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Articles by M Wright
Total Records ( 3 ) for M Wright
  C Glicksman , D. J Pournaras , M Wright , R Roberts , D Mahon , R Welbourn , R Sherwood , J Alaghband Zadeh and C. W. le Roux
  Background

Bile acids can act as signalling molecules via various receptors including the nuclear farnesoid X receptor (FXR) and pregnane X receptor (PXR), and the cell surface G-protein-coupled receptor TGR5. The signalling has been implicated in the release of peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), which improves glycaemic control and energy expenditure. We investigated whether morbidly obese subjects have altered postprandial bile acid responses in comparison to normal weight subjects.

Method

Blood samples were taken every 30 min from 0 to 180 min following a 400 kcal test meal. Samples were taken from 12 normal weight subjects with a body mass index (BMI) of 23.2 (2.8) kg/m2 (median [interquartile range (IQR)]) and seven obese patients with a BMI of 47.2 (7.2) kg/m2. Fractionated bile acids were measured on these samples using high-performance liquid chromatography tandem mass spectrometry.

Results

The obese subjects showed a lower postprandial response in total bile acids compared with the normal weight subjects. An increase of 6.4 (5.0) and 2.6 (3.3) µmol/L (median [IQR]) in normal weight and obese subjects was observed, respectively (P = 0.02). The difference was predominantly due to the glycine-conjugated fraction (P = 0.03). There was no difference in the increase of the unconjugated or taurine-conjugated fractions.

Conclusions

The decreased postprandial bile acid response in obese subjects compared with normal weight subjects may partly explain the suboptimal GLP-1 and PYY responses and could affect appetite, glycaemic control and energy expenditure.

  Peterson The NIH HMP Working Group , S Garges , M Giovanni , P McInnes , L Wang , J. A Schloss , V Bonazzi , J. E McEwen , K. A Wetterstrand , C Deal , C. C Baker , V Di Francesco , T. K Howcroft , R. W Karp , R. D Lunsford , C. R Wellington , T Belachew , M Wright , C Giblin , H David , M Mills , R Salomon , C Mullins , B Akolkar , L Begg , C Davis , L Grandison , M Humble , J Khalsa , A. R Little , H Peavy , C Pontzer , M Portnoy , M. H Sayre , P Starke Reed , S Zakhari , J Read , B Watson and M. Guyer
 

The Human Microbiome Project (HMP), funded as an initiative of the NIH Roadmap for Biomedical Research (http://nihroadmap.nih.gov), is a multi-component community resource. The goals of the HMP are: (1) to take advantage of new, high-throughput technologies to characterize the human microbiome more fully by studying samples from multiple body sites from each of at least 250 "normal" volunteers; (2) to determine whether there are associations between changes in the microbiome and health/disease by studying several different medical conditions; and (3) to provide both a standardized data resource and new technological approaches to enable such studies to be undertaken broadly in the scientific community. The ethical, legal, and social implications of such research are being systematically studied as well. The ultimate objective of the HMP is to demonstrate that there are opportunities to improve human health through monitoring or manipulation of the human microbiome. The history and implementation of this new program are described here.

  A Bouissou , C Verollet , A Sousa , P Sampaio , M Wright , C. E Sunkel , A Merdes and B. Raynaud Messina
 

Independently of their nucleation activity, -tubulin ring complex proteins localize along microtubules, limiting catastrophe events during interphase.

 
 
 
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