Relationships between blood lipids and backfat thickness in growing pigs

1997 ◽  
Vol 1997 ◽  
pp. 62-62
Author(s):  
Teck-Chwen Loh ◽  
Ian J. Lean ◽  
Peter F. Dodds
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Late Pregnancy ◽  
Blood Stream ◽  
Fat Deposition ◽  
Growing Pigs ◽  
Neonatal Pigs ◽  
Piglet Mortality ◽  
Heparin Affinity

Adipose triacylglycerol is mobilised during late pregnancy in humans and rats: the liberated fatty acids are incorporated into very low density lipoprotein (VLDL) by the liver and secreted into the blood stream. Similar hypertriacylglycerolaemia was also found in late-pregnant sows (Wright et al, 1995). It has been shown that VLDL can be separated into two subfractions by heparin-affinity chromatography. The proportion of VLDL-subfraction 2 (higher affinity for heparin) from pregnant sows was related to piglet mortality. The purpose of this investigation was to extend the study to seek relationships between fat deposition and plasma lipids, VLDL lipids and VLDL-subfractions in growing pigs. As most of the fat deposited in the adipose tissue of neonatal pigs is derived from the plasma lipoprotein, it seemed likely that the rate of fat deposition would be influenced by the concentration and nature of available lipoprotein in the plasma.

Dihomo-γ-Linolenic Acid in Patients with Atherosclerosis: Effects on Platelet Aggregation, Plasma Lipids and Low-Density Lipoprotein-Induced Inhibition of Prostacyclin Generation

1984 ◽  
Vol 51 (02) ◽  
pp. 186-188 ◽  
Author(s):  
A Szczeklik ◽  
R J Gryglewski ◽  
K Sladek ◽  
E Kostka-Trąbka ◽  
A Żmuda
Keyword(s):  
Linolenic Acid ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Thromboxane A2 ◽  
Low Density ◽  
Red Cell ◽  
Double Blind ◽  
Daily Dose ◽  
Antithrombotic Effects

SummaryDihomo-γ-linolenic acid (DHLA), a precursor of monoenoic anti-aggregatory prostaglandins (PGE1, PGD2), was administered for 4 weeks in a daily dose of 1.0 g into 33 patients with atherosclerosis on a basis of a double-blind trial. Comparison of treatment and placebo groups revealed elevation of DHLA in red cell lipids in DHLA-treated subjects. No differences, however, between the two groups could be observed in platelet aggregability, thromboxane A2 generation by platelets, serum cholesterol, PGE1 and PGE2 levels, and in inhibitory activity of low-density lipoproteins against prostacyclin synthetizing system in arteries. The dietary supplementation used did not lead to distinct antithrombotic effects.

Abstract P560: Delipid Extracorporeal Lipoprotein Filter System: A New Lipid-Lowering Therapy for Acute Ischemic Stroke Patients

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Yuqiong Jiao ◽  
Ting Ye ◽  
Xiang Han
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Adsorption System ◽  
Stroke Patients ◽  
Safety Parameters

Objectives: The purpose of this study was to illustrate a new low-density lipoprotein cholesterol (LDL-C) adsorption system, Delipid Extracorporeal Lipoprotein filter from Plasma (DELP) system, and evaluate its safety and efficacy in acute ischemic stroke patients. Methods: This is an observational study of 22 acute ischemic stroke patients who underwent DELP treatment from March to August 2019. The DELP system was composed of a plasma filter JX-DELP, a COM.TEC cell separator and Tubing P1R Plasma Treatment Set. Clinical data and laboratory results including plasma lipids and some safety parameters before and after the apheresis were collected and analyzed. Results: The present study included 22 patients (15 males, 7 females, 59.95±13.71 years). The mean LDL-C was significantly reduced from 3.36±0.64 mmol/L to 2.30±0.53 mmol/L (31.5%, p <0.001, n=22) during a single DELP treatment, and from 3.59±0.48 mmol/L to 1.85±0.50 mmol/L (48.2%, p <0.001, n=13) after two apheresis, respectively. No clinically relevant changes were observed in hematologic safety parameters during DELP treatments. Conclusions: We concluded that the new LDL-C adsorption system is a promising method for timely and controllable LDL-C administration in acute ischemic stroke patients in view of its high efficacy, simple operation, and safety.

scholarly journals Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Dietary Fats ◽  
Low Density ◽  
Mrna Levels ◽  
Expression Of Genes ◽  
Coa Reductase

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.

