Abstract
A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Dietary sodium intake was measured by sodium excretion in two complete consecutive 24 h urine collections in 6132 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Fatty Liver Index (FLI) ≥60 and Hepatic Steatosis Index (HSI) >36 were used as proxies of suspected NAFLD. 1936 (31.6%) participants had an FLI ≥60, coinciding with the increased prevalence of type 2 diabetes (T2D), metabolic syndrome, hypertension and history of cardiovascular disease. Sodium intake was higher in participants with an FLI ≥60 (163.63 ± 61.81 mmol/24 h vs. 136.76 ± 50.90 mmol/24 h, p < 0.001), with increasing incidence in ascending quartile categories of sodium intake (p < 0.001). Multivariably, an FLI ≥60 was positively associated with a higher sodium intake when taking account for T2D, a positive cardiovascular history, hypertension, alcohol intake, smoking and medication use (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.44–1.64, p < 0.001). Additional adjustment for the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) diminished this association (OR 1.30, 95% CI 1.21–1.41, p < 0.001). HSI >36 showed similar results. Associations remained essentially unaltered after adjustment for body surface area or waist/hip ratio. In conclusion, suspected NAFLD is a feature of higher sodium intake. Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis in the absence of excessive alcohol use, and is emerging as the most common cause of chronic liver disease [1,2]
Model 4: adjusted for age, sex, presence of type 2 diabetes, history of cardiovascular disease, presence of hypertension, alcohol intake, current smoking, estimated glomerular filtration rate, urinary albumin excretion, use of antihypertensive medication, glucose lowering drugs and lipid lowering drugs and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). In this large-scale, cross-sectional study in a predominantly Caucasian population we have demonstrated, to the best of our knowledge, for the first time a positive association of higher sodium intake, determined by two consecutive 24 h urinary sodium excretions, with suspected NAFLD
In multivariable regression analyses, accounting for various clinical variables, including BSA, as a measure of body size, Estimated glomerular filtration rate (eGFR) and Urinary albumin excretion (UAE), suspected NAFLD remained independently associated with a higher sodium intake
Summary
Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis in the absence of excessive alcohol use, and is emerging as the most common cause of chronic liver disease [1,2]. The spectrum of NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and eventually cirrhosis [1,3]. NAFLD coincides with obesity and insulin resistance, and is seen as the liver manifestation of the metabolic syndrome (MetS) [4]. NAFLD may in itself increase the risk for the development of MetS and type 2 diabetes mellitus (T2D) [5,6]. The pathophysiological mechanisms underlying the development of NAFLD are not fully clarified, but multifactorial contributors including environmental factors (diet), central obesity, insulin resistance, alterations in gut microbiota and genetic factors are likely to play an important role [10]
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