Liver fat content investigated by magnetic resonance spectroscopy in obese children and youths included in multidisciplinary treatment

2012 ◽  
Vol 2 (1-2) ◽  
pp. 41-49 ◽  
Author(s):  
D. S. Bille ◽  
E. Chabanova ◽  
M. Gamborg ◽  
C. E. Fonvig ◽  
T. R. H. Nielsen ◽  
...  

2014 ◽  
Vol 171 (5) ◽  
pp. 561-569 ◽  
Author(s):  
Daniel J Cuthbertson ◽  
Martin O Weickert ◽  
Daniel Lythgoe ◽  
Victoria S Sprung ◽  
Rebecca Dobson ◽  
...  

Background and aimsSimple clinical algorithms including the fatty liver index (FLI) and lipid accumulation product (LAP) have been developed as surrogate markers for non-alcoholic fatty liver disease (NAFLD), constructed using (semi-quantitative) ultrasonography. This study aimed to validate FLI and LAP as measures of hepatic steatosis, as determined quantitatively by proton magnetic resonance spectroscopy (1H-MRS).MethodsData were collected from 168 patients with NAFLD and 168 controls who had undergone clinical, biochemical and anthropometric assessment. Values of FLI and LAP were determined and assessed both as predictors of the presence of hepatic steatosis (liver fat >5.5%) and of actual liver fat content, as measured by 1H-MRS. The discriminative ability of FLI and LAP was estimated using the area under the receiver operator characteristic curve (AUROC). As FLI can also be interpreted as a predictive probability of hepatic steatosis, we assessed how well calibrated it was in our cohort. Linear regression with prediction intervals was used to assess the ability of FLI and LAP to predict liver fat content. Further validation was provided in 54 patients with type 2 diabetes mellitus.ResultsFLI, LAP and alanine transferase discriminated between patients with and without steatosis with an AUROC of 0.79 (IQR=0.74, 0.84), 0.78 (IQR=0.72, 0.83) and 0.83 (IQR=0.79, 0.88) respectively although could not quantitatively predict liver fat. Additionally, the algorithms accurately matched the observed percentages of patients with hepatic steatosis in our cohort.ConclusionsFLI and LAP may be used to identify patients with hepatic steatosis clinically or for research purposes but could not predict liver fat content.





Obesity ◽  
2009 ◽  
Vol 17 (12) ◽  
pp. 2239-2244 ◽  
Author(s):  
Mireille A. Edens ◽  
Peter M.A. van Ooijen ◽  
Wendy J. Post ◽  
Mark J.F. Haagmans ◽  
Wisnumurti Kristanto ◽  
...  


2009 ◽  
Vol 35 (8) ◽  
pp. S185
Author(s):  
Marcello Mancini ◽  
Anna Prinster ◽  
Raffaele Liuzzi ◽  
Gianni Annuzzi ◽  
Rosalba Giacco ◽  
...  




2009 ◽  
Vol 160 (4) ◽  
pp. 593-602 ◽  
Author(s):  
Anna Kotronen ◽  
Hannele Yki-Järvinen ◽  
Anna Aminoff ◽  
Robert Bergholm ◽  
Kirsi H Pietiläinen ◽  
...  

AimsWe investigated whether polymorphisms in candidate genes involved in lipid metabolism and type 2 diabetes are related to liver fat content.MethodsLiver fat content was measured using proton magnetic resonance spectroscopy (1H-MRS) in 302 Finns, in whom single nucleotide polymorphisms (SNPs) in acyl-CoA synthetase long-chain family member 4 (ACSL4), adiponectin receptors 1 and 2 (ADIPOR1andADIPOR2), and the three peroxisome proliferator-activated receptors (PPARA,PPARD, andPPARG) were analyzed. To validate our findings, SNPs significantly associated with liver fat content were studied in two independent cohorts and related to surrogate markers of liver fat content.ResultsIn the Finnish subjects, polymorphisms inACSL4(rs7887981),ADIPOR2(rs767870), andPPARG(rs3856806) were significantly associated with liver fat content measured with1H-MRS after adjusting for age, gender, and BMI. Anthropometric and circulating parameters were comparable between genotypes. In the first validation cohort of ∼ 600 Swedish men,ACSL4rs7887981 was related to fasting insulin and triglyceride concentrations, andADIPOR2rs767870 to serum γ glutamyltransferase concentrations after adjusting for BMI. The SNP inPPARG(rs3856806) was not significantly associated with any relevant metabolic parameter in this cohort. In the second validation cohort of ∼3000 subjects from Western Finland,ADIPOR2rs767870, but notACSL4rs7887981 was related to fasting triglyceride concentrations.ConclusionsGenetic variation, particularly in theADIPOR2gene, contributes to variation in hepatic fat accumulation in humans.



2015 ◽  
Vol 83 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Hongxi Zhang ◽  
Huiping Yang ◽  
Can Lai ◽  
Xiaoqin Xu ◽  
Ke Huang ◽  
...  


2018 ◽  
Vol 43 (6) ◽  
pp. 553-557
Author(s):  
Dong-Woo Kang ◽  
Ji-Hye Park ◽  
Mi Kyung Lee ◽  
YoonMyung Kim ◽  
In Deok Kong ◽  
...  

Nonalcoholic fatty liver disease is the most common chronic liver disease and can present with advanced fibrosis or nonalcoholic steatohepatitis. The purpose of this study was to investigate the effect of a 7-day intense physical activity intervention on liver fat content in children with obesity. Fifty-seven obese children (mean body mass index: 26.5 ± 3.2 kg/m2; mean age: 12.0 ± 0.8 years) participated in a 7-day physical activity program. All participants were housed together, and their food intake and energy expenditure were strictly controlled. Anthropometric measurements, abdominal computerized tomography scans, and blood analyses were conducted at baseline and post-intervention. Participants lost weight by 2.53 ± 0.85 kg on average (61.0 ± 9.8 vs. 58.5 ± 9.5 kg, p < 0.05), fat mass (16.7 ± 5.1 vs. 15.7 ± 4.9 kg, p < 0.05), and serum insulin (13.7 ± 6.7 vs. 3.5 ± 2.0 μU/mL, p < 0.05). However, liver fat content was increased, presented as liver-to-spleen ratio (LSR) where lower LSR represents higher liver fat content. The intervention increased aspartate transaminase level (29.42 ± 6.78 IU/L vs. 33.50 ± 9.60 IU/L, p < 0.001). The change in liver fat content was not associated with the change in fasting insulin and liver enzymes. Short-term intense physical activity increased liver fat content independent of change in fasting insulin level and liver enzymes. This is the first human study to report increased liver fat content after physical activity-induced rapid weight loss.



Sign in / Sign up

Export Citation Format

Share Document