The number of surviving children born prematurely has increased substantially during the last 2 decades. The major goal of enteral nutrient supply to these infants is to achieve growth similar to foetal growth coupled with satisfactory functional development. The accumulation of knowledge since the previous guideline on nutrition of preterm infants from the Committee on Nutrition of the European Society of Paediatric Gastroenterology and Nutrition in 1987 has made a new guideline necessary. Thus, an ad hoc expert panel was convened by the Committee on Nutrition of the European Society of Paediatric Gastroenterology, Hepatology, and Nutrition in 2007 to make appropriate recommendations. The present guideline, of which the major recommendations are summarised here (for the full report, see http://links.lww.com/A1480), is consistent with, but not identical to, recent guidelines from the Life Sciences Research Office of the American Society for Nutritional Sciences published in 2002 and recommendations from the handbook Nutrition of the Preterm Infant. Scientific Basis and Practical Guidelines, 2nd ed, edited by Tsang et al, and published in 2005. The preferred food for premature infants is fortified human milk from the infant's own mother, or, alternatively, formula designed for premature infants. This guideline aims to provide proposed advisable ranges for nutrient intakes for stable-growing preterm infants up to a weight of approximately 1800 g, because most data are available for these infants. These recommendations are based on a considered review of available scientific reports on the subject, and on expert consensus for which the available scientific data are considered inadequate.

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The plasma profile of subjects with non-alcoholic fatty liver disease (NAFLD), steatosis and steatohepatitis (NASH), was examined using an untargeted global metabolomic analysis in order to identify specific disease-related pattern/s and to identify potential non-invasive biomarkers. Plasma samples were obtained after an overnight fast from histologically confirmed non-diabetic subjects with hepatic steatosis (N=11) or NASH (N=24), and compared with healthy, age and sexmatched controls (n=25). Subjects with NAFLD were obese, were insulin resistant and had higher plasma concentration of homocysteine and total cysteine and lower plasma concentrations of total glutathione. Metabolomic analysis showed markedly higher levels of glycocholate, taurocholate and glycochenodeoxycholate in subjects with NAFLD. Plasma concentrations of long chain fatty acids were lower and concentrations of free carnitine, butyrylcarnitine and methylbutyryl carnitine were higher in NASH. Several glutamyl dipeptides were higher, while cysteine-glutathione levels were lower in NASH and steatosis. Other changes included higher branched chain amino acids, phosphocholine, carbohydrates (glucose, mannose), lactate, pyruvate, and several unknown metabolites. Random forest analysis and recursive partitioning of the metabolomic data could separate healthy subjects from NAFLD with an error rate of ~8%, and NASH from healthy controls with an error rate of 4%. Hepatic steatosis and steatohepatitis could not be separated using the metabolomic profile.Conclusion-Plasma metabolomic analysis revealed marked changes in bile salts and in biochemicals related to glutathione in subjects with non-alcoholic fatty liver disease. Statistical analysis identified a panel of biomarkers that could effectively separate healthy controls from NAFLD and healthy controls from NASH. These biomarkers can potentially be used to follow response to therapeutic interventions.

Our nontargeted analytical approach detected a large number of metabolites, including those that were found to be statistically altered with age, sex or race. Age-associated changes were more pronounced than those related to differences in sex or race in the population group we studied. Age, sex and race can be confounding factors when comparing different groups in clinical studies. Future studies to determine the influence of diet, lifestyle and medication are also warranted.