Changes in plasma lipids and low-density lipoprotein peak particle size during and after acute myocardial infarction

2002 ◽  
Vol 89 (4) ◽  
pp. 460-462 ◽  
Author(s):  
Carlo M Barbagallo ◽  
Manfredi Rizzo ◽  
Angelo B Cefalù ◽  
Davide Noto ◽  
Antonio Scimeca ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Particle Size ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density

Effect of aging and obesity on the expression of dyslipidaemia in children from families with familial combined hyperlipidaemia

2006 ◽  
Vol 112 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Ewoud ter Avest ◽  
Allan D. Sniderman ◽  
Sebastian J. H. Bredie ◽  
Albert Wiegman ◽  
Anton F. H. Stalenhoef ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Indirect Evidence ◽  
Low Density ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
And Gender ◽  
Genetically Determined

The aim of the present study was to delineate the mechanism(s) responsible for the increased secretion of VLDL (very-low-density lipoprotein) particles in patients with FCH (familial combined hyperlipidaemia). In 194 young adults (<25 years of age) recruited from families with FCH, we investigated how plasma lipids, (apo)lipoproteins and BMI (body mass index) varied with age. Furthermore, we performed a 5-year follow-up study of clinical and biochemical characteristics of a subset of this population (n=85) stratified by apoB (apolipoprotein B) levels (below or above the 75th percentile adjusted for age and gender). Plasma apoB concentration (r=0.45, P<0.0001), triacylglycerol (triglyceride) concentration (r=0.45, P<0.0001), LDL (low-density lipoprotein) subfraction profile (r=−0.46, P<0.0001) and BMI (r=0.51, P<0.0001) were significantly associated with age. Plasma apoB concentration in the hyperapoB group was already elevated at a young age, whereas other characteristics of FCH, as observed in adults, including triacylglycerol levels >1.5 mmol/l and/or small-dense LDL, were observed only sporadically. After the 5-year follow-up, BMI increased in both groups, and this increase was associated with changes in apoB (r=0.27, P<0.05), triacylglycerol (r=0.30, P<0.01), VLDL cholesterol (r=0.22, P<0.05), VLDL triacylglycerol (r=0.25, P<0.05) and high-density lipoprotein cholesterol (r=−0.27, P<0.05). In conclusion, we have found indirect evidence of a primary, presumably genetically determined, increase in plasma apoB concentration occurring early in life of offspring from families with FCH. However, aging-related post-maturation increases in adipose tissue mass also appear to contribute to an aggravation and/or modulation of this genetically determined apoB overproduction.

Association of osteocalcin, insulin resistance and oxidative stress during noncomplicated pregnancy

2016 ◽  
Vol 40 (4) ◽  
Author(s):  
Marina Pijanović ◽  
Aleksandra Stefanović ◽  
Milica Miljković ◽  
Snežana Marić-Krejović ◽  
Slavica Spasić
Keyword(s):  
Repeated Measures ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Late Pregnancy ◽  
Progressive Increase ◽  
Oxidative Status ◽  
Insulin Resistant ◽  
Uncomplicated Pregnancy ◽  
Lipid Status

AbstractBackground:The aim of this study was to explore longitudinal changes of serum osteocalcin during normal, uncomplicated pregnancy and after delivery, and its correlations with parameters of glucose homeostasis, lipid status, and oxidative status in late pregnancy.Methods:Osteocalcin, glucose, insulin, lipid status parameters, total oxidative status (TOS), and total antioxidant capacity (TAC) were measured in sera of 38 healthy pregnant women. The sera were collected at the midpoint of the 1Results:Repeated measures analysis of variance showed a progressive increase in total cholesterol, triglycerides, and low density lipoprotein (LDL)-cholesterol, with a postpartum decrease. High density lipoprotein (HDL)-cholesterol increased in the 2Conclusions:We observed the changes in pregnancy that may lead towards atherogenic, prooxidant and insulin resistant state, which are possibly counterbalanced by various protective systems, one of which might be osteocalcin.

Longitudinal Genetic Analysis of Plasma Lipids

2006 ◽  
Vol 9 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Rita P. Middelberg ◽  
Nicholas G. Martin ◽  
John B. Whitfield
Keyword(s):  
Environmental Factors ◽  
Measurement Errors ◽  
Genetic Factors ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Study Participant ◽  
Biological Variation ◽  
Long Term Effects

AbstractThe consensus from published studies is that plasma lipids are each influenced by genetic factors, and that this contributes to genetic variation in risk of cardiovascular disease. Heritability estimates for lipids and lipoproteins are in the range .48 to .87, when measured once per study participant. However, this ignores the confounding effects of biological variation measurement error and ageing, and a truer assessment of genetic effects on cardiovascular risk may be obtained from analysis of longitudinal twin or family data. We have analyzed information on plasma high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, and triglycerides, from 415 adult twins who provided blood on two to five occasions over 10 to 17 years. Multivariate modeling of genetic and environmental contributions to variation within and across occasions was used to assess the extent to which genetic and environmental factors have long-term effects on plasma lipids. Results indicated that more than one genetic factor influenced HDL and LDL components of cholesterol, and triglycerides over time in all studies. Nonshared environmental factors did not have significant long-term effects except for HDL. We conclude that when heritability of lipid risk factors is estimated on only one occasion, the existence of biological variation and measurement errors leads to underestimation of the importance of genetic factors as a cause of variation in long-term risk within the population. In addition our data suggest that different genes may affect the risk profile at different ages.

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