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| Página principal > Artículos > Artículos publicados > Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese |
(Universitat de Barcelona. Departament de Bioquímica i Biologia Molecular) (Hospital Universitari Vall d'Hebron. Institut de Recerca) (Hospital Universitari Vall d'Hebron) (Hospital Universitari Vall d'Hebron) (Hospital Universitari Vall d'Hebron)| 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. |
| Ayudas: | Instituto de Salud Carlos III PI030024 Instituto de Salud Carlos III PI030042 Instituto de Salud Carlos III PI070079 Instituto de Salud Carlos III 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.  |
| Lengua: | Anglès |
| Documento: | Article ; recerca ; Versió publicada |
| 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 |
