Gene Expression Of Metabolizing Enzymes Research Articles

The effect of fibroblast growth factor 15 deficiency on the development of high fat diet induced non-alcoholic steatohepatitis

Non-alcoholic steatohepatitis (NASH) is a form of non-alcoholic fatty liver disease (NAFLD) characterized by steatosis, inflammation, and fibrosis often associated with metabolic syndrome. Fibroblast growth factor 15 (FGF15), an endocrine factor mainly produced in the distal part of small intestine, has emerged to be a critical factor in regulating bile acid homeostasis, energy metabolism, and liver regeneration. We hypothesized that FGF15 alters the development of each of the listed features of NASH. To test this hypothesis, four-week old male Fgf15−/− and their corresponding wild-type (WT) mice were fed either a high fat diet (HFD) or a control chow diet for six months. The results confirmed that HFD feeding for six months in WT mice recapitulated human NASH phenotype, including macrovesicular steatosis, inflammation, and fibrosis. Whereas FGF15 deficiency had no effect on the severity of liver steatosis or inflammation, it was associated with decreased liver fibrosis. Furthermore, FGF15 deficiency resulted in abnormal bile acid homeostasis, increased insulin resistance, increased HFD-induced serum triglycerides, decreased inductions of hepatic cholesterol content by HFD, and altered gene expression of lipid metabolic enzymes. These data suggest that FGF15 improves lipid homeostasis and reduces bile acid synthesis, but promotes fibrosis during the development of NASH.

Mechanisms of transcriptional control of glucose metabolism in hepatocytes

The hepatic tissue plays a key role in the regulation and maintenance of stable blood glucose levels. The liver is the main gluconeogenesis organ of the body and is under constant hormonal control to determine the metabolic activity of hepatocytes. Hormonal signals trigger multiple post-translational regulatory mechanisms that alter the activity of key enzymes of glucose metabolism. A crucial role in the long-term control of glucose production and metabolism is played by pre-translational regulation at the level of gene expression of metabolic enzymes. There is growing evidence that this regulation, which is realised via control of the activity of transcription factors, provides constant adjustment of the body to changing environmental conditions and that its disruption leads to the development of metabolic diseases associated with insulin resistance. Therefore, the study of transcription factors that regulate glucose metabolism in the liver and the search for mechanisms to control them is of great biomedical importance in the context of metabolic disease treatment research.

Impact of high-fat diet on liver genes expression profiles in mice model of nonalcoholic fatty liver disease.

Evidences have shown that NAFLD influences expression of some drug metabolic enzyme genes. This study aims to investigate the role of HFD-induced NAFLD in regulating the transcription of genes, particularly the drug metabolizing genes variation. Transcriptome analysis demonstrated that HFD feeding caused the 150 genes expression to change, most genes associated with lipid metabolism, inflammatory, oxidative stress and oxidoreductase activity up-regulated, whereas most genes involved in nucleic acid metabolism repressed. The genes involved in drug metabolism had 16 down-regulated and 21 up-regulated in NAFLD. The over-4-fold change genes included the down-regulation of Cyp8b1, Cyp7a1, Sult3a1, Sult1e1, Cyp17a1, Cyp3a41a, Gstt3, Cyp51, Cyp2c54 and Cyp4f14, and the up-regulation of Asns, Past1, Cyp2c55, Gstm2, Cyp2e1 and Gstaα1. In conclusion, significant alterations in the expression of drug metabolizing enzymes may affect the clearance of therapeutic drugs, with the potential to result in adverse drug reactions or drug toxicity in nonalcoholic fatty liver disease.