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Aims/hypothesis: Adiponectin is upregulated during adipogenesis and downregulated in insulin-resistant states. The mechanism(s) governing the re-arrangements from adipogenesis to facilitated lipolysis during pregnancy are unknown. Our purpose was to analyse the role of adiponectin relative to the metabolic changes in human pregnancy. Subjects, materials and methods: Lean women (BMI <25 kg/m²) were evaluated longitudinally before conception, and in early (12-14 weeks) and late (34-36 weeks) pregnancy. Insulin sensitivity was measured using the glucose clamp technique. Venous blood and subcutaneous adipose tissue biopsies were obtained at each time point. Results: Adiponectin concentrations were lower in the third trimester than in the pregravid condition (9.9±1.4 vs 13.5±1.8 μg/ml). The hypoadiponectinaemia was reflected by a 2.5-fold decrease in white adipose tissue adiponectin mRNA. These changes were associated with a 25% increase in fat mass (23.7±2.9 vs 18.9±2.9 kg). Insulin infusion decreased high molecular weight adiponectin complexes in pregravid women (9.9±0.6 vs 6.2±0.06) and the suppressive effect of insulin was lost during pregnancy. The pregnancy-mediated changes in adiponectin were strongly correlated with basal insulin levels and insulin sensitivity (p<0.0001). The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. Conclusions/interpretation: These data demonstrate that pregnancy is associated with adiponectin changes in lean women. Hypoadiponectinaemia is reflected by a lower amount of high molecular weight adiponectin and by the ratio of high to low molecular weight multimers. The adiponectin changes relate to decreased insulin sensitivity of glucose disposal rather than alterations of lipid metabolism.

Serine is generally classified as a nutritionally nonessential (dispensable) amino acid, but metabolically, serine is indispensible and plays an essential role in several cellular processes. Serine is the major source of one-carbon units for methylation reactions that occur via the generation of S-adenosylmethionine. The regulation of serine metabolism in mammalian tissues is thus of critical importance for the control of methyl group transfer. In addition to the well known role of D-serine in the brain, L-serine has recently been implicated in breast cancer and other tumors due in part to the genomic copy number gain for 3-phosphoglycerate dehydrogenase, the enzyme that controls the entry of glycolytic intermediates into the pathway of serine synthesis. Here, we review recent information regarding the synthesis of serine and the regulation of its metabolism and discuss the role played by phosphoenolpyruvate carboxykinase in this process.The regulation of methyl group transfer is critical in controlling cellular processes, ranging from the synthesis of key metabolic intermediates, such as creatine, phosphatidylcholine, and epinephrine, to the methylation of proteins, DNA, and RNA. Serine, a nutritionally nonessential amino acid, plays a key role in this process by providing one-carbon units to tetrahydrofolate (THF) 2 to form N 5 ,N 10 -methylene-THF and, subsequently, 5-methyl-THF, an intermediate in the methylation of homocysteine to methionine, via homocysteine methyltransferase (methionine synthase) (Fig. 1). This ensures sufficient methionine for optimal functioning of the methionine cycle and for synthesis of S-adenosylmethionine, the key methyl donor in all cells. The regulation of the cellular levels of S-adenosylmethionine in response to metabolic changes and the role of the enzyme glycine N-methyltransferase in this process have been discussed recently in a minireview by Luka et al. (1). This minireview was particularly timely because it details the pioneering work on methyl group transfer of Conrad Wagner and colleagues.Serine is also involved in the ultimate disposal of methionine carbon by condensing with homocysteine to form cystathionine, a reaction that is catalyzed by cystathionine ␤-synthase. Cystathionine is subsequently split into cysteine and ␣-ketobutyrate by cystathionine ␥-lyase. This cascade of cysteine synthesis has been termed the "transsulfuration pathway" (Fig. 1). Over the past decade, the importance of the two enzymes of this pathway in the generation of hydrogen sulfide has been recognized. In addition, the metabolism of serine has been linked to the growth of breast cancer cells (2). The scope of the metabolism of sulfur-containing compounds in the generation of hydrogen sulfide and the role of the latter in the control of blood pressure and the reduction of ischemia/reperfusion injury have been reviewed in detail elsewhere (3-6). Here, we focus on the key role of serine in methyl group transfer and the factors that regulate its metabolism. Metabolism of Serine in Vivo and Sour...