scholarly journals Effects of a low-energy diet associated with egg supplementation on plasma cholesterol and lipoprotein levels in normal subjects: results of a cross-over study

1986 ◽  
Vol 56 (3) ◽  
pp. 561-575 ◽  
Author(s):  
Christiane R. Lacombe ◽  
Geneviève R. Corraze ◽  
Maryse M. Nibbelink ◽  
Danièle Boulze ◽  
Philippe Douste-Blazy ◽  
...  
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Energy ◽  
Low Density ◽  
High Cholesterol ◽  
Dietary Regimen ◽  
Cholesterol Intake ◽  
Usual Diet ◽  
Low Energy Diet

1. The influence of a low-energy diet when associated with high-cholesterol intake was investigated in seventeen normal men during an 8-week cross-over study. The subjects were given a daily supplement of two whole eggs and two egg yolks (approximately 1 g cholesterol) either with their usual diet for 4 weeks or with a low-energy diet for 4 weeks. Each subject took part randomly in both dietary periods.2. During the first part of the study, no changes occurred in the plasma cholesterol of the subjects with egg supplementation of the usual diet.3. In contrast, the low-energy diet and associated weight loss markedly decreased the tolerance to high- cholesterol intake resulting in increased plasma cholesterol. The mean rise was 22.7% but with wide individual variations in the response. This was almost completely normalized when the subjects returned to their usual energy intake indicating the involvement of weight reduction in the increase observed.4. Changes in low-density-lipoprotein (LDL) cholesterol were parallel to those of total plasma cholesterol with an increase following the low-energy diet and normalization after body-weight recovery.5. The opposite effect was shown with the low-energy diet after previous adaptation to the consumption of four eggs per day. This dietary regimen resulted in a decrease in plasma cholesterol although it was not significant. Moreover, the lipoprotein profile was improved with a decrease in very-low-density-lipoprotein (VLDL) cholesterol and an increase in high-density-lipoprotein (HDL) cholesterol.6. High-cholesterol intake induced significant changes in lipoprotein composition whatever the energy ration. LDL and HDL were enriched in cholesterol esters as early as the 1st month of egg supplementation of the diet.7. Taken together, the results emphasize the possible adverse effect of slimming diets when associated with high-cholesterol intake. The existence of ‘high-responders’ to these dietary conditions calls for special attention to be paid to the cholesterol content of restricted diets.

Methionine supplementation of low-protein diet and subsequent feeding of low-energy diet on the performance and blood chemical profile of broiler chickens

2018 ◽  
Vol 58 (5) ◽  
pp. 878 ◽  
Author(s):  
P. Jariyahatthakij ◽  
B. Chomtee ◽  
T. Poeikhampha ◽  
W. Loongyai ◽  
C. Bunchasak
Keyword(s):  
Broiler Chickens ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Conversion Ratio ◽  
Low Energy ◽  
Control Group ◽  
Low Density ◽  
Productive Performance ◽  
Conventional Diet ◽  
Low Energy Diet

The effects were investigated of supplementing methionine (Met) in a low-crude protein diet (Low-CP+Met) during Days 11–24 post-hatch and subsequent feeding with a low-metabolisable energy diet (Low-ME; –0.31 MJ/kg) during Days 25–42 on the productive performance and blood chemistry profile of broiler chickens. The 1600 broiler chicks were divided into four groups and fed as follows: (1) Control diet; (2) Low-CP (Met deficiency) diet during Days 11–24, then re-feeding with conventional diet; (3) Low-CP+Met diet during days 11–24, then re-feeding with conventional diet; and (4) Low-CP+Met+Low-ME diet (Low-CP+Met diet during Days 11–24, then re-feeding with Low-ME diet). During Days 11–24, the growth performance of the Control group was better than the other groups (P < 0.01), although the Low-CP+Met diet improved bodyweight, feed conversion ratio and improved the protein conversion ratio compare to the Low-CP group (P < 0.01). During the re-feeding phase (Days 25–42), reducing the dietary energy resulted in better growth performance and a better protein conversion ratio and energy conversion ratio than in the Control group (P < 0.05). Triglyceride, very low-density lipoprotein, low-density lipoprotein-cholesterol and total cholesterol in serum were higher, and non-esterified fatty acid was lower in the Control group than those of the Low-CP+Met+Low-ME group (P < 0.05). In conclusion, reducing dietary protein with balanced amino acids during the grower period and subsequent feeding with a low-energy diet promoted productive performance, improved protein utilisation and reduced fat accumulation via increasing lipolysis and/or disruption of the triglyceride transportation in broiler chickens.