Prenatal corticosterone altered glucocorticoid receptor and glucocorticoid metabolic enzyme gene expression in chicken ovary

Abstract Objective The acute stress response is an adaptive physiological mechanism which allows an organism to respond and survive deleterious stimuli in the surrounding environment. In mammals, prenatal glucocorticoids exposure (GCs) reprograms offspring phenotype and reproductive performance. In the present study, we investigated potential prenatal GC exposure on the glucocorticoid receptor (GR), mineralocorticoid receptor (MR) and GC metabolic genes mRNA expression in the ovary of chickens. Methods We injected low (0.2 μg) and high (1.0 μg) doses of corticosterone (CORT) in ovo before incubation and measured the changes in GCs metabolic enzymes genes in ovarian follicles 1 (F1), F2 and F3 post hatching. Results The high dose CORT treatment significantly ( P P in ovo injection of high dose CORT significantly ( P Conclusions Prenatal CORT exposure modified GR, MR and GC metabolic enzymes gene expression in ovarian follicles, thus it may reprogram reproductive function.

MP62-11 CHARACTERIZATION OF PROSTATE CANCER IN A FUNCTIONAL EUNUCH

You have accessJournal of UrologyProstate Cancer: Basic Research & Pathophysiology I1 Apr 2016MP62-11 CHARACTERIZATION OF PROSTATE CANCER IN A FUNCTIONAL EUNUCH Michael Fiandalo, John Stocking, Elena Pop, John Wilton, Gissou Azabdaftari, and James Mohler Michael FiandaloMichael Fiandalo More articles by this author , John StockingJohn Stocking More articles by this author , Elena PopElena Pop More articles by this author , John WiltonJohn Wilton More articles by this author , Gissou AzabdaftariGissou Azabdaftari More articles by this author , and James MohlerJames Mohler More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.919AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Prostate cancer (CaP) development and growth rely on androgen receptor (AR) and its ligands, testosterone (T) and dihydrotestosterone (DHT). CaP that recurs in spite of castrate levels of circulating T has been shown to contain levels of T and DHT sufficient for AR transactivation that are produced by intratumoral intracrine metabolism. We report a case of CaP that developed in a functional eunuch male, which provided the opportunity to characterize fully serum and prostate tissue androgen levels and gene and protein expression profiles. Patient suffered mumps orchitis at age 13, developed secondary sex characteristics poorly, was married briefly and never fathered a child. T replacement therapy (TRT) was begun to treat hypogonadal symptoms at age 60 when prostate exam was benign, prostate-specific antigen (PSA) was 0.43 ug/dl and PSA doubling time was 3.18 years. TRT was halted and prostate biopsy using transrectal prostate ultrasound (TRUS) revealed a 14.6 g prostate with Gleason grade 4+4=8 adenocarcinoma. Radical prostatectomy revealed Gleason grade 3+4=7 (PT3aN0) CaP that invaded bladder neck but surgical margins were negative. PSA was low detectable 2 years later. METHODS Serum, CaP and benign prostate tissue androgen levels were measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay. The assay measures T, DHT, the adrenal androgens androstenedione (ASD) and dehydroepiandrosterone and the androgen metabolite, androsterone. Androgen metabolism enzyme, AR and AR-regulated gene expression levels were measured using qRT-PCR and immunohistochemistry (IHC) for protein. RESULTS LC-MS/MS showed that T was not measurable in benign prostate or CaP tissues. DHT levels were higher in benign prostate than CaP tissues. Serum T, DHT and ASD levels were at the limit of detection. Androgen metabolism enzyme gene and AR and AR-regulated gene and protein expression levels were lower in CaP than benign tissues. CONCLUSIONS Androgen levels, AR and AR-gene expression levels were lower in CaP than benign prostate tissues, which is similar to what investigators have reported for castration-recurrent CaP. The benign prostate had no T and low ASD levels, which suggest that the benign prostate may have used the primary backdoor androgen metabolism pathway to generate DHT. The benign prostate grew in a castrate microenvironment and may have created a microenvironment conducive for growth of CaP with characteristics of castration-recurrent instead of androgen-stimulated CaP. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e816 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Michael Fiandalo More articles by this author John Stocking More articles by this author Elena Pop More articles by this author John Wilton More articles by this author Gissou Azabdaftari More articles by this author James Mohler More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Trichloroethylene-induced hypersensitivity dermatitis was associated with hepatic metabolic enzyme genes and immune-related genes.

