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#ETGA-200 EnzyChrom™ Triglyceride Assay Kit
Product name : EnzyChrom™ Triglyceride Assay Kit
Catalog number : ETGA-200
Quantity: 200 Tests
Supplier name : Bioassays
Data sheet: Ask more or other datasheet now !
More Details about
For quantitative determination of triglyceride and evaluation of drug effects on triglyceride metabolism.
Samples: serum, plasma etc.
Procedure: 30 min.
Size: 200 tests.
Detection limit: 0.01 mmol/L (0.88 mg/dL).
TRIGLYCERIDE, also known as TRIACYLTRIGLYCERIDE or TRIACYLGLYCERIDE,
is the main constituent in vegetable oil and animal fats.
Triglycerides play an important role as energy sources and transporters
of dietary fat. In the human body, high levels of triglycerides in the
bloodstream have been linked to atherosclerosis, heart disease and
pancreatitis. Simple, direct and automation-ready procedures for
measuring triglyceride concentrations find wide applications in research
and drug discovery. BioAssay Systems' triglyceride assay uses a single
Working Reagent that combines triglyceride hydrolysis and glycerol
determination in one step, in which a dye reagent is oxidized to form a
colored product. The color intensity at 570nm is directly proportional to
triglyceride concentration in the sample.
Sensitive and accurate. Use as little as 10 μL samples. Linear detection
range 0.01 mmol/L to 1.0 mmol/L (0.88 mg/dL to 88.5 mg/dL) triglyceride.
Simple and convenient. The procedure involves addition of a single
working reagent and incubation for 30 min at room temperature,
compatible for HTS assays.
Improved reagent stability. The optimized formulation has greatly
enhanced the reagent and signal stability.
Direct Assays: triglyceride in biological samples (e.g. serum and
Drug Discovery/Pharmacology: effects of drugs on triglyceride
Assay Buffer: 24 mL ATP: 250 μL Dye Reagent: 220 μL
Enzyme Mix: 500 μL Lipase: 1000 μL
Standard: 100 μL (equivalent to 100 mmol/L Triglyceride)
Storage conditions. The kit is shipped on ice. Store Assay Buffer at 4°C
and other reagents at -20°C. Shelf life of 12 months after receipt.
Precautions: reagents are for research use only. Normal precautions for
laboratory reagents should be exercised while using the reagents.
Please refer to Material Safety Data Sheet for detailed information.
Sample Type: serum
References: Tam J et al (2010). Peripheral CB1 cannabinoid receptor blockade improves cardiometabolic risk in mouse models of obesity. J Clin Invest. 120(8):2953-66.
Pubmed ID: 20664173
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20664173
Abstract: Obesity and its metabolic consequences are a major public health concern worldwide. Obesity is associated with overactivity of the endocannabinoid system, which is involved in the regulation of appetite, lipogenesis, and insulin resistance. Cannabinoid-1 receptor (CB1R) antagonists reduce body weight and improve cardiometabolic abnormalities in experimental and human obesity, but their therapeutic potential is limited by neuropsychiatric side effects. Here we have demonstrated that a CB1R neutral antagonist largely restricted to the periphery does not affect behavioral responses mediated by CB1R in the brains of mice with genetic or diet-induced obesity, but it does cause weight-independent improvements in glucose homeostasis, fatty liver, and plasma lipid profile. These effects were due to blockade of CB1R in peripheral tissues, including the liver, as verified through the use of CB1R-deficient mice with or without transgenic expression of CB1R in the liver. These results suggest that targeting peripheral CB1R has therapeutic potential for alleviating cardiometabolic risk in obese patients.
- J Clin Invest. 2010 Aug 2;120(8):2646-8.
PMID: 20664173 [PubMed - indexed for MEDLINE] PMCID: PMC2912197
References: Bytautiene, E et al (2011). Prepregnancy obesity and sFlt1-induced preeclampsia in mice: developmental programming model of metabolic syndrome. Am J Obstet Gynecol 204(5):398 e1-8.
Pubmed ID: 21444063
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21444063
We sought to establish a model of fetal programming of metabolic syndrome by exposure to soluble fms-like tyrosine kinase-1 (sFlt1)-induced preeclampsia (PE) and preexisting maternal obesity (MO).
CD-1 female mice were placed on either standard or high-fat diet for 3 months. On day 8 of pregnancy, mice were injected with either adenovirus-carrying sFlt1 or adenovirus-carrying murine immunoglobulin G2α Fc fragment. Offspring were studied at 6 months of age.
