Web of Science: 9 citas, Scopus: 9 citas, Google Scholar: citas,
Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese
Pardina, Eva (Universitat de Barcelona.Departament de Bioquímica i Biologia molecular)
Ferrer, Roser (Hospital Universitari Vall d'Hebron)
Rossell, Joana (Universitat de Barcelona.Departament de Bioquímica i Biologia molecular)
Baena-Fustegueras, Juan Antonio (Hospital Universitari Arnau de Vilanova. Unitat de Cirurgia.Universitat de Lleida)
Lecube, Albert (Hospital Universitari Arnau de Vilanova. Departament d'Endocrinologia i Nutrició. Universitat de Lleida. Diabetes and Metabolism Research Unit (VHIR, UAB), CIBER de Diabetes y Enfermedades Metabólicas (CIBERDEM) del Instituto de Salud Carlos III)
Fort, Jose Manuel (Hospital Universitari Vall D'Hebron, Unitat de Cirurgia endocrinològica)
Caubet, Enric (Hospital Universitari Vall D'Hebron, Unitat de Cirurgia endocrinològica)
González López, Óscar (Hospital Universitari Vall D'Hebron, Unitat de Cirurgia endocrinològica)
Vilallonga, Ramón (Hospital Universitari Vall D'Hebron, Unitat de Cirurgia endocrinològica)
Vargas, Víctor (CIBER de Enfermedades Hepáticas y Digestivas (CIBEREHD) del Instituto de Salud Carlos III (ISCIII), Hospital Universitari Vall D'Hebron)
Balibrea, José María (Hospital Universitari Vall D'Hebron, Unitat de Cirurgia endocrinològica)
Peinado-Onsurbe, Julia (Universitat de Barcelona.Departament de Bioquímica i Biologia molecular)
Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular

Fecha: 2016
Resumen: To study the origin of fat excess in the livers of morbidly obese (MO) individuals, we analysed lipids and lipases in both plasma and liver and genes involved in lipid transport, or related with, in that organ. Thirty-two MO patients were grouped according to the absence (healthy: DM − DL −) or presence of comorbidities (dyslipidemic: DM − DL +; or dyslipidemic with type 2 diabetes: DM + DL +) before and one year after gastric bypass. The livers of healthy, DL and DM patients contained more lipids (9. 8, 9. 5 and 13. 7 times, respectively) than those of control subjects. The genes implicated in liver lipid uptake, including HL, LPL, VLDLr, and FAT / CD36, showed increased expression compared with the controls. The expression of genes involved in lipid-related processes outside of the liver, such as apoB, PPARα and PGC1α, CYP7a1 and HMGCR, was reduced in these patients compared with the controls. PAI1 and TNFα gene expression in the diabetic livers was increased compared with the other obese groups and control group. Increased steatosis and fibrosis were also noted in the MO individuals. Hepatic lipid parameters in MO patients change based on their comorbidities. The gene expression and lipid levels after bariatric surgery were less prominent in the diabetic patients. Lipid receptor overexpression could enable the liver to capture circulating lipids, thus favouring the steatosis typically observed in diabetic and dyslipidaemic MO individuals.
Nota: Número d'acord de subvenció ISCIII/PI030024, PI030042, PI070079 I PI11/01159
Derechos: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, i la comunicació pública de l'obra, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. No es permet la creació d'obres derivades. Creative Commons
Lengua: Anglès
Documento: article ; recerca ; publishedVersion
Materia: DM − DL −, "Healthy" obese patients, or patients without type 2 diabetes or dyslipidaemia ; DM − DL +, Dyslipidemic obese patients ; DM + DL +, Obese patients with type 2 diabetes and dyslipidaemia ; HL, Hepatic lipase ; VLDLr, Very-Low-Density Lipoprotein receptor ; FAT/CD36, Fatty Acid Translocase or Cluster of Differentiation 36 ; LDLr, Low-Density Lipoprotein receptor ; ApoB, Apolipoprotein B ; PPARα, Peroxisome Proliferator-Activated Receptor alpha ; PPARα, Peroxisome Proliferator-Activated Receptor gamma Coactivator 1-alpha ; CYP7a1, Cholesterol 7 Alpha-Hydroxylase ; HMGCR, 3-Hydroxy-3-Methylglutaryl-CoA Reductase ; PAI1, Plasminogen Activator Inhibitor of Type 1 ; TNFα, Tumour Necrosis Factor-alpha ; ATGL, Adipose Tissue Glycerol Lipase ; SCARB1, Scavenger Receptor Class B, Member 1 ; CPT1a, Carnitine Palmitoyltransferase 1a ; UCP2, Uncoupling Protein 2 ; INOS2, Inducible Nitric Oxide Synthase 2 ; ENOS3, Endothelial Nitric Oxide Synthase 3 ; IL6, Interleukin-6 ; TAGs, Triacylglycerides ; NAFLD, Non-alcoholic fatty liver disease ; IR, Insulin resistance ; NASH, Non-alcoholic liver steatohepatitis ; MO, Morbidly obese ; BMI, Body Mass Index ; DM, Type 2 diabetes mellitus ; DL, Dyslipidaemia ; RYGBP, Roux-en-Y gastric bypass ; HTA, Hypertension ; HOMA-IR, Homeostasis Model Assessment of Insulin Resistance ; PLs, Phospholipids ; TC, Total cholesterol ; CLDL, Low-Density Lipoprotein Cholesterol ; CHDL, High-Density Lipoprotein Cholesterol ; NEFA, Non-esterified fatty acid ; AST, Aspartate transaminase ; ALT, Alanine transaminase ; GGT, gamma-glutaryl transferase ; CRP, C-reactive protein ; KBs, Ketone bodies ; ApoA1, Apolipoprotein A1 ; HSL, Hormone-sensitive lipase ; QMs, Chylomicrons ; SAT, Subcutaneous adipose tissue ; VAT, Visceral adipose tissue ; Steatosis ; NAFLD ; Liver ; Lipases ; Diabetes ; Lipids
Publicado en: BBA Clinical, Vol. 5 (january 2016) , p. 54-65, ISSN 2214-6474

DOI: 10.1016/j.bbacli.2015.12.002
PMID: 27051590

12 p, 843.5 KB

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