Trichloroethylene (TCE) is one of the common organic solvents that has been widely used in cleaning or degreasing of metal and electronic products. However, hundreds of cases of hypersensitivity dermatitis have occurred after the workers were occupationally exposed to TCE in China over the past decade. The purpose of this study was to investigate mRNA expression of hepatic metabolic enzyme genes, immune-related genes, apoptosis genes and oncogenes in patients with hypersensitivity dermatitis induced by trichloroethylene. 12 typical patients with TCE-induced hypersensitivity dermatitis were investigated as the study cases, peripheral blood samples were taken from patients and control, and real-time fluorescence PCR assay was applied for detection of mRNA expression of hepatic metabolic enzyme genes, immune-related genes, apoptosis genes and oncogenes. It was found that the relative levels of mRNA expression of CYP1A2, CYP2E1, CYP3A4 and CYP2C9 increased by 723%, 318%, 385% and 216%, respectively, when compared with control (p < 0.01 or p < 0.05); Foxp3, GATA3 and CTLA4 mRNA expression increased by 104%, 106% and 253%, respectively, in TCE patients when compared with control (p < 0.01); T-bet expression decreased by 44% when compared with control (p < 0.01); these findings indicate that some immune-related genes and hepatic metabolic enzyme genes might play an important role in the process of trichloroethylene-induced hypersensitivity dermatitis.

Effects of sex and site on amino acid metabolism enzyme gene expression and activity in rat white adipose tissue.

Background and Objectives. White adipose tissue (WAT) shows marked sex- and diet-dependent differences. However, our metabolic knowledge of WAT, especially on amino acid metabolism, is considerably limited. In the present study, we compared the influence of sex on the amino acid metabolism profile of the four main WAT sites, focused on the paths related to ammonium handling and the urea cycle, as a way to estimate the extent of WAT implication on body amino-nitrogen metabolism.Experimental Design. Adult female and male rats were maintained, undisturbed, under standard conditions for one month. After killing them under isoflurane anesthesia. WAT sites were dissected and weighed. Subcutaneous, perigonadal, retroperitoneal and mesenteric WAT were analyzed for amino acid metabolism gene expression and enzyme activities.Results. There was a considerable stability of the urea cycle activities and expressions, irrespective of sex, and with only limited influence of site. Urea cycle was more resilient to change than other site-specialized metabolic pathways. The control of WAT urea cycle was probably related to the provision of arginine/citrulline, as deduced from the enzyme activity profiles. These data support a generalized role of WAT in overall amino-N handling. In contrast, sex markedly affected WAT ammonium-centered amino acid metabolism in a site-related way, with relatively higher emphasis in males’ subcutaneous WAT.Conclusions. We found that WAT has an active amino acid metabolism. Its gene expressions were lower than those of glucose-lipid interactions, but the differences were quantitatively less important than usually reported. The effects of sex on urea cycle enzymes expression and activity were limited, in contrast with the wider variations observed in other metabolic pathways. The results agree with a centralized control of urea cycle operation affecting the adipose organ as a whole.

In utero bisphenol A concentration, metabolism, and global DNA methylation across matched placenta, kidney, and liver in the human fetus

