The sample selection process.

<p>The sample selection process.</p

Metabolites differing between UQ and GDM groups at 2-y follow-up (<i>p</i>&lt;0.05).

<p>Metabolites have been classified according to their molecular structures or known metabolic functions/pathway participation. Within each class, data have been separated in to those with higher and lower ratios and are then presented in order from lowest to highest <i>p</i> value. The molecular weights, calculated as the monoisotopic mass, are included. Ratios with 95% confidence intervals in parentheses are shown. CE Cholesteryl ester; CEHC, 2,5,7,8-tetramethyl-2-(2'-carboxyethyl)-6-hydroxychroman; DG, diglyceride; HEPE, hydroxy-eicosapentaenoic acid; PC, phosphatidylcholine; PG, phosphatidylglycine; The values in parentheses (for example PC(34∶0)) relate to the total fatty acid carbon chain length and number of carbon double bonds (unsaturation) in each metabolite. *Identification by matching of retention time and accurate mass to authentic chemical standard.</p><p>Metabolites differing between UQ and GDM groups at 2-y follow-up (<i>p</i>&lt;0.05).</p

Long chain fatty acids that differed significantly between control and UQ groups at 2-y follow-up (<i>p</i>&lt;0.05).

<p>PC, phosphatidylcholine; PE, phosphatidylethanolamine; PG, glycerophosphoglycerol; PS, phosphatidylserine.</p

Clinical data for participants during pregnancy and at follow-up in the three study groups.

<p><i>p</i> values calculated applying ANOVA or **Chi-squared tests. #Data are geometric mean and 95% confidence intervals</p><p>Clinical data for participants during pregnancy and at follow-up in the three study groups.</p

Metabolites differing between control and GDM groups at 2-y follow-up (<i>p</i>&lt;0.05).

<p>Metabolites have been classified according to their molecular structures or known metabolic functions/pathway participation. Within each class the data have been separated in to those with higher and lower ratios and are then presented in order from lowest to highest <i>p</i> value. The molecular weights, calculated as the monoisotopic mass, are included. Ratios with 95% confidence intervals in parentheses are shown. CE cholesteryl ester; DG, diglyceride; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PG, phosphatidylglycine; PGF, prostaglandin; PI, phosphatidylinositol; PS, phosphatidylserine; The values in parentheses (for example PC(34∶0)) relate to the total fatty acid carbon chain length and number of carbon double bonds (unsaturation) in each metabolite. *Identification by matching of retention time and accurate mass to authentic chemical standard.</p><p>Metabolites differing between control and GDM groups at 2-y follow-up (<i>p</i>&lt;0.05).</p

Phospholipids that differed significantly between control and UQ groups at 2-y follow-up (<i>p</i>&lt;0.05).

<p>*Identification by matching of retention time and accurate mass to authentic chemical standard.</p

Integration of proteome and metabolic control to show regulation of carbon and nitrogen metabolic fluxes at the protein (enzyme) level

Shown here are the coupling of carbon and nitrogen fluxes at the level of glutamate dehydrogenase (Gdh1p, Gdh2p) and glutamine synthetase (Gln1p), the regulation of arginine biosynthesis at the carbamoyl phosphate synthetase (Cpa1p, Cpa2p) level and amino-acid biosynthesis, and amino-acid sensing by TOR. Selected proteins with levels consistently upregulated (red) with growth independently of culture conditions are shown. Enzymes responsible for the cytosolic 2-oxoglutarate pool: Aco1p and Aco2p, aconitase and putative aconitase isoenzyme; Odc1p and Odc2p, mitochondrial 2-oxoglutarate transporters; Idp2p, NADP-specific isocitrate dehydrogenase. Enzyme subunits coupling the oxidation of succinate to the transfer of electrons to ubiquinone: Sdh1p and Sdh2p, succinate dehydrogenase, flavoprotein, and iron-sulfur protein subunits, respectively. Metabolic diagram from [42, 91, 92] and drawn using Cell Designer [136] and Adobe Illustrator [137].<p><b>Copyright information:</b></p><p>Taken from "Growth control of the eukaryote cell: a systems biology study in yeast"</p><p>http://jbiol.com/content/6/2/4</p><p>Journal of Biology 2007;6(2):4-4.</p><p>Published online 30 Apr 2007</p><p>PMCID:PMC2373899.</p><p></p

Integration of proteome and metabolic control to show regulation of sulfur and C1 (folate) metabolic fluxes at the protein (enzyme) level

Selected proteins with levels consistently upregulated (red) or downregulated (green) with growth independently of culture conditions are shown. Sulfur, C1 metabolism, methyl cycle, methionine and -adenosylmethionine (SAM) fluxes towards methylation of proteins, rRNAs and tRNAs, and protein biosynthesis are shown here. Metabolic pathways and enzymes are from [42,82, 103-105] and the diagram is drawn with Cell Designer [136] and Adobe Illustrator [137]. Reverse methionine biosynthetic pathways [83] have been omitted for clarity. Metabolite abbreviations: THF, tetrahydrofolate; METTHF, 5,10-methylenetetrahydrofolate; MTHPTGLUT, 5-methyltetrahydropteroyltriglutamate (donor of the terminal methyl group in methionine biosynthesis); GT, glutathione; CYS, cysteine; CT, cystathionine; OAHS, -acetylhomoserine; HCYS, homocysteine; MET, methionine; SAM, -adenosylmethionine; SAH, -adenosylhomocysteine; D-SAM, decarboxylated -adenosylmethionine; MTA, methylthioadenosine. Metabolic steps (genes/enzymes): Met10p, sulfite reductase alpha subunit; Ecm17p, sulfite reductase beta subunit; , folylpolyglutamate synthetase (Met7p not detected; the relevance of polyglutamylation in the C1 metabolism branch was demonstrated at the transcriptional level (see text)); Met13p, methylenetetrahydrofolate reductase isozyme; Met6p, methionine synthase; Mes1p, methionyl-tRNA synthetase; Sam1p, S-adenosylmethionine synthetase isozyme; Sam2p, S-adenosylmethionine synthetase isozyme. Sah1p, S-adenosyl-L-homocysteine hydrolase; Ado1p, adenosine kinase.<p><b>Copyright information:</b></p><p>Taken from "Growth control of the eukaryote cell: a systems biology study in yeast"</p><p>http://jbiol.com/content/6/2/4</p><p>Journal of Biology 2007;6(2):4-4.</p><p>Published online 30 Apr 2007</p><p>PMCID:PMC2373899.</p><p></p