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At least 217 records · Page 12Linked to original sources
PubMed2001

Helicobacter pylori alters n-6 fatty acid metabolism and prostaglandin E2 synthesis in rat gastric mucosal cells.

BACKGROUND AND AIMS: Little is known about whether Helicobacter pylori infection alters fatty acid metabolism in gastric mucosal cells. By using cultured rat gastric mucosal cells (RGM-1), we investigated the effect of H. pylori broth culture filtrates on this point. Furthermore, our study aimed to find out whether n-6 long chain polyunsaturated fatty acids from linoleic acid are formed in RGM-1 cells. METHODS: Rat gastric mucosal cells were incubated with 10, 20 and 40 microg/mL of linoleic acid or medium alone. Phosphatidylcholine content extracted from whole RGM-1 cells was quantitated by using a densitometer, and its fatty acid composition was analyzed by using gas chromatography. Prostaglandin E2 concentration in the culture medium was measured by using radioimmunoassay. The expression of cyclooxygenase (COX)-1 and COX-2 was examined by using reverse transcription-polymerase chain reaction. In addition, after incubation with [1-14C] linoleic acid, radioactivities of both linoleic acid and arachidonic acid components of the PC fraction were counted. The effects of H. pylori broth culture filtrates on PC content, its fatty acid composition and prostaglandin (PG)E2 synthesis were also assessed. RESULTS: Linoleic acid addition caused an increase in the composition of arachidonic acid, as well as linoleic acid, and also in PGE2 concentration. Cyclo-oxygenase-2 expression was induced in RGM-1 cells by the addition of linoleic acid. In addition, [1-14C] linoleic acid added to the culture medium was converted to [1-14C] arachidonic acid in RGM-1 cells. Helicobacter pylori broth culture filtrates decreased linoleic acid composition and increased arachidonic acid composition. Moreover, after incubation with H. pylori broth culture filtrates, PGE2 concentrations were higher than that of the controls. CONCLUSIONS: These findings suggest the presence of fatty acid elongase and Delta5- and Delta6-desaturases synthesize arachidonic acid from linoleic acid in RGM-1 cells. Thus, H. pylori infection may enhance PGE2 synthesis and accelerate n-6 fatty acid metabolism in gastric mucosal cells, which could make the gastric mucosal barrier more fragile.

Animals↗
PubMed1998

Non-esterified fatty acid metabolism and postprandial lipaemia.

Non-esterified fatty acids (NEFA, or free fatty acids) are an important metabolic fuel. Both the concentration of NEFA and their flux through the circulation vary widely from hour to hour, reflecting nutritional state and physical activity. Inappropriately elevated plasma NEFA concentrations may have a number of adverse effects on both carbohydrate and lipid metabolism. These adverse effects are likely to be most marked in the postprandial period, when NEFA release from adipose tissue is usually suppressed. Although the regulation of NEFA release in the postabsorptive state is well understood in molecular terms, the predominant pathway for release of NEFA in the postprandial state is the action of lipoprotein lipase (LPL) in adipose tissue capillaries on chylomicron-triacylglycerol (TG). Fatty acids released by LPL may either be sequestered in the adipocytes by esterification, or released as NEFA into the plasma. The regulation of this branch-point, which may be of crucial significance for postprandial metabolism, is not well understood. Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. There is considerable indirect evidence that impaired regulation of this step occurs in insulin resistance and other conditions collectively recognised by an elevated concentration of apolipoprotein B (hyper-apo B). Inappropriate release of NEFA in the postprandial period is likely both to reduce the sensitivity of glucose metabolism to insulin and to accentuate postprandial lipaemia. Further study of the regulation of this pathway is much needed.

Adipose Tissue↗
PubMed2006

Control of energy homeostasis: role of enzymes and intermediates of fatty acid metabolism in the central nervous system.

