Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese
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 pres...
| Autores: | , , , , , , , , , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2016 |
| País: | España |
| Institución: | Universitat Autònoma de Barcelona |
| Repositorio: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglés |
| OAI Identifier: | oai:ddd.uab.cat:185845 |
| Acceso en línea: | https://ddd.uab.cat/record/185845 https://dx.doi.org/urn:doi:10.1016/j.bbacli.2015.12.002 |
| Access Level: | acceso abierto |
| Palabra clave: | 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 |
| Sumario: | 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. |
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