Exposure to MO with/without PE resulted in significant increase in progeny's weight and adiposity. Blood pressure in males was significantly increased due to MO with PE. Metabolic blood analytes were affected in males and females exposed to only PE or MO with/without PE; inflammatory-in females exposed to MO with/without PE and males born to MO with PE; atherosclerotic-in females exposed to MO.
Exposure to maternal prepregnancy obesity and sFlt1-induced preeclampsia alter the offspring's blood pressure, metabolic, inflammatory, and atherosclerotic profiles later in life.
Copyright © 2011 Mosby, Inc. All rights reserved.
PMID: 21444063 [PubMed - in process]
Sample Type: primary hepatocyte
References: Kim HS et al (2010). Hepatic-specific disruption of SIRT6 in mice results in fatty liver formation due to enhanced glycolysis and triglyceride synthesis. Cell Metab. 12(3):224-36
Pubmed ID: 20816089
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20816089
Abstract: Under various conditions, mammals have the ability to maintain serum glucose concentration within a narrow range. SIRT1 plays an important role in regulating gluconeogenesis and fat metabolism; however, the underlying mechanisms remain elusive. Here, we show that SIRT1 forms a complex with FOXO3a and NRF1 on the SIRT6 promoter and positively regulates expression of SIRT6, which, in turn, negatively regulates glycolysis, triglyceride synthesis, and fat metabolism by deacetylating histone H3 lysine 9 in the promoter of many genes involved in these processes. Liver-specific deletion of SIRT6 in mice causes profound alterations in gene expression, leading to increased glycolysis, triglyceride synthesis, reduced beta oxidation, and fatty liver formation. Human fatty liver samples exhibited significantly lower levels of SIRT6 than did normal controls. Thus, SIRT6 plays a critical role in fat metabolism and may serve as a therapeutic target for treating fatty liver disease, the most common cause of liver dysfunction in humans.
2010 Elsevier Inc. All rights reserved.
PMID: 20816089 [PubMed - indexed for MEDLINE] PMCID: PMC2935915
Sample Type: blood
References: Tucci, S et al (2010). Medium-chain triglycerides impair lipid metabolism and induce hepatic steatosis in very long-chain acyl-CoA dehydrogenase (VLCAD)-deficient mice. Mol. Gen. Met. 101(1): 40-47
Pubmed ID: 20580297
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20580297
Abstract: A medium-chain-triglyceride (MCT)-based diet is mainstay of treatment in very-long-chain acyl-CoA dehydrogenase deficiency (VLCADD), a long-chain fatty acid beta-oxidation defect. Beneficial effects have been reported with an MCT-bolus prior to exercise. Little is known about the impact of a long-term MCT diet on hepatic lipid metabolism. Here we investigate the effects of MCT-supplementation on liver and blood lipids in the murine model of VLCADD. Wild-type (WT) and VLCAD-knock-out (KO) mice were fed (1) a long-chain triglyceride (LCT)-diet over 5weeks, (2) an MCT diet over 5 weeks and (3) an LCT diet plus MCT-bolus. Blood and liver lipid content were determined. Expression of genes regulating lipogenesis was analyzed by RT-PCR. Under the LCT diet, VLCAD-KO mice accumulated significantly higher blood cholesterol concentrations compared to WT mice. The MCT-diet induced severe hepatic steatosis, significantly higher serum free fatty acids and impaired hepatic lipid mobilization in VLCAD-KO mice. Expression at mRNA level of hepatic lipogenic genes was up-regulated. The long-term MCT diet stimulates lipogenesis and impairs hepatic lipid metabolism in VLCAD-KO mice. These results suggest a critical reconsideration of a long-term MCT-modified diet in human VLCADD. In contrast, MCT in situations of increased energy demand appears to be a safer treatment alternative.
PMID: 20580297 [PubMed - indexed for MEDLINE]
Sample Type: cellular fractions
Species: mouse, human
References: Guo H et al (2011). Anthocyanin inhibits high glucose-induced hepatic mtGPAT1 activation and prevents fatty acid synthesis through PKCζ. J Lipid Res. 52(5):908-22.