The regulation of energy homeostasis is critical for normal physiology and survival. Energy flux must be rigorously monitored and adjusted to ensure that fuel intake and expenditure remain within acceptable limits. The central nervous system (CNS) is, in large part, responsible for conducting this energy-monitoring function and for integrating the numerous inputs. It has become evident that neurons of the CNS monitor and respond to levels of metabolic intermediates that reflect peripheral energy status. Intermediates in the fatty acid biosynthetic pathway have been implicated as hypothalamic signaling mediators that sense and respond to changes in circulating fuels. Genetic and pharmacologic manipulation of the enzymes of fatty acid metabolism have led to the hypothesis that neuronal metabolic intermediates affect neural outputs that modify both feeding behavior and energy expenditure. This review focuses on the regulatory roles of these enzymes and intermediates in the regulation of food intake and energy balance.

Central Nervous System↗
PubMed2002

Analysis of 3-hydroxydodecanedioic acid for studies of fatty acid metabolic disorders: preparation of stable isotope standards.

Current diagnostic tests to detect disorders of fatty acids metabolism, such as long-chain hydroxyacyl CoA dehydrogenase deficiency (LCHAD), are hampered by insensitivity or a long delay time required for results. Children with LCHAD deficiency are known to excrete 3-hydroxydicarboxylic acids with chain lengths of 10-16 carbons, but a quantitative method to measure excretion of these potentially diagnostically important compounds has not been reported. We report synthetic schemes for synthesis of 3-hydroxydodecanedioic acid and a di-deuterated analog, suitable for use in a stable-isotope dilution mass spectrometric analytical approach. Evaluation of several common derivatization protocols to produce a volatile derivative for gas chromatography determined that trimethylsyl derivatives produced the best efficiency and stability. Positive-ion chemical ionization mass spectrometry provided the greatest yield of characteristic ions. These results indicate the basic reagents needed to develop sensitive and accurate 3-hydroxydodecanedioic acid measurements for diagnosis of LCHAD deficiency and other fatty acid oxidation disorders.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMedDate not supplied

Impact of hormone replacement on myocardial fatty acid metabolism: potential role of estrogen.

BACKGROUND: Estrogen increases fatty acid utilization and oxidation and may decrease glucose use in human skeletal muscle, whereas these effects are attenuated by progesterone. Whether these ovarian hormones exhibit similar effects on myocardial metabolism is unknown. METHODS AND RESULTS: Myocardial blood flow and oxygen consumption, as well as glucose and fatty acid metabolism, were examined retrospectively by use of positron emission tomography in 24 postmenopausal women receiving estrogen (n = 7), estrogen plus progesterone (n = 8), or no hormone replacement (n = 9) and in 22 age-matched men. Myocardial blood flow was higher in women regardless of hormone replacement status. Myocardial oxygen consumption was higher in women taking estrogen only when compared with men (7.3 +/- 1.6 micromol.g(-1).min(-1) vs 4.6 +/- 1.2 micromol.g(-1).min(-1), P < .001). Glucose utilization was not affected by gender or hormone replacement. Whereas fatty acid levels and the degree of myocardial fatty acid uptake were not distinguished by gender or hormone use, myocardial fatty acid utilization was higher in women taking estrogen when compared with men (259 +/- 68 nmol.g(-1).min(-1) vs 176 +/- 50 nmol.g(-1).min(-1), P = .01) and trended higher when compared with women not receiving hormonal therapy (185 +/- 46 nmol.g(-1).min(-1), P = .07) but was not different from that of women taking estrogen plus progesterone (205 +/- 58 nmol.g(-1).min(-1), P = not significant). CONCLUSIONS: In postmenopausal women, estrogen use is associated with increased myocardial fatty acid utilization. Thus, when the cardiac effects of hormone replacement therapy are being assessed, alterations in myocardial substrate metabolism should be considered.

Aged↗
PubMed1989

Altered hepatic fatty acid metabolism in endotoxicosis: effect of L-carnitine on survival.

