Objective: This study examined the prevalence of impaired fasting glucose tolerance in first-episode, drug-naive patients with schizophrenia. Method: In this cross-sectional study, fasting plasma levels of glucose, insulin, lipids, and cortisol were measured in 15 male and 11 female hospitalized Caucasian patients with DSM-IV schizophrenia (mean age=33.6 years) and age-and sexmatched healthy comparison subjects. The patients and comparison subjects were also matched in terms of various lifestyle and anthropometric measures. Results: More than 15% of the drug-naive, first-episode patients with schizophrenia had impaired fasting glucose tolerance, compared to none of the healthy volunteers. Compared with the healthy
BackgroundIn recent years an individual’s ability to respond to an acute dietary challenge has emerged as a measure of their biological flexibility. Analysis of such responses has been proposed to be an indicator of health status. However, for this to be fully realised further work on differential responses to nutritional challenge is needed. This study examined whether metabolic phenotyping could identify differential responders to an oral glucose tolerance test (OGTT) and examined the phenotypic basis of the response.Methods and ResultsA total of 214 individuals were recruited and underwent challenge tests in the form of an OGTT and an oral lipid tolerance test (OLTT). Detailed biochemical parameters, body composition and fitness tests were recorded. Mixed model clustering was employed to define 4 metabotypes consisting of 4 different responses to an OGTT. Cluster 1 was of particular interest, with this metabotype having the highest BMI, triacylglycerol, hsCRP, c-peptide, insulin and HOMA- IR score and lowest VO2max. Cluster 1 had a reduced beta cell function and a differential response to insulin and c-peptide during an OGTT. Additionally, cluster 1 displayed a differential response to the OLTT.ConclusionsThis work demonstrated that there were four distinct metabolic responses to the OGTT. Classification of subjects based on their response curves revealed an “at risk” metabolic phenotype.
BackgroundPharmacists’ completion of medication reconciliation in the community after hospital discharge is intended to reduce harm due to prescribed or omitted medication and increase healthcare efficiency, but the effectiveness of this approach is not clear. We systematically review the literature to evaluate intervention effectiveness in terms of discrepancy identification and resolution, clinical relevance of resolved discrepancies and healthcare utilisation, including readmission rates, emergency department attendance and primary care workload.MethodsThis is a systematic literature review and meta-analysis of extracted data. Medline, Cumulative Index to Nursing and Allied Health Literature (CINAHL), EMBASE, Allied and Complementary Medicine Database (AMED), Education Resources Information Center (ERIC), Scopus, NHS Evidence and the Cochrane databases were searched using a combination of medical subject heading terms and free-text search terms. Controlled studies evaluating pharmacist-led medication reconciliation in the community after hospital discharge were included. Study quality was appraised using the Critical Appraisal Skills Programme. Evidence was assessed through meta-analysis of readmission rates. Discrepancy identification rates, emergency department attendance and primary care workload were assessed narratively.ResultsFourteen studies were included, comprising five randomised controlled trials, six cohort studies and three pre–post intervention studies. Twelve studies had a moderate or high risk of bias. Increased identification and resolution of discrepancies was demonstrated in the four studies where this was evaluated. Reduction in clinically relevant discrepancies was reported in two studies. Meta-analysis did not demonstrate a significant reduction in readmission rate. There was no consistent evidence of reduction in emergency department attendance or primary care workload.ConclusionsPharmacists can identify and resolve discrepancies when completing medication reconciliation after hospital discharge, but patient outcome or care workload improvements were not consistently seen. Future research should examine the clinical relevance of discrepancies and potential benefits on reducing healthcare team workload.
