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Phosphatidylethanolamine N-methyltransferase gene rs7946 polymorphism plays a role in risk of nonalcoholic fatty liver disease: evidence from meta-analysis

Tan HL, Mohamed R, Mohamed Z, Zain SM

Pharmacogenet Genomics, 2016 Feb;26(2):88-95.
PMID: 26636496 DOI: 10.1097/FPC.0000000000000193

Phosphatidylethanolamine N-methyltransferase (PEMT) governs the secretion of hepatic triglycerides in the form of very low-density lipoprotein and has been implicated in nonalcoholic fatty liver disease (NAFLD). Studies on the role of the PEMT rs7946 polymorphism as a genetic modifier of NAFLD have reported inconsistent results. This meta-analysis was carried out to evaluate and summarize the association of PEMT rs7946 with susceptibility to NAFLD.

Matched MeSH terms: Lipoproteins, VLDL
Fulltext Lipoproteins modulate growth and P-glycoprotein expression in drug-resistant HER2-overexpressed breast cancer cells

Siti ZS, Seoparjoo AMI, Shahrul H

Heliyon, 2019 Apr;5(4):e01573.
PMID: 31183434 DOI: 10.1016/j.heliyon.2019.e01573

Background: Drug resistance remains as a challenge in the treatment of HER2-overexpressed breast cancer. Emerging evidence from clinical studies show relation of oxidized low density lipoprotein (LDL) and very low density lipoprotein (VLDL) level with drug resistance. However, the underlying molecular mechanisms for this effect remain unclear. Therefore, the aim of this study was to determine the effects of oxidized-LDL and VLDL in drug-resistant HER2-overexpressed breast cancer cells.
Methods: An in vitro cell model for tamoxifen-resistant HER2 overexpressed UACC732 cells was created using the pulse method. Cells were exposed to oxidized LDL (oxLDL) and very low density lipoprotein (VLDL) separately. Effects on cell morphology was studied using phase contrast microscopic changes. Percentage of cell viability was measured using proliferation assay kit. Development of tamoxifen resistance was determined based on P-gp expression with flow cytometry. Further analysis includedcell death measurement with flow cytometry method.
Results: UACC732 cells exposed to VLDL exhibited fibroblast-like morphology. This was further supported by proliferation assay, where the percentage of cell viability achieved more than 100% with 100 μg/ml of VLDL exposure, indicating cell proliferation. Findings also showed that VLDL caused reduction in expression of Pgp in resistant cells compared to resistant cells alone (p = 0.02).
Conclusion: Results of this study suggest that VLDL may play a role in growth of drug-resistant HER2-overexpressing cells. Lower expression of P-gp in presence of VLDL need to be investigated further.

Matched MeSH terms: Lipoproteins, VLDL
Fulltext Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets

Umpleby AM, Shojaee-Moradie F, Fielding B, Li X, Marino A, Alsini N, et al.

Clin Sci (Lond), 2017 Nov 01;131(21):2561-2573.
PMID: 28923880 DOI: 10.1042/CS20171208

Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD) and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on plasma lipoproteins. To study this further, men with NAFLD (n = 11) and low liver fat 'controls' (n = 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and lipoprotein kinetics were measured after each diet by stable isotope trace-labelling.There were significant differences in the production and catabolic rates of VLDL subclasses between men with NAFLD and controls, in response to the high and low sugar diets. Men with NAFLD had higher plasma concentrations of VLDL1-triacylglycerol (TAG) after the high (P<0.02) and low sugar (P<0.0002) diets, a lower VLDL1-TAG fractional catabolic rate after the high sugar diet (P<0.01), and a higher VLDL1-TAG production rate after the low sugar diet (P<0.01), relative to controls. An effect of the high sugar diet, was to channel hepatic TAG into a higher production of VLDL1-TAG (P<0.02) in the controls, but in contrast, a higher production of VLDL2-TAG (P<0.05) in NAFLD. These dietary effects on VLDL subclass kinetics could be explained, in part, by differences in the contribution of fatty acids from intra-hepatic stores, and de novo lipogenesis. The present study provides new evidence that liver fat accumulation leads to a differential partitioning of hepatic TAG into large and small VLDL subclasses, in response to high and low intakes of sugars.

