Abstract：
Genetic mutations causing defective VLDL secretion and low LDL cholesterol are associated with hepatic steatosis and nonalcoholic fatty liver disease (NAFLD).
Determine if low LDL cholesterol (< 5th percentile) was an independent predictor of hepatic steatosis.
Secondary data analysis of the Dallas Heart study (an urban, multiethnic, probability-based sample), we defined hepatic steatosis utilizing intrahepatic triglyceride (IHTG) analyzed using magnetic resonance spectroscopy in conjunction and available demographic, serological and genetic information. We exclude patients on lipid lowering medications.
Of the 2094 subjects that met our exclusion criteria, 86 had a low LDL cholesterol, of whom 19 (22%) exhibited hepatic steatosis. After matching for age, sex, BMI, and alcohol consumption, low LDL cholesterol was not a risk factor for hepatic steatosis compared to those with normal (50-180 mg/dL) or high (> 180 mg/dL) LDL. When analyzed as a continuous variable, we observed lower IHTG in the low LDL group compared to the normal or high LDL groups (2.2%, 3.5%, 4.6%; all pairwise comparisons p < 0.001). Subjects with both hepatic steatosis and low LDL cholesterol exhibited a more favorable lipid profile but similar insulin resistance and hepatic fibrosis risk compared to other subjects with hepatic steatosis. The distribution of variant alleles associated with NAFLD, including PNPLA3, GCKR, and MTTP was indistinguishable between subjects with hepatic steatosis and low versus high LDL cholesterol.
These findings suggest that low serum LDL levels are not a useful predictor of hepatic steatosis and NAFLD. Moreover, subjects with low LDL exhibit a more favorable lipid profile and lower IHTG.
Determine if low LDL cholesterol (< 5th percentile) was an independent predictor of hepatic steatosis.
Secondary data analysis of the Dallas Heart study (an urban, multiethnic, probability-based sample), we defined hepatic steatosis utilizing intrahepatic triglyceride (IHTG) analyzed using magnetic resonance spectroscopy in conjunction and available demographic, serological and genetic information. We exclude patients on lipid lowering medications.
Of the 2094 subjects that met our exclusion criteria, 86 had a low LDL cholesterol, of whom 19 (22%) exhibited hepatic steatosis. After matching for age, sex, BMI, and alcohol consumption, low LDL cholesterol was not a risk factor for hepatic steatosis compared to those with normal (50-180 mg/dL) or high (> 180 mg/dL) LDL. When analyzed as a continuous variable, we observed lower IHTG in the low LDL group compared to the normal or high LDL groups (2.2%, 3.5%, 4.6%; all pairwise comparisons p < 0.001). Subjects with both hepatic steatosis and low LDL cholesterol exhibited a more favorable lipid profile but similar insulin resistance and hepatic fibrosis risk compared to other subjects with hepatic steatosis. The distribution of variant alleles associated with NAFLD, including PNPLA3, GCKR, and MTTP was indistinguishable between subjects with hepatic steatosis and low versus high LDL cholesterol.
These findings suggest that low serum LDL levels are not a useful predictor of hepatic steatosis and NAFLD. Moreover, subjects with low LDL exhibit a more favorable lipid profile and lower IHTG.
摘要：
背景：导致VLDL分泌缺陷和低LDL胆固醇的基因突变与肝性脂肪变性和非酒精性脂肪性肝病（NAFLD）相关。
目标：确定低LDL胆固醇（<5百分位数）是否是肝脂肪变性的独立预测因子。
方法：达拉斯心脏研究的次要数据分析(城市，多民族,基于概率的样本)，我们使用结合磁共振波谱分析的肝内甘油三酯（IHTG）和可用的人口统计学定义肝脂肪变性，血清学和遗传信息。我们排除了服用降脂药物的患者。
结果：在符合我们排除标准的2094名受试者中，86有一个低低密度脂蛋白胆固醇，其中19人（22％）表现为肝脂肪变性。年龄匹配后，性别,BMI,和酒精消费，与正常（50-180mg/dL）或高（>180mg/dL）LDL患者相比，低LDL胆固醇不是肝脂肪变性的危险因素。当作为连续变量分析时，我们观察到低LDL组的IHTG低于正常或高LDL组（2.2％，3.5%,4.6%；所有成对比较p<0.001)。与其他患有肝性脂肪变性的受试者相比，患有肝性脂肪变性和低LDL胆固醇的受试者表现出更有利的脂质特征，但胰岛素抵抗和肝纤维化风险相似。与NAFLD相关的变异等位基因的分布，包括PNPLA3、GCKR、和MTTP在肝性脂肪变性和低LDL胆固醇与高LDL胆固醇之间没有区别。
结论：这些研究结果表明，低血清LDL水平不是肝脂肪变性和NAFLD的有用预测因子。此外，具有低LDL的受试者表现出更有利的脂质分布和更低的IHTG。
目标：确定低LDL胆固醇（<5百分位数）是否是肝脂肪变性的独立预测因子。
方法：达拉斯心脏研究的次要数据分析(城市，多民族,基于概率的样本)，我们使用结合磁共振波谱分析的肝内甘油三酯（IHTG）和可用的人口统计学定义肝脂肪变性，血清学和遗传信息。我们排除了服用降脂药物的患者。
结果：在符合我们排除标准的2094名受试者中，86有一个低低密度脂蛋白胆固醇，其中19人（22％）表现为肝脂肪变性。年龄匹配后，性别,BMI,和酒精消费，与正常（50-180mg/dL）或高（>180mg/dL）LDL患者相比，低LDL胆固醇不是肝脂肪变性的危险因素。当作为连续变量分析时，我们观察到低LDL组的IHTG低于正常或高LDL组（2.2％，3.5%,4.6%；所有成对比较p<0.001)。与其他患有肝性脂肪变性的受试者相比，患有肝性脂肪变性和低LDL胆固醇的受试者表现出更有利的脂质特征，但胰岛素抵抗和肝纤维化风险相似。与NAFLD相关的变异等位基因的分布，包括PNPLA3、GCKR、和MTTP在肝性脂肪变性和低LDL胆固醇与高LDL胆固醇之间没有区别。
结论：这些研究结果表明，低血清LDL水平不是肝脂肪变性和NAFLD的有用预测因子。此外，具有低LDL的受试者表现出更有利的脂质分布和更低的IHTG。
