High density lipoprotein2. Relationship of the plasma levels of this lipoprotein species to its composition, to the magnitude of postprandial lipemia, and to the activities of lipoprotein lipase and hepatic lipase.

Patsch, Josef R.; Prasad, Sarada C.; Gotto, Antonio M.; Patsch, Wolfgang

doi:10.1172/jci113078

Cited by 378 publications

(142 citation statements)

References 37 publications

(31 reference statements)

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“…Circulating VLDLs are hydrolysed by two lipolytic enzymes, lipoprotein lipase and hepatic lipase. Both a decrease in lipoprotein lipase and an increase in hepatic lipase activity have previously been shown to be associated with the accumulation of pro-atherogenic small dense LDL particles, a lipoprotein composition that is particularly evident in the presence of increased VLDL concentrations [17,18]. Consistent with the above, we found an independent association between RPB4 levels and hepatic lipase activity in patients with type 2 diabetes and in those with CAD.…”

Section: Discussionsupporting

confidence: 89%

Retinol-binding protein 4 is associated with components of the metabolic syndrome, but not with insulin resistance, in men with type 2 diabetes or coronary artery disease

et al. 2007

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Aims/hypothesis Retinol-binding protein 4 (RBP4) has recently been reported to be associated with insulin resistance and the metabolic syndrome. This study tested the hypothesis that RBP4 is a marker of insulin resistance and the metabolic syndrome in patients with type 2 diabetes or coronary artery disease (CAD) or in non-diabetic control subjects without CAD. Methods Serum RBP4 was measured in 365 men (126 with type 2 diabetes, 143 with CAD and 96 control subjects) and correlated with the homeostasis model assessment of insulin resistance index (HOMA-IR), components of the metabolic syndrome and lipoprotein metabolism. RBP4 was detected by ELISA and validated by quantitative Western blotting. Results RBP4 concentrations detected by ELISA were shown to be strongly associated with the results gained in quantitative Western blots. There were no associations of RBP4 with HOMA-IR or HbA 1c in any of the groups studied. In patients with type 2 diabetes there were significant positive correlations of RBP4 with total cholesterol, LDL-cholesterol, VLDL-cholesterol, plasma triacylglycerol and hepatic lipase activity. In patients with CAD, there were significant associations of RBP4 with VLDLcholesterol, plasma triacylglycerol and hepatic lipase activity, while non-diabetic control subjects without CAD showed positive correlations of RBP4 with VLDLcholesterol and plasma triacylglycerol. Conclusions/interpretation RBP4 does not seem to be a valuable marker for identification of the metabolic syndrome or insulin resistance in male patients with type 2 diabetes or CAD. Independent associations of RBP4 with pro-atherogenic lipoproteins and enzymes of lipoprotein metabolism indicate a possible role of RBP4 in lipid metabolism.

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Section: Discussionsupporting

confidence: 89%

Retinol-binding protein 4 is associated with components of the metabolic syndrome, but not with insulin resistance, in men with type 2 diabetes or coronary artery disease

et al. 2007

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“…However, this effect could very well be desireable in obesity and type 2 diabetes; in both conditions plasma triglyceride levels are frequently increased accompanied with CETPmediated loss of HDL-cholesterol. 10,11 In both situations, leptin and insulin levels are high reducing PLTP and CETP levels and consequently loss of HDL cholesterol.…”

Section: Leptin and Insulin On Lipid Transfer Proteins S Kaser Et Almentioning

confidence: 99%

“…6,7 CETP catalyzes the transfer of cholesteryl esters (CE) from HDL to apoB-containg lipoproteins in exchange for triglycerides 8,9 resulting in the conversion of larger to smaller particles and low HDL cholesterol levels. 10,11 Thus, both PLTP and CETP stimulate several critical steps of reverse cholesterol transport.…”

Section: Introductionmentioning

confidence: 99%

Influence of leptin and insulin on lipid transfer proteins in human hepatoma cell line, HepG2

et al. 2001

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AIM: Phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) are key enzymes in lipoprotein metabolism facilitating the transfer and exchange of cholesteryl esters, triglycerides and phospholipids between lipoproteins. In the study presented here, we investigated the influence of two hormones -the adipocyte-derived hormone leptin as well as insulin on the hepatic secretion of both, PLTP and CETP. METHODS: PLTP activity and CETP concentration -measured by exogenous substrate assay and enzyme-linked immunosorbent assay -were determined in supernatant of human hepatoma cell line HepG2 after single or combined exposure to leptin and insulin at physiological and supraphysiological concentrations, respectively. Messenger-RNA of PLTP and CETP was quantified by Northern blot analysis. RESULTS: Leptin suppressed PLTP activity and CETP-concentration by up to 33% and 23%, respectively. Insulin also suppressed PLTP activity by up to 11% and CETP-concentration by up to 16%. In combination, the two hormones had additive suppressive effects for both, PLTP activity and CETP-concentration. Northern blot analysis showed no difference in m-RNA levels after exposure to leptin or insulin. CONCLUSIONS: Leptin and insulin, both known to increase with body fat mass, suppress production of PLTP and CETP in HepG2 cells. When extrapolated to the in vivo situation, this suppressive effect may constitute a mechanism counteracting the potentially harmful action of lipid transfer proteins, particularly reduction of HDL-cholesterol, in conditions frequently associated with increased plasma triglyceride levels such as obesity and insulin resistance.