The activities of palmitoyl-coenzyme A (CoA) synthetase, carnitine acetyltransferase (CAT), and carnitine palmitoyltransferase (CPT) and the levels of ketone bodies, reduced coenzyme A (CoASH), carnitine, and their esters, which are involved in fatty acid metabolism, in rat liver and plasma were measured after the administration of Escherichia coli lipopolysaccharide (LPS). We also studied the effect of L-carnitine treatment before LPS administration on survival and on hepatic fatty acid metabolism. The activities of CAT and CPT and the concentrations of ketone bodies, CoA, and carnitine derivatives (except for malonyl-CoA) declined in the liver after LPS administration. The activity of palmitoyl-CoA synthetase was changed little after LPS administration, and the level of hepatic malonyl-CoA increased significantly, suggesting that LPS causes activated fatty acids to undergo esterification and lipogenesis rather than oxidation. Treatment of rats with L-carnitine before LPS greatly increased the survival rate, but did not affect enzymes that metabolize fatty acids, CoA, or carnitine derivatives in the liver. Further studies are necessary to elucidate the mechanism of the effect of carnitine on post-LPS survival.

Animals↗
PubMed2003

Cross-talk between peroxisome proliferator-activated receptor (PPAR) alpha and liver X receptor (LXR) in nutritional regulation of fatty acid metabolism. II. LXRs suppress lipid degradation gene promoters through inhibition of PPAR signaling.

Fatty acid metabolism is transcriptionally regulated by two reciprocal systems: peroxisome proliferator-activated receptor (PPAR) alpha controls fatty acid degradation, whereas sterol regulatory element-binding protein-1c activated by liver X receptor (LXR) regulates fatty acid synthesis. To explore potential interactions between LXR and PPAR, the effect of LXR activation on PPARalpha signaling was investigated. In luciferase reporter gene assays, overexpression of LXRalpha or beta suppressed PPARalpha-induced peroxisome proliferator response element-luciferase activity in a dose-dependent manner. LXR agonists, T0901317 and 22(R)-hydroxycholesterol, dose dependently enhanced the suppressive effects of LXRs. Gel shift assays demonstrated that LXR reduced binding of PPARalpha/retinoid X receptor (RXR) alpha to peroxisome proliferator response element. Addition of increasing amounts of RXRalpha restored these inhibitory effects in both luciferase and gel shift assays, suggesting the presence of RXRalpha competition. In vitro protein binding assays demonstrated that activation of LXR by an LXR agonist promoted formation of LXR/RXRalpha and, more importantly, LXR/PPARalpha heterodimers, leading to a reduction of PPARalpha/RXRalpha formation. Supportively, in vivo administration of the LXR ligand to mice and rat primary hepatocytes substantially decreased hepatic mRNA levels of PPARalpha-targeted genes in both basal and PPARalpha agonist-induced conditions. The amount of nuclear PPARalpha/RXR heterodimers in the mouse livers was induced by treatment with PPARalpha ligand, and was suppressed by superimposed LXR ligand. Taken together with data from the accompanying paper (Yoshikawa, T., T. Ide, H. Shimano, N. Yahagi, M. Amemiya-Kudo, T. Matsuzaka, S. Yatoh, T. Kitamine, H. Okazaki, Y. Tamura, M. Sekiya, A. Takahashi, A. H. Hasty, R. Sato, H. Sone, J. Osuga, S. Ishibashi, and N. Yamada, Endocrinology 144:1240-1254) describing PPARalpha suppression of the LXR-sterol regulatory element-binding protein-1c pathway, we propose the presence of an intricate network of nutritional transcription factors with mutual interactions, resulting in efficient reciprocal regulation of lipid degradation and lipogenesis.

ATP Binding Cassette Transporter 1↗
PubMed2003

Angiotensin-converting enzyme inhibition improves cardiac fatty acid metabolism in patients with congestive heart failure.

