owl liver publications
Obesity-dependent metabolic signatures associated with nonalcoholic Fatty liver disease progression.
We studied 467 biopsied individuals with normal liver histology or diagnosed with NAFLD. Qualitative determinations of 540 serum metabolite variables were performed using UPLC-MS. The metabolic profile was dependent on patient body-mass index (BMI), suggesting that the NAFLD pathogenesis mechanism may be quite different depending on an individual's level of obesity. A BMI-stratified multivariate model based on the NAFLD serum metabolic profile was used to separate patients with and without NASH. The area under the receiver operating characteristic curve was 0.87 in the estimation and 0.85 in the validation group. The cutoff (0.54) corresponding to maximum average diagnostic accuracy (0.82) predicted NASH with a sensitivity of 0.71 and a specificity of 0.92 (negative/positive predictive values = 0.82/0.84).
Journal of Proteome Research 2012, 11,2521-2532
Nonalcoholic fatty liver disease (NAFLD) is a
common liver disease associated with obesity
and insulin resistance. Due to the rising
prevalence of obesity and diabetes, NAFLD is presently
the most common cause of liver disease in the
Western world, both in adults and children. The prevalence
of NAFLD in Western adults is between 20%
and 30%. NAFLD associates with increased hepaticrelated
mortality. NAFLD ranges from the simple
accumulation of triacylglycerol (TAG) in the liver
(hepatic steatosis) to nonalcoholic steatohepatitis
(NASH), which is characterized by steatosis, hepatocyte
ballooning, scattered inflammation, fibrosis, and
necrosis.
Hepatology 54,4,1115-1117
This article describes a parallel animal model / human NAFLD exploratory metabolomics study, using ultra performance liquid chromatography-mass spectrometry (UPLC®-MS) to analyze 42 serum samples collected from non-diabetic, morbidly obese, biopsy-proven NAFLD patients, and 17 animals belonging to the glycine Nmethyltransferase knockout (GNMT-KO) NAFLD mouse model. Many of the altered metabolites observed could be associated with biochemical perturbations associated with liver dysfunction (e.g. reduced Creatine) and inflammation (e.g. eicosanoid signaling).
Journal of Proteome Research 2010, 9,4501-4512.
DOI: 10.1021/pr1002593
J. Caballería(1), J. Barr (2), A. Domínguez-Diez(3), A. Martin-Duce(4), O. Lo Iacono(5), Y. Le Marchand-Brustel(6), SC. Lu(7), and JM. Mato (8)
(1) Unidad de Hepatología, Hospital Clinic, Ciberehd. Barcelona. (2) OWL Genomics. Derio, (3) Hospital Universitario Marques de Valdecilla. Universidad de Cantabria. Santander, (4) Hospital de Alcalá de Henares Universidad de. Madrid, (5) Hospital del Tajo. Aranjuez, Madrid, (6) Institut National de la Sante et de la Recherche Medicale (INSERM). Nice, France. (7) Division of Gastrointestinal and Liver diseases, USC. Los Angeles, USA. (8) CIC bioGUNE, Unidad de Metabolomica. Ciberehd. Derio.
Gastroenterología y Hepatogía. Volumen 33, Especial Congreso AEEH. Febrero 2010.