While urine has been an easily accessible and feasible matrix for human biomonitoring, analytical measurements in internal tissues and organs can provide more accurate exposure assessments to understand disease etiology. This is especially important for the endocrine active compound, bisphenol A (BPA), where studies investigating internal doses at sensitive periods of human development are currently lacking. Herein, BPA concentrations, BPA-specific metabolizing enzyme gene expression, and global DNA methylation were characterized across three matched tissues from elective pregnancy terminations of 2nd trimester human fetuses: the placenta, liver, and kidney (N=12 each; N=36 total). Compared to liver (free: 0.54–50.5ngg−1), BPA concentrations were lower in matched placenta (<0.05–25.4ngg−1) and kidney (0.08–11.1ngg−1) specimens. BPA-specific metabolism gene expression of GUSB, UGT2B15, STS, and SULT1A1 differed across each tissue type; however, conjugation and deconjugation expression patterns were similar across the fetus. Average LINE1 and CCGG global methylation were 58.3% and 59.2% in placenta, 79.5% and 66.4% in fetal liver, and 77.9% and 77.0% in fetal kidney, with significant tissue-specific DNA methylation differences in both LINE1 (p-value<0.001) and CCGG content (p-value<0.001). Total BPA concentrations were positively associated with global methylation for the placenta only using the LINE1 assay (p-value: 0.002), suggesting organ-specific biological effects after fetal exposure. Utilizing sensitive human clinical specimens, results are informative for BPA toxicokinetics and toxicodynamics assessment in the developing human fetus.

Effect of nitrite stress on gene expression of antioxidant enzymes, heat shock protein 70, and metabolic enzymes in gill tissue of adult red swamp crayfish, Procambarus clarkii

The effect of acute nitrite stress on gene expression of antioxidant enzymes, Hsp70 and metabolic enzymes in gill tissue of adult Procambarus clarkii (Girard, 1852) was evaluated. A 48 hours nitrite exposure was conducted, using four test concentrations (NO2-N = 1, 2, 3 and 4 mg l−1) plus a control group. Significantly increased mRNA expression was observed for all the antioxidant enzymes. A significant increase of Hsp70 mRNA expression was observed when exposed to 2 mg l−1 nitrite-N at 12 h. An elevation in AST mRNA expression occurred in the 3 mg l−1 nitrite-N group at 12 h. No significant variation was observed for ALT. Elevations in SDH and Na+/K+-ATPase α-subunit mRNA expression were found throughout the experiment. This study shows that gene expression of antioxidant and metabolic enzymes could be helpful in predicting sublethal nitrite toxicity and it will also improve our understanding of the toxicological mechanisms of nitrite on crustacean.

Analysis of gene expression changes, caused by exposure to nitrite, in metabolic and antioxidant enzymes in the red claw crayfish, Cherax quadricarinatus

We evaluated the effect of acute exposure to nitrite on expression of antioxidant and metabolic enzyme genes in gill tissue of advanced juvenile Cherax quadricarinatus. A 48h nitrite exposure was conducted, using four test concentrations (NO2–N=0.5, 1, 1.5 and 2mgL−1) plus a control group. The relative mRNA expression of mitochondrial manganese superoxide dismutase (mMnSOD), cytosolic MnSOD (cMnSOD), extracellular copper/zinc SOD (exCu/ZnSOD), catalase (CAT), glutathione S-transferase (GST), arginine kinase (AK), glutamate dehydrogenase (GDH), mitochondrial malate dehydrogenase (mMDH), Na+/K+-ATPase α-subunit and phosphoenolpyruvate carboxykinase (PEPCK) in gill tissue was measured. Significantly increased mRNA expression was observed for all the antioxidant enzymes after 12 and 24h. After 48h, they all decreased at high nitrite concentrations. The gene expression levels of AK, GDH, mMDH and Na+/K+-ATPase α-subunit showed similar trends as the antioxidant enzymes. Significant depression of gene expression levels of PEPCK occurred throughout the experimental time at high nitrite concentrations. The results indicated that nitrite could induce oxidative and metabolic stress in C. quadricarinatus, in a time dependent manner, which suggests they could be helpful in predicting sublethal nitrite toxicity and useful in environmental monitoring studies.

