scholarly journals Adipose Tissue Inflammation and Increased Ceramide Content Characterize Subjects With High Liver Fat Content Independent of Obesity

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


2020 ◽  
Vol 112 (2) ◽  
pp. 354-363
Author(s):  
Ilka Ratjen ◽  
Jakub Morze ◽  
Janna Enderle ◽  
Marcus Both ◽  
Jan Borggrefe ◽  
...  

ABSTRACT Background Better adherence to plant-based diets has been linked to lower risk of metabolic diseases but the effect on abdominal fat distribution and liver fat content is unclear. Objectives We aimed to examine the association between different plant-based diet indices and measures of abdominal fat distribution and liver fat content. Methods In a population-based sample of 578 individuals from Northern Germany (57% male, median age 62 y), diet was assessed with a validated FFQ and an overall, a healthy, and an unhealthy plant-based diet index were derived. Participants underwent MRI to assess volumes of visceral and subcutaneous abdominal adipose tissue and liver signal intensity (LSI), a measure of liver fat content. Fatty liver disease (FLD) was defined as log LSI ≥3.0. Cross-sectional associations of the plant-based diet indices with visceral and subcutaneous abdominal fat volumes, LSI, and FLD were assessed in linear and logistic regression analyses. The most comprehensive model adjusted for age, sex, education, smoking, alcohol, physical activity, energy intake, diabetes, hyperlipidemia, and BMI. Results Higher overall and healthy plant-based diet indices both revealed statistically significant associations with lower visceral and subcutaneous abdominal adipose tissue volumes and with lower odds of FLD in multivariable-adjusted models without BMI. Upon additional adjustment for BMI, only the association of the healthy plant-based diet with visceral adipose tissue remained statistically significant (per 10-point higher healthy plant-based diet index, percentage change in visceral adipose tissue: −4.9%, 95% CI: −8.6%, −2.0%). None of the plant-based diet indices was associated with LSI. The unhealthy plant-based diet index was unrelated to any of the abdominal or liver fat parameters. Conclusions Adherence to healthy plant-based diets was associated with lower visceral adipose tissue. None of the other examined associations remained statistically significant after adjustment for BMI.


2008 ◽  
Vol 295 (1) ◽  
pp. E85-E91 ◽  
Author(s):  
Ksenia Sevastianova ◽  
Jussi Sutinen ◽  
Katja Kannisto ◽  
Anders Hamsten ◽  
Matti Ristola ◽  
...  

In this cross-sectional study, we sought to determine whether gene expression of macrophage markers and inflammatory chemokines in lipoatrophic subcutaneous abdominal adipose tissue and liver fat content are increased and interrelated in human immunodeficiency virus (HIV)-1-positive, highly active antiretroviral therapy (HAART)-treated patients with lipodystrophy (HAART+LD+; n = 27) compared with those without (HAART+LD−; n = 13). The study groups were comparable with respect to age, gender, and body mass index. The HAART+LD+ group had twofold more intra-abdominal ( P = 0.01) and 1.5-fold less subcutaneous ( P = 0.091) fat than the HAART+LD− group. As we have reported previously, liver fat was 10-fold higher in the HAART+LD+ compared with the HAART+LD− group ( P = 0.00003). Inflammatory gene expression was increased in HAART-lipodystrophy: CD68 4.5-fold ( P = 0.000013), tumor necrosis factor (TNF)-α 2-fold ( P = 0.0094), chemokine (C-C motif) ligand (CCL) 2 2.5-fold ( P = 0.0024), CCL3 7-fold ( P = 0.0000017), integrin αM (ITGAM) 3-fold ( P = 0.00067), epidermal growth factor-like module containing, mucin-like, hormone receptor-like (EMR)1 2.5-fold ( P = 0.0038), and a disintegrin and metalloproteinase domain (ADAM)8 3.5-fold ( P = 0.00057) higher in the HAART+LD+ compared with the HAART+LD− group. mRNA concentration of CD68 ( r = 0.37, P = 0.019), ITGAM ( r = 0.35, P = 0.025), CCL2 ( r = 0.39, P = 0.012), and CCL3 ( r = 0.54, P = 0.0003) correlated with liver fat content. In conclusion, gene expression of markers of macrophage infiltration and adipose tissue inflammation is increased in lipoatrophic subcutaneous abdominal adipose tissue of patients with HAART-associated lipodystrophy compared with those without. CD68, ITGAM, CCL2, and CCL3 expression is significantly associated with accumulation of liver fat.


2011 ◽  
Vol 34 (6) ◽  
pp. 1205-1212 ◽  
Author(s):  
Markus M. Lindroos ◽  
Ronald Borra ◽  
Nina Mononen ◽  
Terho Lehtimäki ◽  
Kirsi A. Virtanen ◽  
...  