Pubmed ID: 21343633
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21343633
Abstract: Mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 (mtGPAT1) controls the first step of triacylglycerol (TAG) synthesis and is critical to the understanding of chronic metabolic disorders such as primary nonalcoholic fatty liver disease (NAFLD). Anthocyanin, a large group of polyphenols, was negatively correlated with hepatic lipid accumulation, but its impact on mtGPAT1 activity and NAFLD has yet to be determined. Hepatoma cell lines and KKAy mice were used to investigate the impact of anthocyanin on high glucose-induced mtGPAT1 activation and hepatic steatosis. Treatment with anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g) reduced high glucose-induced GPAT1 activity through the prevention of mtGPAT1 translocation from the endoplasmic reticulum to the outer mitochondrial membrane (OMM), thereby suppressing intracellular de novo lipid synthesis. Cy-3-g treatment also increased protein kinase C ζ phosphorylation and membrane translocation in order to phosphorylate the mtF0F1-ATPase β-subunit, reducing its enzymatic activity and thus inhibiting mtGPAT1 activation. In vivo studies further showed that Cy-3-g treatment significantly decreases hepatic mtGPAT1 activity and its presence in OMM isolated from livers, thus ameliorating hepatic steatosis in diabetic KKAy mice. Our findings reveal a novel mechanism by which anthocyanin regulates lipogenesis and thereby inhibits hepatic steatosis, suggesting its potential therapeutic application in diabetes and related steatotic liver diseases.
PMID: 21343633 [PubMed - indexed for MEDLINE] PMCID: PMC3073470 [Available on 2012/5/1]
Sample Type: lipid droplets
Species: cells, bovine
References: Orban T et al (2011). Retinyl ester storage particles (retinosomes) from the retinal pigmented epithelium resemble lipid droplets in other tissues. J Biol Chem. 286(19):17248-58.
Pubmed ID: 21454509
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21454509
Abstract: Levels of many hydrophobic cellular substances are tightly regulated because of their potential cytotoxicity. These compounds tend to self-aggregate in cytoplasmic storage depots termed lipid droplets/bodies that have well defined structures that contain additional components, including cholesterol and various proteins. Hydrophobic substances in these structures become mobilized in a specific and regulated manner as dictated by cellular requirements. Retinal pigmented epithelial cells in the eye produce retinyl ester-containing lipid droplets named retinosomes. These esters are mobilized to replenish the visual chromophore, 11-cis-retinal, and their storage ensures proper visual function despite fluctuations in dietary vitamin A intake. But it remains unclear whether retinosomes are structures specific to the eye or similar to lipid droplets in other organs/tissues that contain substances other than retinyl esters. Thus, we initially investigated the production of these lipid droplets in experimental cell lines expressing lecithin:retinol acyltransferase, a key enzyme involved in formation of retinyl ester-containing retinosomes from all-trans-retinol. We found that retinosomes and oleate-derived lipid droplets form and co-localize concomitantly, indicating their intrinsic structural similarities. Next, we isolated native retinosomes from bovine retinal pigmented epithelium and found that their protein and hydrophobic small molecular constituents were similar to those of lipid droplets reported for other experimental cell lines and tissues. These unexpected findings suggest a common mechanism for lipid droplet formation that exhibits broad chemical specificity for the hydrophobic substances being stored.
PMID: 21454509 [PubMed - indexed for MEDLINE] PMCID: PMC3089567 [Available on 2012/5/13]
Sample Type: blood
References: Lee, SM et al (2008).GCG-rich tea catechins are effective in lowering cholesterol and triglyceride concentrations in hyperlipidemic rats. Lipids 43(5): 419-429.
Pubmed ID: 18365267
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=18365267
Abstract: The (-)-gallocatechin gallate (GCG) concentration in some tea beverages can account for as much as 50% of the total catechins, as a result of sterilization. The present study aims to examine the effects of GCG-rich tea catechins on hyperlipidemic rats and the mechanisms associated with regulating cholesterol metabolism in the liver. By performing heat epimerization of (-)-epigallocatechin gallate (EGCG), we manufactured a mixture of catechins that had a GCG content of approximately 50% (w/w). In sucrose-rich diet-induced hyperlipidemic rats, the GCG-rich tea catechins exhibited strong activity in reducing plasma cholesterol and triglyceride concentrations. Furthermore, the hepatic cholesterol and triglyceride concentrations that had increased as a result of the sucrose-rich diet were reduced due to GCG-rich tea catechins consumption. In order to investigate the hyperlipidemic mechanism of GCG-rich tea catechins, we examined the hepatic expressions of LDL receptor and HMG-CoA reductase in hyperlipidemic rats. We further evaluated the action of purified GCG on LDL receptor activity, which is a key contributor to the regulation of cholesterol concentrations. We found that purified GCG increased LDL receptor protein level and activity to a greater extent than EGCG. In conclusion, our study indicates that GCG-rich tea catechins in tea beverages may be effective in preventing hyperlipidemia by lowering plasma and hepatic cholesterol concentrations.
PMID: 18365267 [PubMed - indexed for MEDLINE]
Sample Type: plasma
References: Oh TW et al (2010). Semipurified fractions from the submerged-culture broth of Agaricus blazei Murill reduce blood glucose levels in streptozotocin-induced diabetic rats. J Agric Food Chem. 58(7):4113-9.