This study aimed to examine whether angiotensin-converting enzyme (ACE) inhibition improved cardiac fatty acid metabolism in patients with congestive heart failure (CHF). Myocardial 123I-beta-methyl-iodophenylpentadecanoic acid (123I-BMIPP) imaging was performed in 25 patients with CHF and in 10 control subjects. Myocardial 123I-BMIPP images were obtained 30 min and 4 h after tracer injection. The heart-to-mediastinum (H/M) ratio of 123I-BMIPP uptake and the washout rate of 123I-BMIPP from the myocardium were calculated. Patients were given enalapril for 6 months, and 123I-BMIPP imaging was repeated. H/M ratios on early and delayed images were lower in CHF patients than in normal controls (P<0.01). The washout rate of 123I-BMIPP from the myocardium was faster in CHF patients than in controls (P<0.01). As the severity of the New York Heart Association (NYHA) functional class increased, the H/M ratio decreased and the washout rate increased. The washout rate of 123I-BMIPP was inversely correlated with left ventricular fractional shortening (R=-0.62, P<0.01). ACE inhibition with enalapril increased the H/M ratio on delayed images (P<0.05) and reduced the washout rate of 123I-BMIPP (P<0.05) in CHF patients. These data suggest that: (1) angiotensin II-mediated intracellular signalling activation may be a possible mechanism for the decreased myocardial uptake and enhanced washout of 123I-BMIPP in heart failure patients; and (2) the improvement in fatty acid metabolism by ACE inhibition may represent a new mechanism for the beneficial effect of this therapy in heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

[Glycolytic and fatty acid metabolic enzyme changes early after acute myocardial ischemia].

OBJECTIVE: To explore the changes of mRNA and protein expressions of glycolytic and fatty acid metabolic enzymes early after acute myocardial ischemia. METHODS: Twelve dogs were randomly divided into 3 groups (sham, 20 min ischemia and 40 min ischemia, n = 4 each). Myocardial samples from ischemic and nonischemic zone were obtained for histology examination, and the mRNA expressions for Phosphofructokinase (PFK), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), GLUT1, GLUT4, Medium-chain acyl-CoA dehydrogenase (MCAD) and Heart-fatty acid binding protein (H-FABP) were determined by Real Time PCR-SYBR Green RT-PCR. GLUT1 protein expression was determined by immunohistochemistry. The apoptotic cardiomyocytes was evaluated by TUNEL. RESULTS: Compared to sham hearts, H-FABP mRNA was decreased in nonischemic and ischemic zone (P < 0.05) while GLUT1 mRNA expression was significantly increased in nonischemic and ischemic zone (P < 0.05) in dogs underwent 20 and 40 min ischemia. PFK mRNA tended to be higher in ischemic myocardium (P = 0.065) and GAPDH, MCAD as well as GLUT4 remained unchanged post ischemia (all P > 0.05). Positive GLUT1 protein staining was visualized in ischemic myocardium of hearts underwent 20 and 40 min ischemia. The myocardial apoptosis cells was 6.4% +/- 0.9% in sham hearts, 28.0% +/- 3.7% in hearts underwent 20 min ischemia (P < 0.05 vs. sham) and 38.4% +/- 1.9% in hearts underwent 40 min ischemia (P < 0.05 vs. sham). CONCLUSIONS: Significant down and up-regulated glycolytic and fatty acid metabolic enzymes early after myocardial ischemia suggested that these enzymes might play an important role in acute myocardial ischemia.

Animals↗
PubMed2007

Comparative analysis of sesame lignans (sesamin and sesamolin) in affecting hepatic fatty acid metabolism in rats.