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 (&gt;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.


2017 ◽  
Vol 117 (02) ◽  
pp. 286-294 ◽  
Author(s):  
Susanna Lallukka ◽  
Panu K. Luukkonen ◽  
You Zhou ◽  
Elina Isokuortti ◽  
Marja Leivonen ◽  
...  

SummaryIncreased liver fat may be caused by insulin resistance and adipose tissue inflammation or by the common I148M variant in PNPLA3 at rs738409, which lacks both of these features. We hypothesised that obesity/insulin resistance rather than liver fat increases circulating coagulation factor activities. We measured plasma prothrombin time (PT, Owren method), activated partial thromboplastin time (APTT), activities of several coagulation factors, VWF:RCo and fibrinogen, and D-dimer concentration in 92 subjects divided into groups based on insulin sensitivity [insulin-resistant (‘IR’) versus insulin-sensitive (‘IS’)] and PNPLA3 genotype (PNPLA3148MM/MI vs PNPLA3148II). Liver fat content (1H-MRS) was similarly increased in ‘IR’ (13 ± 1 %) and PNPLA3148MM/MI (12 ± 2 %) as compared to ‘IS’ (6 ± 1 %, p < 0.05) and PNPLA3148II (8 ± 1 %, p < 0.05), respectively. FVIII, FIX, FXIII, fibrinogen and VWF:RCo activities were increased, and PT and APTT shortened in ‘IR’ versus ‘IS’, in contrast to these factors being similar between PNPLA3148MM/MI and PNPLA3148II groups. In subjects undergoing a liver biopsy and entirely lacking the I148M variant, insulin-resistant subjects had higher hepatic expression of F8, F9 and FGG than equally obese insulin-sensitive subjects. Expression of pro-inflammatory genes in adipose tissue correlated positively with PT (% of normal), circulating FVIII, FIX, FXI, VWR:RCo and fibrinogen, and expression of anti-inflammatory genes negatively with PT (%), FIX and fibrinogen. We conclude that obesity/insulin resistance rather than an increase in liver fat is associated with a procoagulant plasma profile. This reflects adipose tissue inflammation and increased hepatic production of coagulation factors and their susceptibility for activation.Supplementary Material to this article is available online at www.thrombosis-online.com.


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

2013 ◽  
pp. n/a-n/a
Author(s):  
Henry J. Jansen ◽  
Gerald M. Vervoort ◽  
Marinette van der Graaf ◽  
Rinke Stienstra ◽  
Cees J. Tack

2019 ◽  
Vol 104 (9) ◽  
pp. 4016-4023 ◽  
Author(s):  
Yeli Wang ◽  
Manja Koch ◽  
Romina di Giuseppe ◽  
Kirsten Evans ◽  
Jan Borggrefe ◽  
...  

Abstract Context CD36 is a class B scavenger-receptor involved in the uptake of fatty acids in liver and adipose tissue. It is unknown whether plasma CD36 levels are related to liver fat content or adipose tissue in the general population. Methods We measured plasma CD36 from 575 participants of the community-based PopGen cohort who underwent MRI to quantify visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and liver signal intensity (LSI), a proxy for liver fat content. Nonalcoholic fatty liver disease (NAFLD) was defined as LSI ≥3.0 in the absence of high alcohol intake. The relations between plasma CD36 and body mass index (BMI), VAT, SAT, LSI, and NAFLD were evaluated via multivariable-adjusted linear and logistic regression analysis. Results Plasma CD36 concentrations were correlated with BMI (r = 0.11; P = 0.01), SAT (r = 0.16; P &lt; 0.001), and VAT (r = 0.15, P &lt; 0.001) but not with LSI (P = 0.44). In multivariable-adjusted regression models, mean BMI values rose across CD36 quartiles [quartile 1 (Q1), 27.8 kg/m2; Q4, 28.9 kg/m2; P-trend = 0.013). Similarly, VAT (Q1, 4.13 dm3; Q4, 4.71 dm3; P-trend &lt; 0.001), and SAT (Q1, 7.61 dm3; Q4, 8.74 dm3; P-trend &lt; 0.001) rose across CD36 quartiles. Plasma CD36 concentrations were unrelated to LSI (P-trend = 0.36) and NAFLD (P-trend = 0.64). Participants with NAFLD and elevated alanine aminotransferase (ALT), a marker for liver damage, had higher CD36 compared with participants with NAFLD and normal ALT. Conclusions Higher plasma concentrations of CD36 were associated with greater general and abdominal adiposity but not with liver fat content or NAFLD in this community-based sample. However, plasma CD36 may reflect more severe liver damage in NAFLD.


Sign in / Sign up

Export Citation Format

Share Document