H igh-density lipoprotein (HDL) particles play a pivotal role in reverse cholesterol transport (RCT) by facilitating cholesterol efflux from peripheral cells and delivering acquired lipid to the liver for elimination in the feces. 1 Obesity increases the risk of developing cardiovascular disease (CVD) 2 ; however, little is known about the impact of obesity on HDL function and RCT. Chronic inflammation is a classic hallmark of obesity 3 and CVD, 4 and it is plausible there is a common inflammatory-driven mechanism Background-Acute inflammation impairs reverse cholesterol transport (RCT) and reduces high-density lipoprotein (HDL) function in vivo. This study hypothesized that obesity-induced inflammation impedes RCT and alters HDL composition, and investigated if dietary replacement of saturated (SFA) for monounsaturated (MUFA) fatty acids modulates RCT. Methods and Results-Macrophage-to-feces RCT, HDL efflux capacity, and HDL proteomic profiling was determined in C57BL/6j mice following 24 weeks on SFA-or MUFA-enriched high-fat diets (HFDs) or low-fat diet. The impact of dietary SFA consumption and insulin resistance on HDL efflux function was also assessed in humans. Both HFDs increased plasma 3 H-cholesterol counts during RCT in vivo and ATP-binding cassette, subfamily A, member 1-independent efflux to plasma ex vivo, effects that were attributable to elevated HDL cholesterol. By contrast, ATP-binding cassette, subfamily A, member 1-dependent efflux was reduced after both HFDs, an effect that was also observed with insulin resistance and high SFA consumption in humans. SFA-HFD impaired liver-to-feces RCT, increased hepatic inflammation, and reduced ABC subfamily G member 5/8 and ABC subfamily B member 11 transporter expression in comparison with low-fat diet, whereas liver-to-feces RCT was preserved after MUFA-HFD. HDL particles were enriched with acute-phase proteins (serum amyloid A, haptoglobin, and hemopexin) and depleted of paraoxonase-1 after SFA-HFD in comparison with MUFA-HFD. Conclusions-Ex vivo efflux assays validated increased macrophage-to-plasma RCT in vivo after both HFDs but failed to capture differential modulation of hepatic cholesterol trafficking. By contrast, proteomics revealed the association of hepatic-derived inflammatory proteins on HDL after SFA-HFD in comparison with MUFA-HFD, which reflected differential hepatic cholesterol trafficking between groups. Acute-phase protein levels on HDL may serve as novel biomarkers of impaired liver-to-feces RCT in vivo. Correspondence to Fiona C. McGillicuddy, UCD Conway Institute, School of Medicine, University College Dublin, Dublin 4, Ireland. E-mail fiona.mcgillicuddy@ucd.ie © 2016 The Authors. Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited and is not used for commercial pur...
The role of metabolomics in the field of nutrition is continuing to grow and it has the potential to assist in the understanding of metabolic regulation and explain how minor perturbations can have a multitude of biochemical endpoints. It is this development, which creates the potential to provide the knowledge necessary to facilitate a more targeted approach to nutrition. In recent years, there has been interest in applying metabolomics to examine alterations in the metabolic profile according to weight gain/obesity. Emerging from these studies is the strong evidence that alterations in the amino acid (AA) profiles are associated with obesity. Several other studies have also shown a relationship between branched-chain amino acids (BCAA), obesity and insulin resistance. The present review focuses on the proposed link between AA and in particular BCAA, obesity and insulin resistance. In conclusion, a wealth of information is accumulating to support the role of AA, and in particular of the BCAA, in obesity. Metabolomics: Amino acids: BMI: Branched-chain amino acidsObesity is now considered as a major global health problem, and the WHO has demonstrated that obesity levels have reached epidemic proportions worldwide with approximately 2 . 3 billion adults predicted to be overweight or obese by the year 2015(1) . It is well recognised that obesity plays a central role in insulin resistance, the metabolic syndrome and type-2 diabetes mellitus. Despite many years of research the exact mechanisms underlying the role of obesity in the development of these disorders and diseases are still not fully elucidated. However, in recent years, the application of 'omic' technologies to studies comparing lean and obese subjects has enhanced our understanding of this research area. This review will focus on the literature, which has utilised metabolomic techniques to investigate the altered metabolic profile in obesity and the subsequent effect on insulin resistance. MetabolomicsMetabolomics is the comprehensive study of metabolites in biofluids, tissues or cellular extracts. The metabolic profile of a sample may be assessed using a variety of techniques including Proton NMR spectroscopy, LC-MS and GC-MS. The role of metabolomics in the field of nutrition is continuing to grow and its utility in a number of studies has been demonstrated (2,3) . Earlier applications of metabolomics in this field compared metabolic profiles of lean and obese subjects (Table 1). Pietiläinen et al.(4) investigated whether acquired obesity was associated with changes in global serum lipid profiles independent of genetic factors in young adult monozygotic twins. In this study, fourteen healthy monozygotic pairs discordant for obesity (10-25 kg weight Abbreviations: AA, amino acid; BCAA, branched-chain amino acid; GBP, gastric bypass surgery; HF, high fat.
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