regulated by the availability of lipids, and the characterization of transport vesicles transporting primordial apoB containing particles to the Golgi. The lipase maturation factor 1, glycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1 and an angiopoietin-like protein play a role in lipoprotein lipase (LPL)-mediated hydrolysis of secreted CMs and VLDL so that the right amount of fatty acid is delivered to the right tissue at the right time. Expression of the low density lipoprotein (LDL) receptor is regulated at both transcriptional and posttranscriptional level. Proprotein convertase subtilisin/ kexin type 9 (PCSK9) has a pivotal role in the degradation of LDL receptor. Plasma remnant lipoproteins bind to specific receptors in the liver, the LDL receptor, VLDL receptor and LDL receptor-like proteins prior to removal from the plasma. Reverse cholesterol transport occurs when lipid free apoAI recruits cholesterol and phospholipid to assemble high density lipoprotein (HDL) particles. The discovery of ABC transporters (ABCA1 and ABCG1) and scavenger receptor class B type I (SR-BI) provided further information on the biogenesis of HDL. In humans HDLcholesterol can be returned to the liver either by direct uptake by SR-BI or through cholesteryl ester transfer protein exchange of cholesteryl ester for triglycerides in apoB lipoproteins, followed by hepatic uptake of apoB containing particles. Cholesterol content in cells is regulated by several transcription factors, including the liver X receptor and sterol regulatory element binding protein. This review summarizes recent advances in knowledge of the molecular mechanisms regulating lipoprotein metabolism.Keywords: ABCA1; angiopoietin-like proteins; apoC; apoAI; apolipoprotein E (apoE); cholesterol ester transfer protein; chylomicron; LDL receptor; lecithin cholesterol acyl transferase; lipoprotein(a); lipoprotein lipase; microsomal transfer protein; propertin convertase subtilisin/ kexin type 9; SR-BI; phospholipid transfer protein; very low density lipoproteins (VLDL). Abstract 1695

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Section: Lipoprotein Lipase and Chylomicron Metabolismmentioning

confidence: 99%

Recent advances in physiological lipoprotein metabolism

Ramasamy

2014

Clinical Chemistry and Laboratory Medicine (CCLM)

184

159

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“…lomicrons (3) which are generated when these lipoproteins are cleared from the circulation by the lipolytic action of lipoprotein lipase (LPL) and hepatic lipase (4).…”

mentioning

confidence: 99%

Exercise Training Reduces Liver Fat and Increases Rates of VLDL Clearance But Not VLDL Production in NAFLD

Shojaee‐Moradie

Cuthbertson

Barrett

et al. 2016

The Journal of Clinical Endocrinology & Metabolism

118

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Context Randomised controlled trials in non-alcoholic fatty liver disease (NAFLD) have shown that regular exercise, even without calorie restriction, reduces liver steatosis. A previous study has shown that 16 weeks supervised exercise training in NAFLD did not affect total VLDL kinetics. Objective:To determine the effect of exercise training on intrahepatocellular fat (IHCL) and the kinetics of large triglyceride-(TG)-rich VLDL 1 and smaller denser VLDL 2 which has a lower TG content.Design A 16 week randomised controlled trial. Patients 27 sedentary patients with NAFLD.Intervention Supervised exercise with moderate-intensity aerobic exercise or conventional lifestyle advice (control).Main outcome Very low density lipoprotein1 (VLDL 1 ) and VLDL 2 -TG and apolipoproteinB (apoB) kinetics investigated using stable isotopes before and after the intervention. Results:In the exercise group VO 2max increased by 31Ϯ6% (meanϮSEM) and IHCL decreased from 19.6% (14.8, 30.0) to 8.9% (5.4, 17.3) (median (IQR)) with no significant change in VO 2max or IHCL in the control group (change between groups pϽ0.001 and pϭ0.02, respectively). Exercise training increased VLDL 1 -TG and apoB fractional catabolic rates, a measure of clearance, (change between groups pϭ0.02 and pϭ0.01, respectively), and VLDL 1 -apoB production rate (change between groups pϭ0.006), with no change in VLDL 1 -TG production rate. Plasma TG did not change in either group. Conclusion:An increased clearance of VLDL 1 may contribute to the significant decrease in liver fat following 16 weeks of exercise in NAFLD. A longer duration or higher intensity exercise interventions may be needed to lower plasma TG and VLDL production rate.

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“…Insulin blocks the VLDL1 formation in the liver. In the conditions of insulin resistance this effect and the elevated intercellular TAG content stimulate formation and secretion predominantly of VLDL1 by the liver [37].…”

Section: Discussionmentioning

confidence: 99%