Effects of temperature acclimation on Pacific bluefin tuna (Thunnus orientalis) cardiac transcriptome

Little is known about the mechanisms underpinning thermal plasticity of vertebrate hearts. Bluefin tuna hearts offer a unique model to investigate processes underlying thermal acclimation. Their hearts, while supporting an endothermic physiology, operate at ambient temperature, and are presented with a thermal challenge when migrating to different thermal regimes. Here, we examined the molecular responses in atrial and ventricular tissues of Pacific bluefin tuna acclimated to 14°C, 20°C, and 25°C. Quantitative PCR studies showed an increase in sarcoplasmic reticulum Ca(2+) ATPase gene expression with cold acclimation and an induction of Na(+)/Ca(2+)-exchanger gene at both cold and warm temperatures. These data provide evidence for thermal plasticity of excitation-contraction coupling gene expression in bluefin tunas and indicate an increased capacity for internal Ca(2+) storage in cardiac myocytes at 14°C. Transcriptomic analysis showed profound changes in cardiac tissues with acclimation. A principal component analysis revealed that temperature effect was greatest on gene expression in warm-acclimated atrium. Overall data showed an increase in cardiac energy metabolism at 14°C, potentially compensating for cold temperature to optimize bluefin tuna performance in colder oceans. In contrast, metabolic enzyme activity and gene expression data suggest a decrease in ATP production at 25°C. Expression of genes involved in protein turnover and molecular chaperones was also decreased at 25°C. Expression of genes involved in oxidative stress response and programmed cell death suggest an increase in oxidative damage and apoptosis at 25°C, particularly in the atrium. These findings provide insights into molecular processes that may characterize cardiac phenotypes at upper thermal limits of teleosts.

The effect of green tea extract on fat oxidation at rest and during exercise: evidence of efficacy and proposed mechanisms.

Green tea is made from the leaves of the Camellia sinensis L plant, which is rich in polyphenol catechins and caffeine. There is increasing interest in the potential role of green tea extract (GTE) in fat metabolism and its influence on health and exercise performance. A number of studies have observed positive effects of GTE on fat metabolism at rest and during exercise, following both shorter and longer term intake. However, overall, the literature is inconclusive. The fact that not all studies observed effects may be related to differences in study designs, GTE bioavailability, and variation of the measurement (fat oxidation). In addition, the precise mechanisms of GTE in the human body that increase fat oxidation are unclear. The often-cited in vitro catechol-O-methyltransferase mechanism is used to explain the changes in substrate metabolism with little in vivo evidence to support it. Also, changes in expression of fat metabolism genes with longer term GTE intake have been implicated at rest and with exercise training, including the upregulation of fat metabolism enzyme gene expression in the skeletal muscle and downregulation of adipogenic genes in the liver. The exact molecular signaling that activates changes to fat metabolism gene expression is unclear but may be driven by PPAR-γ coactivator 1-α and PPARs. However, to date, evidence from human studies to support these adaptations is lacking. Clearly, more studies have to be performed to elucidate the effects of GTE on fat metabolism as well as improve our understanding of the underlying mechanisms.

Gestational Age-Dependent Changes in Gene Expression of Metabolic Enzymes and Transporters in Pregnant Mice

Pregnancy-induced changes in drug pharmacokinetics can be explained by changes in expression of drug-metabolizing enzymes and transporters and/or normal physiology. In this study, we determined gestational age-dependent expression profiles for all metabolic enzyme and transporter genes in the maternal liver, kidney, small intestine, and placenta of pregnant mice by microarray analysis. We specifically examined the expression of genes important for xenobiotic, bile acid, and steroid hormone metabolism and disposition, namely, cytochrome P450s (Cyp), UDP-glucuronosyltranserases (Ugt), sulfotransferases (Sult), and ATP-binding cassette (Abc), solute carrier (Slc), and solute carrier organic anion (Slco) transporters. Few Ugt and Sult genes were affected by pregnancy. Cyp17a1 expression in the maternal liver increased 3- to 10-fold during pregnancy, which was the largest observed change in the maternal tissues. Cyp1a2, most Cyp2 isoforms, Cyp3a11, and Cyp3a13 expression in the liver decreased on gestation days (gd) 15 and 19 compared with nonpregnant controls (gd 0). In contrast, Cyp2d40, Cyp3a16, Cyp3a41a, Cyp3a41b, and Cyp3a44 in the liver were induced throughout pregnancy. In the placenta, Cyp expression on gd 10 and 15 was upregulated compared with gd 19. Notable changes were also observed in Abc and Slc transporters. Abcc3 expression in the liver and Abcb1a, Abcc4, and Slco4c1 expression in the kidney were downregulated on gd 15 and 19. In the placenta, Slc22a3 (Oct3) expression on gd 10 was 90% lower than that on gd 15 and 19. This study demonstrates important gestational age-dependent expression of metabolic enzyme and transporter genes, which may have mechanistic relevance to drug disposition in human pregnancy.

