scholarly journals Effect of fasting on lipid metabolism and oxidative stability in fattening chicken fed a diet supplemented with organic selenium

2012 ◽  
Vol 55 (5) ◽  
pp. 485-495
Author(s):  
B. Beer-Ljubić ◽  
J. Aladrović ◽  
S. Milinković-Tur ◽  
M. Lazarus ◽  
I. Pušić
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Standard Diet ◽  
Low Density ◽  
Tissue Samples ◽  
Organic Selenium ◽  
Fattening Period

Abstract. The aim of the study was to assess the effect of organic selenium dietary supplementation on serum and tissue lipid composition after fattening period and after 48 h fasting in fattening chicken. The study was performed in the Ross hybrid line chicken divided into two groups: control group fed standard diet and Sel Plex group fed standard diet supplemented with 0.3 ppm organic selenium. Blood, liver, intestine and adipose tissue samples were taken upon fattening completion and after 48 h fasting. Total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triacylglycerol and lipoprotein concentrations were determined in serum, whereas total and free cholesterol, triacylglycerol, lipid peroxide and selenium concentrations and glutathione peroxidase activity (GSH-Px) were determined in tissue samples. During fattening period, the correlation of organic selenium with lipid metabolism manifested as decreased concentrations of serum triacylglycerols and very-low-density lipoprotein (VLDL) (P<0.05), liver triacylglycerols (P<0.05), adipose tissue cholesterol (P<0.05) and small intestine cholesterol (P<0.05), and reduced lipid peroxidation (P<0.05). Upon chicken exposure to 48 h fasting, organic selenium supplementation resulted in increased free cholesterol concentration in adipose tissue (P<0.05), GSH-Px activity in the liver (P<0.05), and selenium (P<0.05) accumulation in the liver.

scholarly journals Cold Exposure Partially Corrects Disturbances in Lipid Metabolism in a Male Mouse Model of Glucocorticoid Excess

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4115-4128 ◽  
Author(s):  
Johanna C. van den Beukel ◽  
Mariëtte R. Boon ◽  
Jacobie Steenbergen ◽  
Patrick C. N. Rensen ◽  
Onno C. Meijer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
White Adipose Tissue ◽  
Cold Exposure ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Bat Activity ◽  
Corticosterone Treatment

High glucocorticoid concentrations are accompanied by metabolic side effects such as high plasma triglyceride (TG) concentrations. Liver, brown adipose tissue (BAT) and white adipose tissue are important regulators of plasma TG. Exposure to 4°C reduces plasma TG concentrations, and we therefore aimed to study the interaction between glucocorticoid excess and 24 hours of exposure to 4°C on lipid metabolism. For this, mice were implanted with 50-mg corticosterone or control pellets and housed for 24 hours at 23°C or 4°C 1 week later, after which various aspects of TG metabolism in liver, BAT, and white adipose tissue were studied. Corticosterone treatment resulted in a 3.8-fold increase of plasma TG concentrations. Increased TG was normalized by cold exposure, an effect still present 24 hours after cold exposure. Corticosterone treatment increased hepatic TG content by 3.5-fold and provoked secretion of large, TG-rich very low density lipoprotein particles. Cold exposure reduced very low density lipoprotein-TG secretion by approximately 50%. Corticosterone strongly decreased BAT activity: BAT weight increased by 3.5-fold, whereas uncoupling protein 1 (Ucp1) mRNA expression and Ucp1 protein content of BAT were reduced by 75% and 60%, respectively. Cold exposure partially normalized these parameters of BAT activity. The uptake of TG by BAT was not affected by corticosterone treatment but was increased 4.5-fold upon cold exposure. In conclusion, cold exposure normalizes corticosterone-induced hypertriglyceridemia, at least partly via activating BAT.

scholarly journals Morphological characterization of the cholesteryl ester cycle in cultured mouse macrophage foam cells.