Effects of sesamin and sesamolin (sesame lignans) on hepatic fatty acid metabolism were compared in rats. Rats were fed either a lignan-free diet, a diet containing 0.6 or 2 g/kg lignan (sesamin or sesamolin), or a diet containing both sesamin (1.4 g/kg) and sesamolin (0.6 g/kg) for 10 d. Sesamin and sesamolin dose-dependently increased the activity and mRNA abundance of various enzymes involved in hepatic fatty acid oxidation. The increase was much greater with sesamolin than with sesamin. These lignans increased parameters of hepatic fatty acid oxidation in an additive manner when added simultaneously to an experimental diet. In contrast, they decreased the activity and mRNA abundance of hepatic lipogenic enzymes despite dose-dependent effects not being necessarily obvious. Sesamin and sesamolin were equally effective in lowering parameters of lipogenesis. Sesamolin accumulated in serum at 33- and 46-fold the level of sesamin at dietary concentrations of 0.6 and 2 g/kg, respectively. The amount of sesamolin accumulated in liver was 10- and 7-fold that of sesamin at the respective dietary levels. Sesamolin rather than sesamin can account for the potent physiological effect of sesame seeds in increasing hepatic fatty acid oxidation observed previously. Differences in bioavailability may contribute to the divergent effects of sesamin and sesamolin on hepatic fatty acid oxidation. Sesamin compared to sesamolin was more effective in reducing serum and liver lipid levels despite sesamolin more strongly increasing hepatic fatty acid oxidation.

Animals↗
PubMed1998

Essential fatty acid metabolism in infants with cholestasis.

Long-chain polyunsaturated fatty acids are important for the growth and early development of the central nervous system. Cholestatic infants suffer from fat malabsorption and disturbed lipid metabolism and therefore may be at risk of developing polyunsaturated fatty acid depletion. The aims of this study were to determine essential fatty acid status in cholestatic infants and to study the relationship to disease severity, degree of undernutrition, antioxidant status and mode of feeding. Twenty-four-hour dietary records were obtained in 34 cholestatic infants, and measurements were taken of skin fold thicknesses, bilirubin levels, activities of serum alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, prothrombin time, serum concentrations of albumin, bile acids, total lipids, phospholipids, cholesterol, vitamins A and E, the fatty acid composition of plasma phospholipids and plasma lipid peroxides expressed as thiobarbiturate reactive substance (TBARS). Plasma phospholipid fatty acids and TBARS were also determined in 12 age-matched healthy control infants. The cholestatic patients had very low percentage values of phospholipid essential fatty acids, particularly linoleic acid ( 18:2omega-6, median 14.74% vs 20.76% in controls, p < 0.001) and its major metabolite arachidonic acid (20:4omega-6, 6.80 vs 7.87%, p=0.04). The patients' essential fatty acid depletion was reflected by increased levels of the non-essential fatty acids, Mead acid (20:3omega-9, 0.74 vs 0.21%, p < 0.001) and palmitoleic acid (16:1omega-7, 2.20 vs 0.43%, p < 0.001). Polyunsaturated fatty acid profiles did not differ between infants with biliary atresia (n=13) and those with intrahepatic cholestasis (n=21), or between 17 infants with severe malnutrition (all skin folds < 10th percentile) and mild malnutrition (at least two skin folds > 10th percentile). TBARS were significantly higher in cholestatic patients than in controls (2.74 vs 0.85 nmol ml(-1), p < 0.001) and correlated with direct (r=0.41, p=0.02) and total bilirubin. The daily dietary intake of linoleic acid (per 100 kcal) correlated with plasma phospholipid linoleic acid (r=0.38,p=0.037) and total omega-6 fatty acids (r=0.38,p=0.036). Breastfed cholestatic infants (n=6) had higher values of the omega-3 long-chain polyunsaturated fatty acids docosapentanoic acid (22:5omega-3, 0.47 vs 0.28%, p=0.0006) and docosahexanoic acid (22:6omega-3, 2.39 vs 1.73%, p=0.01) than formula-fed infants, while disease severity was similar in the two groups. In conclusion, cholestatic infants are at high risk of essential fatty acid depletion, which appears to be related to fat malabsorption, hepatic essential fatty metabolism, enhanced lipid peroxidation and dietary intake.

Body Height↗
PubMed2005

Proteome analysis reveals adaptation of Pseudomonas aeruginosa to the cystic fibrosis lung environment.

