scholarly journals Postprandial Lipemia Associates with Liver Fat Content

2007 ◽  
Vol 92 (8) ◽  
pp. 3052-3059 ◽  
Author(s):  
Niina Matikainen ◽  
Sakari Mänttäri ◽  
Jukka Westerbacka ◽  
Satu Vehkavaara ◽  
Nina Lundbom ◽  
...  

Abstract Context/Objective: Postprandial lipemia and low adiponectin represent novel risk factors for vascular disease. This study aimed to determine whether liver fat content and adiponectin are predictors of postprandial triglyceride (TG)-rich lipoproteins (TRL). Patients/Interventions: Twenty-nine men were allocated into subgroups with either low (≤5%) or high (>5%) liver fat measured with magnetic resonance proton spectroscopy. Subjects underwent an oral fat tolerance test with measurements of postprandial TG, cholesterol, apolipoprotein B-48 (apoB-48), and apoB-100 in TRL fractions, a euglycemic hyperinsulinemic clamp, and determination of abdominal fat volumes by magnetic resonance imaging. Results: Subjects with high liver fat displayed increased response of postprandial lipids in plasma, chylomicron, and very-low-density lipoprotein 1 (VLDL1) (Svedberg flotation rate 60–400) fractions. Liver fat correlated positively with postprandial responses (area under the curve) of TG (r = 0.597; P = 0.001), cholesterol (r = 0.546; P = 0.002), apoB-48 (r = 0.556; P = 0.002), and apoB-100 (r = 0.42; P = 0.023) in the VLDL1 fraction. Respective incremental areas under the curve correlated significantly with liver fat. Fasting adiponectin levels were inversely correlated with both postprandial lipids and liver fat content. Liver fat remained the only independent correlate in a multiple linear regression analysis for chylomicron and VLDL1 responses. Conclusions: Liver fat content is a close correlate of postprandial lipids predicting the responses of TRL in chylomicrons and VLDL1 better than measures of glucose metabolism or body adiposity. Low adiponectin concentration is closely linked to high liver fat content and impaired TRL metabolism. High liver fat content associated with postprandial lipemia represents potential risk factors for cardiovascular disease.


2006 ◽  
Vol 291 (2) ◽  
pp. E282-E290 ◽  
Author(s):  
Riikka Lautamäki ◽  
Ronald Borra ◽  
Patricia Iozzo ◽  
Markku Komu ◽  
Terho Lehtimäki ◽  
...  

Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [15O]H2O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[18F]fluoro-d-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 ± 2.0%) and high (17.4 ± 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level ( P = 0.012) and muscle ( P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake ( P = 0.040) and glucose extraction rate ( P = 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 ( P < 0.05) and lower coronary flow reserve ( P = 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function.





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.



2017 ◽  
Vol 234 (12) ◽  
pp. 1923-1932 ◽  
Author(s):  
Jong-Hoon Kim ◽  
Jung-Hyun Kim ◽  
Pil-Whan Park ◽  
Jürgen Machann ◽  
Michael Roden ◽  
...  




2011 ◽  
Vol 35 (5) ◽  
pp. 1112-1118 ◽  
Author(s):  
Vasco Herédia ◽  
Miguel Ramalho ◽  
Rafael O.P. de Campos ◽  
Brian Dale ◽  
Rafael Azevedo ◽  
...  


Diabetes ◽  
2007 ◽  
Vol 56 (8) ◽  
pp. 1960-1968 ◽  
Author(s):  
Maria Kolak ◽  
Jukka Westerbacka ◽  
Vidya R. Velagapudi ◽  
Dick Wågsäter ◽  
Laxman Yetukuri ◽  
...  


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