1983 ◽  
Vol 97 (4) ◽  
pp. 1156-1168 ◽  
Author(s):  
D J McGookey ◽  
R G Anderson
Keyword(s):  
Cholesteryl Ester ◽  
Lipase Activity ◽  
Lipid Droplets ◽  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
The Body ◽  
Cyclic Process ◽  
Low Density ◽  
Cholesteryl Esters

Mouse peritoneal macrophages can be induced to accumulate cholesteryl esters by incubating them in the presence of acetylated low density lipoprotein. The cholesteryl esters are sequestered in neutral lipid droplets that remain in the cell even when the acetylated low density lipoprotein is removed from the culture media. Previous biochemical studies have determined that the cholesterol component of cholesteryl ester droplets constantly turns over with a half time of 24 h by a cyclic process of de-esterification and re-esterification. We have used morphologic techniques to determine the spatial relationship of cholesteryl ester, free cholesterol, and lipase activity during normal turnover and when turnover is disrupted. Lipid droplets were surrounded by numerous 7.5-10.0-nm filaments; moreover, at focal sites on the margin of each droplet there were whorles of concentrically arranged membrane that penetrated the matrix. Histochemically detectable lipase activity was associated with these stacks of membrane. Using filipin as a light and electron microscopic probe for free cholesterol, we determined that a pool of free cholesterol was associated with each lipid droplet. Following incubation in the presence of the exogenous cholesterol acceptor, high density lipoprotein, the cholesteryl ester droplets disappeared and were replaced with lipid droplets of a different lipid composition. Inhibition of cholesterol esterification caused cholesteryl ester droplets to disappear and free cholesterol to accumulate in numerous myelin-like structures in the body of the cell.

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.

scholarly journals Pro-atherogenic lipid profile in pulmonary tuberculosis patients with concurrent insulin resistance

2021 ◽  
Vol 8 (2) ◽  
pp. 111-114
Author(s):  
Olga Shvets ◽  
Olga Shevchenko ◽  
Zoriana Piskur ◽  
Hanna Stepanenko ◽  
Olha Pohorielova
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Pulmonary Tuberculosis ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Tuberculosis Patients ◽  
Group 2 ◽  
Group 1

Background. The problem of studying lipid metabolism in patients with tuberculosis is of interest to scientists around the world. The purpose of the study - to investigate lipid profile in pulmonary tuberculosis patients with concurrent insulin resistance. Materials and methods. Forty-one patients with pulmonary tuberculosis were examined. Insulin resistance index (HOMA-IR), total cholesterol level (TC), triglycerides (TG) level, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and atherogenic index (AI) were measured. Results. Group 1 - 26 patients with tuberculosis and insulin resistance (HOMA-IR ˃ 2.7); Group 2 – 15 patients with tuberculosis without insulin resistance (HOMA-IR ˂ 2.7). Group 1 patients had severe course of TB with fever, severe fatigue and weakness, profuse sweating, weight loss, cough and shortness of breath. Median TC indices differed at significant level (p = 0.012): group 1 - 4.82 mmol/l, group 2 - 4.25 mmol/l. TG level was higher in group 1 patients - 1.32 mmol/l than in group 2 patients - 1.28 mmol/l. LDL cholesterol values were higher in group 1 patients - 3.2 mmol/l vs 2.5 mmol/l in group 2. The AI was higher in group1 (p = 0.005): 3.9 units against 2.8 units in group 2 patients. Conclusions. Insulin resistance in pulmonary tuberculosis patients was associated with severe course of the disease, severe clinical manifestations and impaired external respiration. Pro-atherogenic disorders of lipid metabolism in pulmonary tuberculosis patients with concurrent insulin resistance can be considered as the degree of endogenous intoxication.

Carotenoid and retinol concentrations in serum, adipose tissue and liver and carotenoid transport in sheep, goats and cattle

1992 ◽  
Vol 43 (8) ◽  
pp. 1809 ◽  
Author(s):  
A Yang ◽  
TW Larsen ◽  
RK Tume
Keyword(s):  
Adipose Tissue ◽  
Objective Assessment ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Adipose Tissues ◽  
Sheep And Goats ◽  
Different Levels ◽  
Retinol Concentration

Carotenoid and retinol concentrations were determined in various tissues of sheep, goats and cattle, ruminants known to have widely different levels of pigmentation of their adipose tissues. An objective assessment of fat colour confirmed the whiteness of sheep and goat fat compared with that of cattle. No G-carotene was detected in the serum or fat of sheep and goats, but it was the predominant carotenoid present in the serum and fat of cattle. The major pigment present in serum and fat of sheep and goat was lutein, although its concentration was only 5-10% of that found in cattle. G-carotene was present in the liver of all three species with the highest concentration in cattle. Although lutein was the only carotenoid found in the serum and fat of sheep and goats, it could not be detected in their livers. The concentrations of retinol in serum and fat were similar for each species, but the liver of sheep had about three times the retinol concentration of the liver of goats and cattle. The transport of carotenoids in plasma was investigated. In sheep and goats, the pigments were associated mainly with very low density lipoprotein (VLDL) and low density lipoprotein (LDL), whereas in cattle, high density lipoprotein (HDL) was the major lipoprotein fraction involved.