Altered expression of hepatic metabolic enzyme and apoptosis-related gene transcripts in human hepatocytes treated with trichloroethylene

Trichloroethylene (TCE) is a common organic solvent that has been widely used in industrial applications. Hundred cases of allergic reactions occurred after the workers were occupationally exposed to TCE in China in the past decade, but the underlying effector mechanisms of TCE remain unclear. The purpose of the present study is to examine the alteration of hepatic metabolic enzyme gene and apoptosis-related gene messenger RNA (mRNA) expression in L02 human hepatocytes (L02 cells) after treatment with TCE. L02 cells were cultured either with various doses of TCE (0.25, 0.5, 1.0 and 2.0 mmol/L) for 24 h or with a single dose of TCE (1.0 mmol/L) for different time intervals, whereas samples treated with dimethyl sulfoxide served as control. Quantitative real-time polymerase chain reaction analysis was performed to detect the mRNA expression of hepatic metabolic enzyme genes (CYP1A2, CYP3A4 and CYP2E1) and apoptosis-related genes (BAX and BAD). It was found that the transcript levels of hepatic metabolic enzyme genes and apoptosis genes including BAX and BAD were significantly increased after TCE treatment at various doses for 24 h when compared with controls. Additionally, when the cells were treated with a single dose of TCE (1.0 mmol/L) for different periods of time (3, 6, 12 and 24 h), the mRNA expression of these genes also increased significantly compared with control (p < 0.05 or p < 0.01). The conclusion of the study is that TCE could induce alteration of mRNA expression of hepatic metabolic enzyme genes and apoptosis genes, which might be implicated in the effector mechanisms of TCE cytotoxicity in vivo.

Gene expression profiling and pathway network analysis of hepatic metabolic enzymes targeted by baicalein

Ethnopharmacological relevanceBaicalein is a flavone originally isolated from the roots of traditional Chinese medicinal herb, Scutellaria baicalensis, which has been proved as a promising chemopreventive compound for many chronic human diseases. Aim of the studyThe present study aimed to clarify the molecular mechanism targeted by baicalein. Materials and methodsGene expression profiling of HepG2 cells treated with baicalein was carried out, using the Affymetrix 42K oligonucleotide microarray in the present study. Microarray data analyzed by Ingenuity Pathway Analysis (IPA), further study performed by real time PCR, reporter gene assay, and Western blot. ResultsAmong total 42K gene probes, baicalein treatment up-regulated the signals of 440 gene probes (1.04% of total gene probes) and down-regulated signals of 254 gene probes (0.6% of total gene probes) by ≥2-fold. These genes were categorized into 35 groups and hit for biological processes, molecular functions, and signaling pathways. The network and pathway analyses of these data further revealed that an Nrf2 (nuclear factor-erythroid 2 p45-related factor 2)-mediated ARE (antioxidant response element) pathway is involved in baicalein-induced gene expression of hepatic metabolic enzymes. The representative enzymes involved in Nrf2/ARE pathway were further confirmed at mRNA level by real time PCR and at protein level by Western blot analysis. Moreover, the ARE-reporter gene assay demonstrated that baicalein stimulated Nrf2-mediated ARE transactivation. ConclusionsOur results provide a comprehensive data for understanding the hepatic metabolism, bioactive role and the molecular mechanisms of baicalein.