Matched MeSH terms: Lipoproteins, VLDL/blood; Lipoproteins, VLDL/metabolism*
Fulltext Effects of feeding fat during pregnancy and lactation on growth performance, milk composition and very low density lipoprotein composition in rats

Loh, Teck Chwen, Foo, Hooi Ling, Zurina Abdul Wahab, Tan Bee Koon

Malays J Nutr, 2002;8(2):125-135.
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The effects of dietary fat during pregnancy and lactation on growth performance of pups, milk composition and very low density lipoprotein composition in rats were studied. A total of 33 dams were used in this study and each litter was adjusted to 8 pups per dam. The dams were fed on high fat (150 g fat/kg diet, HF), medium fat (75 g fat/kg of diet, MF) and low fat (2.5 g fat/kg diet, LF) diets. The body weights of dams increased during pregnancy and decreased after pregnancy. The HF pups had a higher body weight and higher weight gain than those of LF pups. The amount of feed intake of HF dams was significantly higher than LF and MF dams. The HF dams had significantly higher milk fat and water concentrations than LF dams. The milk protein was not significantly different among the treatment groups. All dams showed hypertriacylglycerolaemia in their very low density lipoprotein (VLDL) in late pregnancy. The VLDL-protein concentrations increased during the first week after parturition. The HF dams showed a greater response to the dietary fat than that of LF and MF dams. The findings suggest that addition of fat in the diet during pregnancy and lactation may improve the milk quality through modifying the composition of VLDL contents, leading to better growth of pups.

Matched MeSH terms: Lipoproteins, VLDL
Vitamin E and factors affecting atherosclerosis in rabbits fed a cholesterol-rich diet

Ismail NM, Abdul Ghafar N, Jaarin K, Khine JH, Top GM

Int J Food Sci Nutr, 2000;51 Suppl:S79-94.
PMID: 11271860

The present study aims to examine the effects of a palm-oil-derived vitamin E mixture containing tocotrienol (approximately 70%) and tocopherol (approximately 30%) on plasma lipids and on the formation of atherosclerotic plaques in rabbits given a 2% cholesterol diet. Eighteen New Zealand White rabbits (2.2-2.8 kg) were divided into three groups; group 1 (control) was fed a normal diet, group 2 (AT) was fed a 2% cholesterol diet and group 3 (PV) was fed a 2% cholesterol diet with oral palm vitamin E (60 mg/kg body weight) given daily for 10 weeks. There were no differences in the total cholesterol and triacylglycerol levels between the AT and PV groups. The PV group had a significantly higher concentrations of HDL-c and a lower TC/HDL-c ratio compared to the AT group (P < 0.003). The aortic tissue content of cholesterol and atherosclerotic lesions were comparable in both the AT and PV groups. However, the PV group had a lower content of plasma and aortic tissue malondialdehyde (P < 0.005). Our findings suggest that despite a highly atherogenic diet, palm vitamin E improved some important plasma lipid parameters, reduced lipid peroxidation but did not have an effect on the atherosclerotic plaque formation.

Matched MeSH terms: Lipoproteins, VLDL/blood
Fulltext Unleashing the untold and misunderstood observations on vitamin E

Gee PT

Genes Nutr, 2011 Feb;6(1):5-16.
PMID: 21437026 DOI: 10.1007/s12263-010-0180-z

Paradoxically, meta-analysis of human randomized controlled trials revealed that natural but not synthetic α-tocopherol supplementation significantly increases all-cause mortality at 95% confidence interval. The root cause was that natural α-tocopherol supplementation significantly depressed bioavailability of other forms of vitamin E that have better chemo-prevention capability. Meta-analysis outcome demonstrated flaws in the understanding of vitamin E. Reinterpretation of reported data provides plausible explanations to several important observations. While α-tocopherol is almost exclusively secreted in chylomicrons, enterocytes secrete tocotrienols in both chylomicrons and small high-density lipoproteins. Vitamin E secreted in chylomicrons is discriminately repacked by α-tocopherol transfer protein into nascent very low-density lipoproteins in the liver. Circulating very low-density lipoproteins undergo delipidation to form intermediate-density lipoproteins and low-density lipoproteins. Uptake of vitamin E in intermediate-density lipoproteins and low-density lipoproteins takes place at various tissues via low-density lipoproteins receptor-mediated endocytosis. Small high-density lipoproteins can deliver tocotrienols upon maturation to peripheral tissues independent of α-tocopherol transfer protein action, and uptake of vitamin E takes place at selective tissues by scavenger receptor-mediated direct vitamin E uptake. Dual absorption pathways for tocotrienols are consistent with human and animal studies. α-Tocopherol depresses the bioavailability of α-tocotrienol and has antagonistic effect on tocotrienols in chemo-prevention against degenerative diseases. Therefore, it is an undesirable component for chemo-prevention. Future research directions should be focused on tocotrienols, preferably free from α-tocopherol, for optimum chemo-prevention and benefits to mankind.

Matched MeSH terms: Lipoproteins, VLDL