Evidence map›Paper›PMID 27051590›Full record

ArticleBBA clinical2016

Diabetic and dyslipidaemic morbidly obese exhibit more liver alterations compared with healthy morbidly obese.

Eva Pardina, Roser Ferrer, Joana Rossell, Juan Antonio Baena-Fustegueras, Albert Lecube, Jose Manuel Fort, Enric Caubet, Óscar González, Ramón Vilallonga, Víctor Vargas and 2 more

Abstract read
In one paragraph

Article in BBA clinical, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Trial
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  3. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Eva PardinaBiochemistry and Molecular Biology Department, Biology Faculty, Barcelona University, Spain.
Roser FerrerBiochemistry Department, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Joana RossellBiochemistry and Molecular Biology Department, Biology Faculty, Barcelona University, Spain.
Juan Antonio Baena-FusteguerasSurgery Unit, Arnau de Vilanova University Hospital (UdL), Spain.
Albert LecubeEndocrinology and Nutrition Department, Arnau de Vilanova University Hospital (UdL), Diabetes and Metabolism Research Unit (VHIR, UAB), CIBER de Diabetes y Enfermedades Metabólicas (CIBERDEM) del Instituto de Salud Carlos III, Spain.
Jose Manuel FortEndocrinology Surgery Unit, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Enric CaubetEndocrinology Surgery Unit, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Óscar GonzálezEndocrinology Surgery Unit, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Ramón VilallongaEndocrinology Surgery Unit, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Víctor VargasCIBER de Enfermedades Hepáticas y Digestivas (CIBEREHD) del Instituto de Salud Carlos III (ISCIII), Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
José María BalibreaEndocrinology Surgery Unit, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Spain.
Julia Peinado-OnsurbeBiochemistry and Molecular Biology Department, Biology Faculty, Barcelona University, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsTo 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.

methodsThirty-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.

resultsThe 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.

conclusionsHepatic 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.

Indexed as

ALT, Alanine transaminaseApoA1, Apolipoprotein A1apoB, Apolipoprotein BAST, Aspartate transaminaseATGL, Adipose Tissue Glycerol LipaseBMI, Body Mass IndexcHDL, High-Density Lipoprotein CholesterolcLDL, Low-Density Lipoprotein CholesterolCPT1a, Carnitine Palmitoyltransferase 1aCRP, C-reactive proteinCYP7a1, Cholesterol 7 Alpha-HydroxylaseDiabetesDL, DyslipidaemiaDM − DL +,  Dyslipidemic obese patientsDM − DL −, “Healthy” obese patients, or patients without type 2 diabetes or dyslipidaemiaDM + DL +,  Obese patients with type 2 diabetes and dyslipidaemiaDM, Type 2 diabetes mellituseNOS3, Endothelial Nitric Oxide Synthase 3FAT/CD36, Fatty Acid Translocase or Cluster of Differentiation 36GGT, gamma-glutaryl transferaseHL, Hepatic lipaseHMGCR, 3-Hydroxy-3-Methylglutaryl-CoA ReductaseHOMA-IR, Homeostasis Model Assessment of Insulin ResistanceHSL, Hormone-sensitive lipaseHTA, HypertensionIL6, Interleukin-6iNOS2, Inducible Nitric Oxide Synthase 2IR, Insulin resistanceKBs, Ketone bodiesLDLr, Low-Density Lipoprotein receptorLipasesLipidsLiverMO, Morbidly obeseNAFLDNAFLD, Non-alcoholic fatty liver diseaseNASH, Non-alcoholic liver steatohepatitisNEFA, Non-esterified fatty acidPAI1, Plasminogen Activator Inhibitor of Type 1PLs, PhospholipidsPPARα, Peroxisome Proliferator-Activated Receptor alphaPPARα, Peroxisome Proliferator-Activated Receptor gamma Coactivator 1-alphaQMs, ChylomicronsRYGBP, Roux-en-Y gastric bypassSAT, Subcutaneous adipose tissueSCARB1, Scavenger Receptor Class B, Member 1SteatosisTAGs, TriacylglyceridesTC, Total cholesterolTNFα, Tumour Necrosis Factor-alphaUCP2, Uncoupling Protein 2VAT, Visceral adipose tissueVLDLr, Very-Low-Density Lipoprotein receptor

Identifiers

PMID27051590
PMCPMC4802404

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.