Altered expression of hepatic metabolic enzyme genes, immune-related genes, oncogene and apoptotic genes in patients with trichloroethylene-induced allergic disorder

Altered expression of hepatic metabolic enzyme genes, immune-related genes, oncogene and apoptotic genes in patients with trichloroethylene-induced allergic disorder

Cold-modulated expression of genes encoding for key enzymes of the sugar metabolism in spring and autumn cvs. ofBeta vulgarisL.

An integrated approach based on the use of bioinformatics and gene expression analysis tools was carried out to evaluate the organ-specific transcription modulation of nine genes relevant to sugar metabolism ofBeta vulgarisL. plantlets of the autumn cv. Franca and spring cv. Bianca, in response to low-temperature (LT) treatments. Different growth cycles imply different plant capability to adapt to the environment that includes variations in gene expression of key metabolic enzymes. The transcriptional response was evaluated by quantitative PCR analysis before, during and after the LT treatments. The results were correlated with the LT-induced electrolyte leakage measure and the carbohydrate content. Stress-induced transcript level alterations were detected in the two cultivars, suggesting a modulation of sucrose synthesis and carbohydrate partitioning. Cold stress induced deep changes in the autumn cultivar, especially in fructose-1,6-biphosphatase gene expression, irrespective of temperature or exposure time. These differential features of expression profiles constitute first clues on the molecular basis of the differential LT response of sugarbeet autumn and spring cultivars.

Relationship Between Gene Expression of 5-Fluorouracil Metabolic Enzymes and 5-Fluorouracil Sensitivity in Primary Cancer Cells Isolated from Malignant Ascites

This study was designed to investigate the predictive role of 5-FU metabolic enzymes in malignant ascites. Forty-three malignant ascites were collected and primary cancer cells were isolated. Gene expression was detected by quantitative RT-PCR. We found that DPD mRNA was higher in patients with pancreatic cancers than those with gastric cancers, colon cancers, and liver cancers. Significant correlations were found between expression of DPD and TP, and between TS and OPRT. mRNA levels of TS and OPRT correlated significantly with the chemosensitivity of 5-FU. Assessing gene expression would be useful in predicting 5-FU sensitivity for patients with malignant ascites.

Rhizoctonia solani infection in two rice lines increases mRNA expression of metabolic enzyme genes in glycolytic, oxidative pentose phosphate pathways and secondary metabolism

Rhizoctonia solani infection in two rice lines increases mRNA expression of metabolic enzyme genes in glycolytic, oxidative pentose phosphate pathways and secondary metabolism

Enzyme Activities and Gene Expression of Yak Skeletal Muscles

Zheng, Y.C., Lin, Y.Q., Xu, Y.O., Wang, G.S., Jin, S.Y. and Li, Y.P. 2010. Enzyme activities and gene expression of yak skeletal muscles. J. Appl. Anim. Res., 38: 135–138. The purpose of the present study was to characterize the metabolic enzyme activities and gene expression levels in yak skeletal muscles. Yak longissimus dorsi had higher lactate dehydrogenase (LDH) activity, lower activities ofmalate dehydrogenase (MDH), β-hydroxyacyl-CoA dehydrogenase (HOAD) and cytocrome c oxidase (COX) compared with biceps femoris. Meanwhile, native PAGE of muscle extracts revealed that longissimus dorsi had higher proportion of LDH5 compared with biceps femoris. These data indicate the less oxidative metabolic orientation of yak longissimus dorsi. Semi-quantitative RT-PCR analysis revealed no significant difference in the expression of four genes including adipocyte fatty acid-binding protein (A-FABP), peroxisome proliferator-activated receptor gamma 2 (PPARγ2), myosin heavy chain 1 (MyHC1) and peroxisome proliferator-activated receptor coactivator lα (PGC-1α) between yak longissimus dorsi and biceps femoris.