Pseudomonas aeruginosa is known for the chronic lung colonization of cystic fibrosis (CF) patients in addition to eye, ear and urinary tract infections. With the underlying disease CF patients are predisposed to P. aeruginosa chronic lung infection, which leads to morbidity and mortality. In this study, we compared the protein expression profile of a CF lung-adapted P. aeruginosa strain C with that of the burn-wound isolate PAO. Differentially expressed proteins from the whole-cell, membrane, periplasmic as well as extracellular fraction were identified. The whole-cell proteome of strain C showed down-regulation of several proteins involved in amino acid metabolism, fatty acid metabolism, energy metabolism and adaptation leading to a highly distinct proteome pattern for strain C in comparison to PAO. Analysis of secreted proteins by strain C compared to PAO revealed differential expression of virulence factors under non-inducing conditions. The membrane proteome of strain C showed modulation of the expression of porins involved in nutrient and antibiotic influx. The proteome of the periplasmic space of strain C showed retention of elastase despite that the equal amounts were secreted by strain C and PAO. Altogether, our results elucidate adaptive strategies of P. aeruginosa towards the nutrient-rich CF lung habitat during the course of chronic colonization.

Adaptation, Physiological↗
PubMed1978

Fatty acid metabolism in L1210 murine leukemia cells: differences in modification of fatty acids incorporated into various lipids.

L1210 leukemia cells can utilize all of the main fatty acids that normally are present in the ascites fluid in which they grow. This finding is consistent with the view that L1210 cells derive most of their fatty acids from the ascites fluid. From 80--90% of each fatty acid was incorporated into cell lipids without structural modification, suggesting that the lipid composition of these cells can be altered by changing the type of fatty acids to which they are exposed. Most importantly, the palmitate that was subsequently incorporated into total cell phospholipids was elongated and desaturated somewhat more than that incorporated into triglycerides. This difference was due primarily to more extensive modification of the palmitate incorporated into the ethanolamine phosphoglycerides fraction. Although there was no difference between total phospholipids and triglycerides with linoleate, more of the linoleate incorporated into ethanolamine phosphoglycerides was elongated and further desaturated than that incorporated into choline phosphoglycerides and triglycerides. These findings indicate fatty acids incorporated into various cell lipid fractions are not structurally modified to the same extent. There appears to be greater modification of fatty acid used for ethanolamine phosphoglyceride synthesis as compared with triglyceride and choline phosphoglyceride synthesis.

Animals↗
PubMed1990

Fatty acid metabolism in human lymphocytes. I. Time-course changes in fatty acid composition and membrane fluidity during blastic transformation of peripheral blood lymphocytes.

The time-course changes in fatty acid composition of human T-lymphocytes during blastic transformation were analysed, as well as the variations in membrane fluidity determined by fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene (DPH), using a fluorescence-activated cell sorter. The more important changes observed, in activated relative to quiescent cells, started after 24 h and consisted in an increase in the proportion of oleic (18:1(n - 9)), docosapentaenoic (22:5(n - 3)) and docosahexaenoic (22:6(n - 3)) acids and a decrease in that of linoleic (18:2(n - 6)) and arachidonic (20:4(n - 6)) acids. This represented a relative increase of 26% for 18:1, 56% for 22:5 and 84% for 22:6 in peripheral blood mononuclear cells (PBMC) and 35%, 182% and 94%, respectively, in purified T-lymphocytes, both activated for 72 h. The decrease in n - 6 fatty acids was of 42% for 18:2 and 14% for 20:4 in PBMC and 30% and 19%, respectively, for 72 h. The decrease in n - 6 fatty acids was of 42% for 18:2 and 14% for 20:4 in PBMC and 30% and phosphatidylethanolamine) rather than neutral lipids. The 18:1/18:0 ratio increased greatly in major cell phospholipids. The proportion of 20:4, 22:5 and 22:6 in phosphatidylinositol was not significantly altered after 72 h of activation. The molar ratio cholesterol/phospholipids was reduced in 72-h-activated lymphocytes (0.29) compared to quiescent cells (0.5). On the other hand, the stimulation of human T-lymphocytes caused a significant decrease in the order parameter (S) of DPH, according to the observed changes in lipid composition. After 72 h in culture, the S value for quiescent and stimulated T-lymphocytes was 0.530 and 0.326, respectively. In conclusion, the blastic transformation of human T-lymphocytes is associated with changes in lipid composition which modify the physical properties of their membranes. These modifications could modulate, in turn, the activity of membrane proteins implicated in the process of blastic transformation.