Emodin alleviated hyperlipidemia and hepatic lipid metabolism in zebrafish larvae fed a high-cholesterol diet via AMPK/SREBP-2/PCSK9/LDLR signaling pathway

2021 ◽  
Author(s):  
Linfeng He ◽  
Cheng Wang ◽  
Yafang Zhang ◽  
Chaocheng Guo ◽  
Yan Wan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Cholesterol Diet ◽  
Low Density ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Cholesterol Accumulation ◽  
Hepatic Lipid ◽  
Zebrafish Larvae

Abstract BackgroundEmodin (EM) is one of bioactive components extracted from Rheum palmatum L. (Dahuang), which possesses numerous pharmacological activities including hypolipidemic effect. However, the potential action of EM on hyperlipidemia (HLP) remains unclear. Here, the theraputic effect of EM against HLP were investigated.MethodsIn this study, the hypolipidemic properties of EM were evaluated using high-cholesterol diet (HCD)-stimulated zebrafish larvae model. The body weight, body length and body mass index (BMI) was measured. The total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) as well as the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by corresponding assay kits. Tg (flil: eGFP) zebrafish were utilized to observe vascular cholesterol accumulation and Tg (mpx: eGFP) zebrafish to visualize and quantify neutrophil inflammation. The hepatic lipid deposition and hepatic histopathology were analyzed by Oil red O staining and H&E staining, respectively. Finally, the underlying mechanism of EM were investigated using real-time quantitative PCR (RT-qPCR) analysis to assess the gene levels of adenosine monophosphate-activated protein kinase alpha (AMPKα), sterol regulatory element binding protein 2 (SREBP-2), proprotein convertase subtilisin kexin 9 (PCSK9), low-density lipoprotein receptor (LDLR), 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR), adenosine triphosphate binding cassette transporter A1 (ABCA1) and adenosine triphosphate binding cassette transporter G1 (ABCG1).ResultsOur data indicated that EM reduced obesity of zebrafish as evidenced by the decrease in body weight, body length and BMI. EM significantly reduced TC, TG, and LDL-C, and increased HDL-C contents. Moreover, it displayed a prominent inhibitory effect on blood cholesterol accumulation, hepatic lipid accumulation, and neutrophil inflammation in vascular site. Additionally, EM improved the liver function through decreasing ALT and AST levels of zebrafish with HCD-induced hepatosteatosis. Further investigation showed that EM treatment attenuated lipid accumulation via upregulating the expression of AMPKα, LDLR, ABCA1 and ABCG1, and downregulating the expression of SREBP-2, PCSK9 and HMGCR.ConclusionTo conclude, EM alleviated lipid metabolism disorder symptoms caused by HCD via modulating AMPK/SREBP-2/PCSK9/LDLR pathway in larvae, suggesting that EM may be developed into hypolipidmic agent for treating lipid metabolism related diseases.

Abstract 566: MicroRNA-146a Deficiency Prevents PCSK9 Gain-of-Function Mutation-induced Hypercholesterolemia in Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Shayan Mohammadmoradi ◽  
Aida Javidan ◽  
Weihua Jiang ◽  
Jessica Moorleghen ◽  
Venkateswaran Subramanian
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Western Diet ◽  
Size Exclusion ◽  
Gel Chromatography ◽  
Low Density ◽  
Distribution Analysis ◽  
Gain Of Function ◽  
Ldl Particles

