Abstract
Few studies on humans have comprehensively evaluated the intake composition of methyl-donor nutrients (MDNs: choline, betaine, and folate) in relation to visceral obesity (VOB)-related hepatic steatosis (HS), the hallmark of non-alcoholic fatty liver diseases. In this case–control study, we recruited 105 patients with HS and 104 without HS (controls). HS was diagnosed through ultrasound examination. VOB was measured using a whole-body analyzer. MDN intake was assessed using a validated quantitative food frequency questionnaire. After adjustment for multiple HS risk factors, total choline intake was the most significant dietary determinant of HS in patients with VOB (Beta: −0.41, p = 0.01). Low intake of choline (<6.9 mg/kg body weight), betaine (<3.1 mg/kg body weight), and folate (<8.8 μg/kg body weight) predicted increased odds ratios (ORs) of VOB-related HS (choline: OR: 22, 95% confidence interval [CI]: 6.5–80; betaine: OR: 14, 95% CI: 4.4–50; and folate: OR: 19, 95% CI: 5.2–74). Combined high intake of choline and betaine, but not folate, was associated with an 81% reduction in VOB-related HS (OR: 0.19, 95% CI: 0.05–0.69). Our data suggest that the optimal intake of choline and betaine can minimize the risk of VOB-related HS in a threshold-dependent manner.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, affecting a quarter of the population in Western countries and Asia [1]
Combined high betaine and choline intake composition was associated with an 81% reduced odds ratios (ORs) of hepatic steatosis (HS), independent of all tested HS risk factors (Model 4: OR: 0.19, 95% confidence interval (CI): 0.05–0.69)
Adding high folate intake to this choline and betaine intake composition negated the relationship (Model 2: OR: 0.37, 95% CI: 0.12–1.14)
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, affecting a quarter of the population in Western countries and Asia [1]. The severity of intrahepatic fat accumulation in NAFLD is related with an increase in oxidative stress, proinflammation status, and chronic kidney disease complications [2,3], all of which are strongly linked to overweight and obesity (OB) [4]. Hepatic steatosis (HS), the hallmark of NAFLD, is associated with a 60–90% prevalence among obese patients [5]. Visceral obesity (VOB) is associated with a higher risk of type 2 diabetes mellitus, dyslipidemia, and insulin resistance [6] and is more associated with HS severity and NAFLD-related mortality across ethnicities [7]. Dietary modification to reduce excess adiposity can help reduce OB-related HS and the risks of progression to NAFLD and associated mortality [8]
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