Cells, Cultured↗
PubMed2001

Genomic interspecies microarray hybridization: rapid discovery of three thousand genes in the maize endophyte, Klebsiella pneumoniae 342, by microarray hybridization with Escherichia coli K-12 open reading frames.

In an effort to efficiently discover genes in the diazotrophic endophyte of maize, Klebsiella pneumoniae 342, DNA from strain 342 was hybridized to a microarray containing 96% (n = 4,098) of the annotated open reading frames from Escherichia coli K-12. Using a criterion of 55% identity or greater, 3,000 (70%) of the E. coli K-12 open reading frames were also found to be present in strain 342. Approximately 24% (n = 1,030) of the E. coli K-12 open reading frames are absent in strain 342. For 1.6% (n = 68) of the open reading frames, the signal was too low to make a determination regarding the presence or absence of the gene. Genes with high identity between the two organisms are those involved in energy metabolism, amino acid metabolism, fatty acid metabolism, cofactor synthesis, cell division, DNA replication, transcription, translation, transport, and regulatory proteins. Functions that were less highly conserved included carbon compound metabolism, membrane proteins, structural proteins, putative transport proteins, cell processes such as adaptation and protection, and central intermediary metabolism. Open reading frames of E. coli K-12 with little or no identity in strain 342 included putative regulatory proteins, putative chaperones, surface structure proteins, mobility proteins, putative enzymes, hypothetical proteins, and proteins of unknown function, as well as genes presumed to have been acquired by lateral transfer from sources such as phage, plasmids, or transposons. The results were in agreement with the physiological properties of the two strains. Whole genome comparisons by genomic interspecies microarray hybridization are shown to rapidly identify thousands of genes in a previously uncharacterized bacterial genome provided that the genome of a close relative has been fully sequenced. This approach will become increasingly more useful as more full genome sequences become available.

Escherichia coli↗
PubMed2006

Gene expression profiles of hepatic cell-type specific marker genes in progression of liver fibrosis.

AIM: To determine the gene expression profile data for the whole liver during development of dimethylni-trosamine (DMN)-induced hepatic fibrosis. METHODS: Marker genes were identified for different types of hepatic cells, including hepatic stellate cells (HSCs), Kupffer cells (including other inflammatory cells), and hepatocytes, using independent temporal DNA microarray data obtained from isolated hepatic cells. RESULTS: The cell-type analysis of gene expression gave several key results and led to formation of three hypotheses: (1) changes in the expression of HSC-specific marker genes during fibrosis were similar to gene expression data in in vitro cultured HSCs, suggesting a major role of the self-activating characteristics of HSCs in formation of fibrosis; (2) expression of mast cell-specific marker genes reached a peak during liver fibrosis, suggesting a possible role of mast cells in formation of fibrosis; and (3) abnormal expression of hepatocyte-specific marker genes was found across several metabolic pathways during fibrosis, including sulfur-containing amino acid metabolism, fatty acid metabolism, and drug metabolism, suggesting a mechanistic relationship between these abnormalities and symptoms of liver fibrosis. CONCLUSION: Analysis of marker genes for specific hepatic cell types can identify the key aspects of fibrogenesis. Sequential activation of inflammatory cells and the self-supporting properties of HSCs play an important role in development of fibrosis.

Alanine Transaminase↗