Background and Objective: Mimetic mediated activation of microRNA 146a (miR-146a) reduces atherosclerosis via suppression of nuclear factor-κB-driven inflammation in mice. The purpose of this study was to determine whether miR-146a influences plasma cholesterol in hypercholesterolemic mice. Methods and Results: To induce hypercholesterolemia, female C57BL/6 miR-146a WT (n=8) and miR-146a KO (n=8) mice were injected intraperitoneally with an adeno-associated viral vector (AAV) expressing the proprotein convertase subtilisin/kexin type 9 (PSCK9 D377Y) gain-of-function mutant at a dose of 3 x 10 10 genomic copies/mouse. After infection, mice were fed a Western diet (21% wt/wt milk fat; 0.15% wt/wt cholesterol) for sixteen weeks, and plasma PCSK9 and total cholesterol concentrations were monitored monthly using an enzymatic assay. Plasma PCSK9 concentrations were profoundly increased 4 weeks post injection (Baseline: WT - 179 ± 12 vs KO - 207 ± 12; Week 4: WT - 1700 ± 148 vs KO - 2689 ± 305 ng/ml) and remained significantly high during 16 weeks (WT - 882 ± 142 vs KO - 718 ± 109 ng/ml; p<0.05 vs baseline) of Western diet feeding. Consistent with increased plasma PCSK9 concentrations, plasma cholesterol concentrations were increased in both groups of mice. Interestingly, miR-146a KO group mice showed less significant increase in plasma cholesterol compared to WT group (Baseline: WT - 88 ± 3 vs KO - 83 ± 3; Week 4: WT - 328 ± 25 vs KO - 195 ± 18 mg/dl) irrespective of the comparable plasma PCSK9 concentrations. Also, lipoprotein distribution analysis with size exclusion gel chromatography revealed that miR-146a KO mice showed a strong reduction in high density lipoprotein (HDL) particles while very low density lipoprotein (VLDL) and low density lipoprotein (LDL) particles were not affected. Conclusion: Our findings suggests that miR146a plays a critical role in the regulation of HDL particles in PCSK9 gain-of-function mutant-induced hypercholesterolemia in mice. Future studies will identify gene targets influenced by miR-146a in regulating HDL-cholesterol in hypercholesterolemic mice.

Plasma lipoprotein profiles of normocholesterolemic and hypercholesterolemic homozygotes for apolipoprotein E2(Arg158-->Cys) compared

1994 ◽  
Vol 40 (8) ◽  
pp. 1559-1566 ◽  
Author(s):  
S P Zhao ◽  
A H Smelt ◽  
A M Van den Maagdenberg ◽  
A Van Tol ◽  
T F Vroom ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Plasma Cholesteryl Ester ◽  
Familial Dysbetalipoproteinemia ◽  
Lipoprotein Profiles

Abstract We compared plasma lipoprotein profiles of 15 individuals with normocholesterolemic (plasma cholesterol 4.81 +/- 0.90 mmol/L) familial dysbetalipoproteinemia (NFD) and 15 patients with hypercholesterolemic (plasma cholesterol 10.61 +/- 2.32 mmol/L) familial dysbetalipoproteinemia (HFD), matched for age and sex. All subjects were homozygous for apoE2(Arg158--&gt;Cys). Compared with 15 normolipidemic controls (plasma cholesterol 5.47 +/- 0.92 mmol/L), subjects with NFD and HFD had greater cholesterol concentrations of large very-low-density lipoprotein (VLDL1), small VLDL (VLDL2), and intermediate-density lipoprotein, each of which was correlated to their plasma total cholesterol concentration. VLDL1 and VLDL2 subfractions were enriched in cholesteryl ester, and plasma cholesteryl ester transfer protein activities were increased in both NFD and HFD; however, absolute changes were larger in HFD than in NFD. Concentrations of low-density lipoprotein cholesterol were lower in HFD (1.89 +/- 0.48 mmol/L) and NFD (1.56 +/- 0.36 mmol/L) than in normolipidemic controls (3.35 +/- 0.73 mmol/L). We conclude that all subjects homozygous for apoE2(Arg158--&gt;Cys) show features of dysbetalipoproteinemia.

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