Fatty liver in familial hypobetalipoproteinemia
Fatty liver is frequent in the apolipoprotein B (apoB)-defective genetic form of familial hypobetalipoproteinemia (FHBL), but interindividual variability in liver fat is large. To explain this, we assessed the roles of metabolic factors in 32 affected family members with apoB-defective FHBL and 33 r...
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Elsevier
2004-05-01
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Series: | Journal of Lipid Research |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520318356 |
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author | Tariq Tanoli Pin Yue Dmitriy Yablonskiy Gustav Schonfeld |
author_facet | Tariq Tanoli Pin Yue Dmitriy Yablonskiy Gustav Schonfeld |
author_sort | Tariq Tanoli |
collection | DOAJ |
description | Fatty liver is frequent in the apolipoprotein B (apoB)-defective genetic form of familial hypobetalipoproteinemia (FHBL), but interindividual variability in liver fat is large. To explain this, we assessed the roles of metabolic factors in 32 affected family members with apoB-defective FHBL and 33 related and unrelated normolipidemic controls matched for age, sex, and indices of adiposity. Two hour, 75 g oral glucose tests, with measurements of plasma glucose and insulin levels, body mass index, and waist-hip ratios were obtained. Abdominal subcutaneous, intraperitoneal (IPAT), and retroperitoneal adipose tissue masses were quantified by MR imaging, and hepatic fat was quantified by MR spectroscopy. Mean ± SD liver fat percentage values of FHBL and controls were 14.8 ± 12.0 and 5.2 ± 5.9, respectively (P = 0.001). Means for these measures of obesity and insulin action were similar in the two groups. Important determinants of liver fat percentage were FHBL-affected status, IPAT, and area under the curve (AUC) insulin in both groups, but the strongest predictors were IPAT in FHBL (partial R2 = 0.55, P < 0.0002) and AUC insulin in controls (partial R2 = 0.59, P = 0.0001). Regression of liver fat percentage on IPAT fat was significantly greater for FHBL than for controls (P < 0.001).In summary, because apoB-defective FHBL imparts heightened susceptibility to liver triglyceride accumulation, increasing IPAT and insulin resistance exert greater liver fat-increasing effects in FHBL. |
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spelling | doaj.art-a93f6fb7a65a460daa1e731aeda8a2932022-12-21T22:09:43ZengElsevierJournal of Lipid Research0022-22752004-05-01455941947Fatty liver in familial hypobetalipoproteinemiaTariq Tanoli0Pin Yue1Dmitriy Yablonskiy2Gustav Schonfeld3Departments of Internal Medicine and Radiology, Washington University School of Medicine, St. Louis, MODepartments of Internal Medicine and Radiology, Washington University School of Medicine, St. Louis, MODepartments of Internal Medicine and Radiology, Washington University School of Medicine, St. Louis, MODepartments of Internal Medicine and Radiology, Washington University School of Medicine, St. Louis, MOFatty liver is frequent in the apolipoprotein B (apoB)-defective genetic form of familial hypobetalipoproteinemia (FHBL), but interindividual variability in liver fat is large. To explain this, we assessed the roles of metabolic factors in 32 affected family members with apoB-defective FHBL and 33 related and unrelated normolipidemic controls matched for age, sex, and indices of adiposity. Two hour, 75 g oral glucose tests, with measurements of plasma glucose and insulin levels, body mass index, and waist-hip ratios were obtained. Abdominal subcutaneous, intraperitoneal (IPAT), and retroperitoneal adipose tissue masses were quantified by MR imaging, and hepatic fat was quantified by MR spectroscopy. Mean ± SD liver fat percentage values of FHBL and controls were 14.8 ± 12.0 and 5.2 ± 5.9, respectively (P = 0.001). Means for these measures of obesity and insulin action were similar in the two groups. Important determinants of liver fat percentage were FHBL-affected status, IPAT, and area under the curve (AUC) insulin in both groups, but the strongest predictors were IPAT in FHBL (partial R2 = 0.55, P < 0.0002) and AUC insulin in controls (partial R2 = 0.59, P = 0.0001). Regression of liver fat percentage on IPAT fat was significantly greater for FHBL than for controls (P < 0.001).In summary, because apoB-defective FHBL imparts heightened susceptibility to liver triglyceride accumulation, increasing IPAT and insulin resistance exert greater liver fat-increasing effects in FHBL.http://www.sciencedirect.com/science/article/pii/S0022227520318356abdominal adipose tissueinsulin resistanceapolipoprotein B |
spellingShingle | Tariq Tanoli Pin Yue Dmitriy Yablonskiy Gustav Schonfeld Fatty liver in familial hypobetalipoproteinemia Journal of Lipid Research abdominal adipose tissue insulin resistance apolipoprotein B |
title | Fatty liver in familial hypobetalipoproteinemia |
title_full | Fatty liver in familial hypobetalipoproteinemia |
title_fullStr | Fatty liver in familial hypobetalipoproteinemia |
title_full_unstemmed | Fatty liver in familial hypobetalipoproteinemia |
title_short | Fatty liver in familial hypobetalipoproteinemia |
title_sort | fatty liver in familial hypobetalipoproteinemia |
topic | abdominal adipose tissue insulin resistance apolipoprotein B |
url | http://www.sciencedirect.com/science/article/pii/S0022227520318356 |
work_keys_str_mv | AT tariqtanoli fattyliverinfamilialhypobetalipoproteinemia AT pinyue fattyliverinfamilialhypobetalipoproteinemia AT dmitriyyablonskiy fattyliverinfamilialhypobetalipoproteinemia AT gustavschonfeld fattyliverinfamilialhypobetalipoproteinemia |