scholarly journals Association of apoE gene polymorphisms with lipid metabolism in renal diseases

2020 ◽  
Vol 20 (3) ◽  
pp. 1368-1381
Author(s):  
Tianbiao Zhou ◽  
Hongyan Li ◽  
Hongzhen Zhong ◽  
Zhiqing Zhong ◽  
Shujun Lin

Background and Objectives: Apolipoprotein E (apoE) plays a central role in the metabolism and homeostasis of lipids. ApoE gene encodes three major isoforms: ε2, ε3 and ε4 forming six phenotypes: Ε2Ε2, Ε2Ε3, Ε2Ε4, Ε3Ε3, Ε3Ε3 and Ε4Ε4 . Disorders of the lipid metabolism and the homeostasis are frequently coexist in renal diseases. The association be- tween gene polymorphisms of apoE and lipid metabolism were not consistent. This meta-analysis was performed to assess the association between gene polymorphisms of apoE and lipid metabolism in renal diseases. Methods: A pre-defined literatures search and selection of eligible relevant investigations were performed to extract and collect data from electronic databases. Results: Sixteen articles were enrolled for the analysis of association between apoE gene polymorphisms and lipid metab- olism. Subjects with E3E4 had a higher total cholesterol (TC) than those with E3E3, and subjects with E2E3 had a lower TC than those with E3E3. Subjects with ε2, ε3 had a lower TC than those with ε2, ε3 or ε4 , and subjects with ε4 had a higher TC than those with ε2, ε3 . Subjects with E2E2, E2E3 or E4E4 had a higher triglyceride (TG) than those with E3E3. Subjects with ε4 had a higher TG than those with ε2, ε3 . Subjects with ε2, ε3 had a higher level of TG than those with non-ε2, ε3 . Subjects with E3E4 had a slightly lower high-density lipoprotein (HDL) than those with E3E3. E3E4 appeared to be associated with lower levels of HDL. Subjects with E2E2, E2E3 had a notably lower low-density lipoprotein (LDL) than those with E3E3. Subjects with ε2, ε3 had a lower LDL than those with ε2, ε3 or ε4 ApoE gene polymorphisms were not associated with very low-density lipoprotein, and lipoprotein (a) [Lp(a)]. Subjects with E2E3 or E2E4 had higher apoE levels than those with E3E3, and subjects with E4E4 had lower apoE levels than those with E3E3. Conclusion: ApoE gene polymorphisms are associated with the expression of TC, TG HDL, LDL, Lp(a) or apoE. Keywords: Apolipoprotein E (ApoE) ; gene polymorphism; total cholesterol (TC) ;triglyceride (TG), high-density lipopro- tein (HDL); low-density lipoprotein (LDL); very low-density lipoprotein (VLDL); lipoprotein (a) [Lp(a)] • Meta-analysis

2000 ◽  
Vol 143 (3) ◽  
pp. 427-430 ◽  
Author(s):  
Y Hozumi ◽  
M Kawano ◽  
VC Jordan

OBJECTIVE: Tamoxifen and raloxifene, selective estrogen receptor modulators, decrease serum concentrations of total cholesterol; however, the effect of these drugs on triglyceride metabolism is unclear. In the present study, we investigated the in vitro effect of raloxifene on lipid metabolism and compared it with that of tamoxifen. DESIGN AND METHODS: Intracellular concentrations of total cholesterol and triglyceride in HepG2 cells were measured by an enzymatic method after tamoxifen or raloxifene treatment with or without oleic acid and with or without very low density lipoprotein. RESULTS: Intracellular concentrations of total cholesterol and triglyceride without oleic acid or very low density lipoprotein were not significantly different after treatment with tamoxifen or raloxifene. In contrast, although raloxifene with oleic acid did not increase the intracellular concentrations of triglyceride, tamoxifen treatment in the presence of oleic acid or very low density lipoprotein significantly increased (P<0.05) the triglyceride concentrations. CONCLUSION: The present study suggests that raloxifene does not increase intracellular triglyceride in the presence of oleic acid or very low density lipoprotein, in contrast to tamoxifen. Therefore, raloxifene might be safer than tamoxifen for treating patients with unstable triglyceride levels or a history of hypertriglyceridemia.