Pubmed ID: 20196600
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20196600
Abstract: Hypoglycemic action of semipurified fractions from hot-water extracts of the submerged-culture broth of Agaricus blazei Murill was examined in streptozotocin (60 mg/kg, intraperitoneal)-induced diabetic male Sprague-Dawley rats, relative to the diabetes drug metformin. The hot-water extract, treated with ethanol to remove beta-glucans and glycoproteins, was freeze-dried, and fractionated into hexane, chloroform, ethyl acetate (EA), and butanol fractions. The EA fraction (EAF; 200 mg/kg body weight) reduced (p < 0.05) the blood glucose level in the oral glucose tolerance test, relative to the other fractions and control. In a 14 day-treatment study, diabetic rats treated with the EAF displayed a suppressed blood glucose level and elevated plasma insulin and glucose transport-4 proteins; the reactions occurred in a dose-dependent manner (200 and 400 mg/kg body weight) compared to those in control animals. The EAF reduced the levels of triglyceride and cholesterol in plasma, the activity of glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase in blood, and the content of thiobarbituric acid reactive substance in the liver and kidney. The hypoglycemic efficacy of the EAF (400 mg/kg body weight) was similar to that of metformin (500 mg/kg body weight). The EAF contained substantial amounts of isoflavonoids including genistein, genistin, daidzein, and daidzin, which could have contributed to the fraction's hypoglycemic action. These results indicate that the hot-water extract of the submerged-culture broth of Agaricus blazei contains an EAF having potent hypoglycemic action, which could be useful in the treatment of diabetes mellitus.
PMID: 20196600 [PubMed - indexed for MEDLINE]
Sample Type: serum
References: Uddin MJ et al (2011). Detection of quantitative trait loci affecting serum cholesterol, LDL, HDL, and triglyceride in pigs. BMC Genet.12:62. PubMed PMID: 21752294
Pubmed ID: 21752294
Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21752294
Serum lipids are associated with many serious cardiovascular diseases and obesity problems. Many quantitative trait loci (QTL) have been reported in the pig mostly for performance traits but very few for the serum lipid traits. In contrast, remarkable numbers of QTL are mapped for serum lipids in humans and mice. Therefore, the objective of this research was to investigate the chromosomal regions influencing the serum level of the total cholesterol (CT), triglyceride (TG), high density protein cholesterol (HDL) and low density protein cholesterol (LDL) in pigs. For this purpose, a total of 330 animals from a Duroc × Pietrain F2 resource population were phenotyped for serum lipids using ELISA and were genotyped by using 122 microsatellite markers covering all porcine autosomes for QTL study in QTL Express. Blood sampling was performed at approximately 175 days before slaughter of the pig.
Most of the traits were correlated with each other and were influenced by average daily gain, slaughter date and age. A total of 18 QTL including three QTL with imprinting effect were identified on 11 different porcine autosomes. Most of the QTL reached to 5% chromosome-wide (CW) level significance including a QTL at 5% experiment-wide (GW) and a QTL at 1% GW level significance. Of these QTL four were identified for both the CT and LDL and two QTL were identified for both the TG and LDL. Moreover, three chromosomal regions were detected for the HDL/LDL ratio in this study. One QTL for HDL on SSC2 and two QTL for TG on SSC11 and 17 were detected with imprinting effect. The highly significant QTL (1% GW) was detected for LDL at 82 cM on SSC1, whereas significant QTL (5% GW) was identified for HDL/LDL on SSC1 at 87 cM. Chromosomal regions with pleiotropic effects were detected for correlated traits on SSC1, 7 and 12. Most of the QTL identified for serum lipid traits correspond with the previously reported QTL for similar traits in other mammals. Two novel QTL on SSC16 for HDL and HDL/LDL ratio and an imprinted QTL on SSS17 for TG were detected in the pig for the first time.
The newly identified QTL are potentially involved in lipid metabolism. The results of this work shed new light on the genetic background of serum lipid concentrations and these findings will be helpful to identify candidate genes in these QTL regions related to lipid metabolism and serum lipid concentrations in pigs.
PMID: 21752294 [PubMed - in process] PMCID: PMC3146427
Sample Type: plasma
Species: horseshoe crab
References: Hu, M et al (2010). Effect of prolonged starvation on body weight and blood-chemistry in two horseshoe crab species: Tachypleus tridentatus and Carcinoscorpius rotundicauda (Chelicerata: Xiphosura). J. Exp. Marine Biol.
Pubmed ID: N/A
Pubmed link: N/A
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