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Clinical Trial
. 2014 Apr 14;9(4):e94059.
doi: 10.1371/journal.pone.0094059. eCollection 2014.

Comparison of liver fat indices for the diagnosis of hepatic steatosis and insulin resistance

Sabine Kahl  1 , Klaus Straßburger  2 , Bettina Nowotny  1 , Roshan Livingstone  2 , Birgit Klüppelholz  3 , Kathrin Keßel  2 , Jong-Hee Hwang  2 , Guido Giani  3 , Barbara Hoffmann  4 , Giovanni Pacini  5 , Amalia Gastaldelli  6 , Michael Roden  7
Affiliations
Clinical Trial

Comparison of liver fat indices for the diagnosis of hepatic steatosis and insulin resistance

Sabine Kahl et al. PLoS One. .

Abstract

Context: Hepatic steatosis, defined as increased hepatocellular lipid content (HCL), associates with visceral obesity and glucose intolerance. As exact HCL quantification by 1H-magnetic resonance spectroscopy (1H-MRS) is not generally available, various clinical indices are increasingly used to predict steatosis.

Objective: The purpose of this study was to test the accuracy of NAFLD liver fat score (NAFLD-LFS), hepatic steatosis index (HSI) and fatty liver index (FLI) against 1H-MRS and their relationships with insulin sensitivity and secretion.

Design, setting and participants: Ninety-two non-diabetic, predominantly non-obese humans underwent clinical examination, 1H-MRS and an oral glucose tolerance test (OGTT) to calculate insulin sensitivity and β-cell function. Accuracy of indices was assessed from the area under the receiver operating characteristic curve (AROC).

Results: Median HCL was 2.49% (0.62;4.23) and correlated with parameters of glycemia across all subjects. NAFLD-LFS, FLI and HSI yielded AROCs of 0.70, 0.72, and 0.79, respectively, and related positively to HCL, insulin resistance, fasting and post-load β-cell function normalized for insulin resistance. Upon adjustment for age, sex and HCL, regression analysis revealed that NAFLD-LFS, FLI and HSI still independently associated with both insulin sensitivity and β-cell function.

Conclusion: The tested indices offer modest efficacy to detect steatosis and cannot substitute for fat quantification by 1H-MRS. However, all indices might serve as surrogate parameters for liver fat content and also as rough clinical estimates of abnormal insulin sensitivity and secretion. Further validation in larger collectives such as epidemiological studies is needed.

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Conflict of interest statement

Competing Interests: Unrelated to this study, M. R. has financial relationships with Boehringer Ingelheim Pharma, Eli Lilly, Novartis Pharma GmbH, Novo Nordisk, Sanofi-Aventis Deutschland GmbH and Takeda Pharma Ges. mbH, Austria. B. N. had travel costs paid by Sanofi-Aventis Deutschland GmbH. There are no patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.

Figures

Figure 1
Figure 1. Performance of indices (all subjects).
(A) ROC curves of NAFLD-LFS (black line), HSI (dotted line) and FLI (dashed line) (B) AROC's of NAFLD-LFS (black line), HSI (dotted line) and FLI (dashed line) for different HCL cut-offs defining steatosis (C) Correlation of HCL with NAFLD-LFS_cont. Black line, linear regression curve; inner broken lines, 95% confidence limits; outer broken lines, 95% prediction limits (D) Evaluation of goodness of fit by plotting residuals against HCL calculated by NAFLD-LFS_cont.
Figure 2
Figure 2. OGTT in subjects with and without steatosis.
Plasma glucose (all: A, LRA: B), insulin and C-peptide (all: C, LRA: D) during OGTT in subjects without (non-FL) (insulin: open triangles, C-peptide: black triangles) and with steatosis (FL) (insulin: open circles, C-peptide: black squares). *, p<0.05; **, p<0.01 for insulin; §, p<0.05 for C-peptide.
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Publication types

Grants and funding

This project was conducted in the context of the pretest studies of the German National Cohort (www.nationale-kohorte.de). These were funded by the Federal Ministry of Education and Research (BMBF), Förderkennzeichen 01ER1001A-I and supported by the participating universities, institutes of the Leibniz Association, the European Foundation for the Study of Diabetes (EFSD Clinical Research Grant in the Field of Diabetes 2010), the German Diabetes Association, the Schmutzler-Stiftung, the ICEMED Helmholtz-Alliance and the German Center for Diabetes Research (DZD e.V.). The study design of the National Cohort, basis for our study, was done by the German national cohort epidemiologic planning committee and project management team, and approved by Prof. Dr. Karl-Heinz Jöckel, chairman of the scientific board of the German National Cohort. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.