2007 ◽  
Vol 79 (3) ◽  
pp. 254-258 ◽  
Author(s):  
Mariarosaria Napolitano ◽  
Alessandro Giuliani ◽  
Tonino Alonzi ◽  
Carmine Mancone ◽  
Gianpiero D'Offizi ◽  
...  

2001 ◽  
Vol 100 (5) ◽  
pp. 517-527 ◽  
Author(s):  
Jason M. R. GILL ◽  
Keith N. FRAYN ◽  
Stephen A. WOOTTON ◽  
George J. MILLER ◽  
Adrianne E. HARDMAN

Moderate exercise reduces postprandial triacylglycerol concentrations, which are a risk marker for coronary heart disease. The present study sought to determine the qualitative nature of exercise-induced changes in lipid metabolism and their association (if any) with changes in factor VII activation. Eleven normotriglyceridaemic men, aged 51.7±6.1 years (mean±S.D.), participated in two oral fat tolerance tests after different pre-conditions: control (no exercise), and exercise (90 min of brisk walking the day before). Venous blood samples were obtained in the fasted state and for 8 h after ingestion of a high-fat meal (1.32 g of fat, 1.36 g of carbohydrate, 0.30 g of protein and 10 mg of [1,1,1-13C] tripalmitin·kg-1 body mass). Prior exercise reduced postprandial plasma triacylglycerol concentrations by 25±3% (mean±S.E.M.), with lower concentrations in the Svedberg flotation rate (Sf) 20–400 (very-low-density lipoprotein) fraction accounting for 79±10% of this reduction. There was no effect on plasma factor VII coagulant activity or on the concentration of the active form of factor VIIa. Prior exercise increased postprandial serum 3-hydroxybutyrate and plasma fatty acid concentrations, decreased serum postprandial insulin concentrations and increased exogenous (8 h 13C breath excretion of 15.1±0.9% of ingested dose compared with 11.9±0.8%; P = 0.00001) and endogenous postprandial fat oxidation. These data raise the possibility that reduced hepatic secretion of very-low-density lipoprotein plays a role in the attenuation of plasma triacylglycerol concentrations seen after exercise, although it is possible that increased triacylglycerol clearance also contributes to this effect.


1990 ◽  
Vol 36 (9) ◽  
pp. 1673-1675 ◽  
Author(s):  
M González Estrada ◽  
C R Rodríguez Ferrer ◽  
I R Astarloa ◽  
E M Lahera

Abstract The values of low-density lipoprotein cholesterol obtained according to the Friedewald formula (Clin Chem 1972; 18:499-502), or by the De Long transformation (J Am Med Assoc 1986;256:2372-7), were compared with the values obtained when the individual cholesterol/triglyceride ratio of very-low-density lipoprotein was used for estimating the contribution of this lipoprotein to the total cholesterol. We found that these formulas gave the greatest errors for individuals with a low serum cholesterol/triglyceride ratio. We propose criteria for deciding when the numerically calculated value of low-density cholesterol is appropriate, and when it is not.


Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2169-2174 ◽  
Author(s):  
Wan Huang ◽  
Anantha Metlakunta ◽  
Nikolas Dedousis ◽  
Heidi K. Ortmeyer ◽  
Maja Stefanovic-Racic ◽  
...  

It is well established that leptin increases the sensitivity of carbohydrate metabolism to the effects of insulin. Leptin and insulin also have potent effects on lipid metabolism. However, the effects of leptin on the regulation of liver lipid metabolism by insulin have not been investigated. The current study addressed the effects of leptin on insulin-regulated hepatic very low-density lipoprotein (VLDL) metabolism in vivo in rats. A 90-min hyperinsulinemic/euglycemic clamp (4 mU/kg · min−1) reduced plasma VLDL triglyceride (TG) by about 50% (P &lt; 0.001 vs. saline control). Importantly, a leptin infusion (0.2 μg/kg · min−1) in combination with insulin reduced plasma VLDL-TG by about 80% (P &lt; 0.001 vs. insulin alone). These effects did not require altered skeletal muscle lipoprotein lipase activity but did include differential effects of insulin and leptin on liver apolipoprotein (apo) B and TG metabolism. Thus, insulin decreased liver and plasma apoB100/B48 levels (∼50%, P &lt; 0.01), increased liver TGs (∼20%, P &lt; 0.05), and had no effect on fatty acid oxidation. Conversely, leptin decreased liver TGs (∼50%, P &lt; 0.01) and increased fatty acid oxidation (∼50%, P &lt; 0.01) but had no effects on liver or plasma apoB levels. Importantly, the TG-depleting and prooxidative effects of leptin were maintained in the presence of insulin. We conclude that leptin additively increases the suppressive effects of insulin on hepatic and systemic VLDL metabolism by stimulating depletion of liver TGs and increasing oxidative metabolism. The net effect of the combined actions of insulin and leptin is to decrease the production and TG content of VLDL particles.


