首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Liver Fat Measured by MR Spectroscopy: Estimate of Imprecision and Relationship with Serum Glycerol Caeruloplasmin and Non-Esterified Fatty Acids
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Liver Fat Measured by MR Spectroscopy: Estimate of Imprecision and Relationship with Serum Glycerol Caeruloplasmin and Non-Esterified Fatty Acids

机译:MR光谱法测定肝脂肪:不精确性及其与血清甘油铜蓝蛋白和非酯化脂肪酸的关系

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摘要

Magnetic resonance spectroscopy (MRS) is a non-invasive method for quantitative estimation of liver fat. Knowledge of its imprecision, which comprises biological variability and measurement error, is required to design therapeutic trials with measurement of change. The role of adipocyte lipolysis in ectopic fat accumulation remains unclear. We examined the relationship between liver fat content and indices of lipolysis, and determine whether lipolysis reflects insulin resistance or metabolic liver disease. Imprecision of measurement of liver fat was estimated from duplicate measurements by MRS at one month intervals. Patients provided fasting blood samples and we examined the correlation of liver fat with indices of insulin resistance, lipolysis and metabolic liver disease using Kendall Tau statistics. The coefficient of variation of liver fat content was 14.8%. Liver fat was positively related to serum insulin (T = 0.48, p = 0.042), homeostasis model assessment (HOMA)-B% (T = −0.48, p = 0.042), and body mass index (BMI) (T = 0.59, p = 0.012); and inversely related to HOMA-S% (T = −0.48, p = 0.042), serum glycerol (T = −0.59, p = 0.014), and serum caeruloplasmin (T = 0.055, p = 0.047). Our estimate of total variability in liver fat content (14.8%) is nearly twice that of the reported procedural variability (8.5%). We found that liver fat content was significantly inversely related to serum glycerol but not to non-esterified fatty acids (NEFA), suggesting progressive suppression of lipolysis. Reduction of caeruloplasmin with increasing liver fat may be a consequence or a cause of hepatic steatosis.
机译:磁共振波谱(MRS)是一种定量评估肝脂肪的非侵入性方法。设计具有变化测量值的治疗性试验需要了解其不精确性,其中包括生物变异性和测量误差。脂肪细胞脂解在异位脂肪积累中的作用尚不清楚。我们检查了肝脂肪含量与脂解指数之间的关系,并确定脂解是否反映胰岛素抵抗或代谢性肝病。肝脂肪测量的不精确度是由MRS每隔一个月进行一次重复测量得出的。患者提供了空腹血液样本,我们使用Kendall Tau统计数据检查了肝脂肪与胰岛素抵抗,脂解和代谢性肝病指数的相关性。肝脂肪含量的变异系数为14.8%。肝脂肪与血清胰岛素(T = 0.48,p = 0.042),体内稳态模型评估(HOMA)-B%(T = -0.48,p = 0.042)和体重指数(BMI)(T = 0.59, p = 0.012);与HOMA-S%(T = -0.48,p = 0.042),血清甘油(T = -0.59,p = 0.014)和血清铜蓝蛋白(T = 0.055,p = 0.047)成反比。我们估计的肝脏脂肪含量的总变异性(14.8%)几乎是所报告的程序变异性(8.5%)的两倍。我们发现,肝脏脂肪含量与血清甘油含量呈显着负相关,而与非酯化脂肪酸(NEFA)没有显着负相关,表明脂肪分解的进行性抑制。随肝脂肪增加而减少的caeruloplasmin可能是肝脂肪变性的结果或原因。

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