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“…Patsch et al 42 have shown that this is a critical factor in controlling postprandial lipemia. We have previously shown in subjects eating cholesterol an increase in HDI_2 cholesterol (as a proportion of total cholesterol), which we postulated might have prevented a rise in total cholesterol.…”

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confidence: 99%

Relationship between sensitivity to dietary fat and dietary cholesterol.

et al. 1990

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A group of 56 hypercholesterolemic and normocholesterolemic men and women were given approximately 700 mg a day of egg yolk cholesterol In a double-blind, crossover study while they were on a background diet containing approximately 30% of energy as fat. Overall there was a 0.23 mmol/l rise In plasma cholesterol (3.7%, p<0.001) after 4 weeks, a 0.19 mmol/l rise in low density lipoprotein (LDL) cholesterol (4.9%, p=0.002), and a 0.07 mmol/l rise In high density lipoprotein (HDL) cholesterol (5.4%, p<0.001). Plasma trlglycerides fell by 0.07 mmol/l (5.1%). Normocholesterolemic Individuals (plasma cholesterol <5.2 mmol/l) experienced small, nonsignificant rises of 0.06, 0.02, and 0.05 mmol/l In total, LDL, and HDL cholesterol, respectively. Hypercholesterolemic sub|ects were classified on the basis of their response to a low fat diet. Diet-sensitive sub|ects were defined by a > 10% fall In plasma cholesterol on a 25% fat, low cholesterol (<200 mg/day) diet These individuals were found to be more responsive to the effect of dietary cholesterol than were dlet-insensltlve subjects; the respective changes In the two groups were rises of 0. A n increase in dietary cholesterol produces a small, but significant, increase in plasma cholesterol in most large experimental groups, but there is great individual variability.1 -8 The response to a change in saturated fat intake tends to be much larger than the response to dietary cholesterol, and although individual variability occurs, few people are truly unresponsive. 9 -13 McNamara et al. 13 in an extensive trial of free-living subjects, found that 70% of people could effectively compensate for an increase in dietary cholesterol by down-regulating cholesterol synthesis. A similar proportion of metabolic "compensators" had earlier been reported by Nestel and Poyser.14 In the former study, only 10% of the individuals had a significant (10%) increase in plasma cholesterol, and these individuals failed to downregulate cholesterol synthesis and tended to have high cholesterol absorption rates. A possible genetic basis has been suggested by Kesaniemi et al. 16 who demonstrated that subjects with the E4 allele for apolipoprotein (apo) E had a higher fractional cholesterol absorption From the CSIRO Division of Human Nutrition, Adelaide, South Australia.This work was partly supported by the National Heart Foundation of Australia and the Egg Industry Research Council of Australia.Address for reprints: Dr. P.J. Nestel, CSIRO Division of Human Nutrition, Kintore Avenue, Adelaide SA 5000, Australia.Received August 3, 1989; revision accepted December 11, 1989. than did subjects with the E2 allele. Individuals carrying an apo E4 allele had a much higher low density lipoprotein (LDL) cholesterol concentration than did those with the E2 allele. 16 Katan et al. 17 have recently shown that there may be a correlation between sensitivity to changes in dietary saturated fat intake and sensitivity to dietary cholesterol in normocholesterolemic individuals. However, hypercholesterolemic ind...

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High density lipoprotein2. Relationship of the plasma levels of this lipoprotein species to its composition, to the magnitude of postprandial lipemia, and to the activities of lipoprotein lipase and hepatic lipase.

Cited by 378 publications

References 37 publications

Retinol-binding protein 4 is associated with components of the metabolic syndrome, but not with insulin resistance, in men with type 2 diabetes or coronary artery disease

Retinol-binding protein 4 is associated with components of the metabolic syndrome, but not with insulin resistance, in men with type 2 diabetes or coronary artery disease

Influence of leptin and insulin on lipid transfer proteins in human hepatoma cell line, HepG2

Relationship between sensitivity to dietary fat and dietary cholesterol.

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