scholarly journals ChREBP-Mediated Regulation of Lipid Metabolism: Involvement of the Gut Microbiota, Liver, and Adipose Tissue

2020 ◽  
Vol 11 ◽  
Author(s):  
Katsumi Iizuka ◽  
Ken Takao ◽  
Daisuke Yabe
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Acid Synthesis ◽  
Whole Body ◽  
Acetyl Coa ◽  
Alcoholic Fatty Liver

Carbohydrate response element-binding protein (ChREBP) plays an important role in the development of type 2 diabetes, dyslipidemia, and non-alcoholic fatty liver disease, as well as tumorigenesis. ChREBP is highly expressed in lipogenic organs, such as liver, intestine, and adipose tissue, in which it regulates the production of acetyl CoA from glucose by inducing Pklr and Acyl expression. It has recently been demonstrated that ChREBP plays a role in the conversion of gut microbiota-derived acetate to acetyl CoA by activating its target gene, Acss2, in the liver. ChREBP regulates fatty acid synthesis, elongation, and desaturation by inducing Acc1 and Fasn, elongation of long-chain fatty acids family member 6 (encoded by Elovl6), and Scd1 expression, respectively. ChREBP also regulates the formation of very low-density lipoprotein by inducing the expression of Mtp. Furthermore, it plays a crucial role in peripheral lipid metabolism by inducing Fgf21 expression, as well as that of Angptl3 and Angptl8, which are known to reduce peripheral lipoprotein lipase activity. In addition, ChREBP is involved in the production of palmitic-acid-5-hydroxystearic-acid, which increases insulin sensitivity in adipose tissue. Curiously, ChREBP is indirectly involved in fatty acid β-oxidation and subsequent ketogenesis. Thus, ChREBP regulates whole-body lipid metabolism by controlling the transcription of lipogenic enzymes and liver-derived cytokines.

scholarly journals Macrophages Create an Acidic Extracellular Hydrolytic Compartment to Digest Aggregated Lipoproteins

2009 ◽  
Vol 20 (23) ◽  
pp. 4932-4940 ◽  
Author(s):  
Abigail S. Haka ◽  
Inna Grosheva ◽  
Ethan Chiang ◽  
Adina R. Buxbaum ◽  
Barbara A. Baird ◽  
...  
Keyword(s):  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Critical Event ◽  
Low Density ◽  
Acid Hydrolases ◽  
Detailed Understanding ◽  
Physical Features

A critical event in atherogenesis is the interaction of macrophages with subendothelial lipoproteins. Although most studies model this interaction by incubating macrophages with monomeric lipoproteins, macrophages in vivo encounter lipoproteins that are aggregated. The physical features of the lipoproteins require distinctive mechanisms for their uptake. We show that macrophages create an extracellular, acidic, hydrolytic compartment to carry out digestion of aggregated low-density lipoproteins. We demonstrate delivery of lysosomal contents to these specialized compartments and their acidification by vacuolar ATPase, enabling aggregate catabolism by lysosomal acid hydrolases. We observe transient sealing of portions of the compartments, allowing formation of an “extracellular” proton gradient. An increase in free cholesterol is observed in aggregates contained in these compartments. Thus, cholesteryl ester hydrolysis can occur extracellularly in a specialized compartment, a lysosomal synapse, during the interaction of macrophages with aggregated low-density lipoprotein. A detailed understanding of these processes is essential for developing strategies to prevent atherosclerosis.

Very low density lipoprotein and low density lipoprotein isolated from patients with hepatitis C infection induce altered cellular lipid metabolism

2007 ◽  
Vol 79 (3) ◽  
pp. 254-258 ◽  
Author(s):  
Mariarosaria Napolitano ◽  
Alessandro Giuliani ◽  
Tonino Alonzi ◽  
Carmine Mancone ◽  
Gianpiero D'Offizi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatitis C ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Cellular Lipid ◽  
Hepatitis C Infection

Effects of prior moderate exercise on exogenous and endogenous lipid metabolism and plasma factor VII activity

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
Keyword(s):  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Factor Vii ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Moderate Exercise ◽  
Prior Exercise ◽  
Plasma Factor ◽  
Plasma Triacylglycerol

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.

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