Author(s):  
N. H. Kopchak ◽  
О. S. Pokotylo ◽  
M. D. Kuhtyn ◽  
M. I. Koval

Introduction. Today, obesity is an extremely common phenomenon that negatively affects on the functional state of the organism, metabolism, and this in turn leads to the increase of a number of diseases. The thyroid gland has a significant effect on lipid metabolism, and especially negative in the case of iodine deficiency in the diet, which leads to hypothyroidism. Comparative study of the effect of various iodine-derived lipid metabolism in obesity is perspective.The aim of the study – to investigate the comparative affect of biologically active iodine in the composition of “Jodis-Concentrate” and inorganic iodine (J-C) as a part of “Iodomarine” on the indicators of lipid metabolism in blood of white male rats with experimental alimentary obesity.Research Methods. The object of the study was the blood serum of white rats, and the subject – separate indicators of lipid metabolism in it. The study was conducted on 48 white male rats. Animals were divided into 3 age groups of 16 animals in each: 1st group – 1.5 months; 2nd – 2.5 months; 3rd – 5th month. In each age group there were 4 subgroups of 4 animals: 1st – control, had a typical diet; 2nd, 3rd and 4th subgroup were with experimental alimentary obesity (EAO), which was formed through the inductor food craving – the sodium salt of glutamic acid in a ratio of 0.6 : 100.0 and high-calorie diet that included standard meals (47 %), sweet condensed milk (44 %), corn oil (8 %) and vegetable starch (1 %). Daily for 45 days, animals of the 3rd subgroup received biologically active iodine in the composition of “Jodis-Concentrate” (J-C) as of 0.1 ml (0.4 mcg of iodine) per kg of body weight a day and 4th subgroup were intragastric administered in the form of inorganic iodine as potassium iodide in medicine “Iodomarin” (IM) as of 0.4 mcg of potassium iodide per kg of body weight a day. In the serum blood, the content of total lipids, total cholesterol, triglycerides, high and low density lipoprotein were determined.Results and Discussion. The obtained results suggest that with the help of biologically active iodine in the composition of “Jodis-Concentrate” there was a significant decrease of the content of common lipids, triglycerides, total cholesterol, low density lipoprotein in blood serum of males with different age than with “Iodomarin”.Conclusions. Given the effective results of the study of the hypolipidemic effect of J-C it is advisable to use it as a preventive and therapeutic agent for reducing the content of common lipids of triglycerides, total cholesterol, and low density lipoproteins in the blood.


PEDIATRICS ◽  
1990 ◽  
Vol 85 (2) ◽  
pp. 155-158
Author(s):  
Wendy Y. Craig ◽  
Glenn E. Palomaki ◽  
A. Myron Johnson ◽  
James E. Haddow

In this meta-analysis it was demonstrated that, when compared with nonsmokers of similar age, smokers in the 8- to 19-year-old age group have significantly higher serum levels of triglyceride (+11.8%), very-low-density lipoprotein (VLDL)-cholesterol (+12.4%) and low-density lipoprotein (LDL)-cholesterol (+4.1%) and significantly lower serum levels of high-density lipoprotein (HDL)-cholesterol (-8.5%) and total cholesterol (-3.7%). All of these smoking-associated changes are in the same direction as those found in adults, with the exception of total cholesterol levels, which are significantly increased in adult smokers. The extent to which mean triglyceride, LDL-cholesterol, and HDL-choles-terol levels are shifted is significantly greater in the 8-to 19-year-old smokers than in adult smokers. The changes in mean total cholesterol levels among smokers in both age groups represent only the net shifts in the lipoprotein fractions and are therefore likely to be a less sensitive indicator of the possible lipid-related excess coronary artery disease risk in smokers.


2019 ◽  
Vol 47 (04) ◽  
pp. 751-767 ◽  
Author(s):  
Li-Shuang Zhang ◽  
Jun-Hua Zhang ◽  
Rui Feng ◽  
Xin-Yao Jin ◽  
Feng-Wen Yang ◽  
...  

To systematically evaluate the efficacy and safety of berberine for the treatment of hyperlipidemia, six electronic literature databases including SinoMed, CNKI, WanFang Data, PubMed, Embase and The Cochrane Library were searched to collect clinical randomized controlled trials (RCTs) of berberine alone or combined with statins for the treatment of hyperlipidemia from the inception to 8 March 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included RCTs. Then, meta-analysis was performed by using RevMan 5.3 software. A total of 11 RCTs involving 1386 patients were finally included. The results of meta-analysis showed that compared with the placebo group, berberine could significantly reduce the total cholesterol and low-density lipoprotein levels and elevate the high density lipoprotein level ([Formula: see text]). Compared with the simvastatin group, berberine was effective only in reducing the level of triglyceride ([Formula: see text], 95% CI: [Formula: see text]0.66, [Formula: see text]0.07, [Formula: see text]). There, however, was no statistical significance between the BBR group and simvastatin group in the low density lipoprotein and high density lipoprotein levels. Compared with the simvastatin group, berberine plus simvastatin was more effective in reducing the level of triglyceride ([Formula: see text], 95% CI: [Formula: see text]0.46, [Formula: see text]0.20, [Formula: see text]) and total cholesterol ([Formula: see text], 95% CI: [Formula: see text]0.60, [Formula: see text]0.12, [Formula: see text]). In terms of adverse reactions, the incidence of adverse reactions including transaminase elevation and muscle aches was lower in the berberine alone or combined with simvastatin group than that in the control group, while the instance of constipation was higher. This study suggests that berberine is effective for hyperlipidemia. The quality and quantity of included studies, however, were dissatisfactory, which might decrease the reliability of the results. Higher quality studies are needed to provide more high quality evidence.


2020 ◽  
Vol 318 (2) ◽  
pp. E262-E275 ◽  
Author(s):  
Jing Zhang ◽  
Ferdous Rastgar Jazii ◽  
Mahdi Montazer Haghighi ◽  
Danielle Alvares ◽  
Lipei Liu ◽  
...  

miR-130b is a microRNA whose expression is particularly elevated within adipose tissue and in the circulation in diabetic states. Hepatic miR-130b expression has been linked to hepatocellular carcinoma and changes in lipid metabolism. Here, we investigated the role of miR-130b in hepatic lipid homeostasis and lipoprotein export. We observed that overexpression of miR-130b-3p or -5p in HepG2 cells markedly enhanced the secretion of very-low-density lipoprotein (VLDL) particles, enhanced the secretion of [3H]glycerol metabolically labeled triglyceride (TG), and significantly increased the number or the average size of lipid droplets (LDs), respectively. Overexpression of miR-130b also altered the expression of key genes involved in lipid metabolism and in particular markedly increased both mRNA and protein expression levels of microsomal triglyceride transfer protein (MTP). Conversely, the miR-130b inhibitor decreased mRNA levels of MTP and fatty acid synthase ( FAS) in HepG2 cells. However, dual-luciferase reporter assays indicated that MTP is not a direct target of miR-130b-3p. miR-130b overexpression did not alter de novo synthesized TG or the stability and secretion of apolipoprotein B 100. Interestingly, knockdown of phosphatase and tensin homolog ( PTEN) blocked the upregulation of MTP mRNA induced by miR-130b. Finally, miR-130b-induced stimulation of VLDL secretion was also observed in a second hepatocyte cell culture model, immortalized human hepatocytes, confirming the effects observed in HepG2 cells. Overall, these data suggest a potential role for miR-130b in promoting hepatic VLDL assembly and secretion mediated by marked stimulation of MTP expression and TG mobilization. Thus miR-130b overexpression corrects the defect in VLDL production in HepG2 cells.


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