Potential role of inflammation in relation to dietary sodium and β-carotene with non-alcoholic fatty liver disease: a mediation analysis

Abstract

Background High sodium intake has been linked to the prevalence of non-alcoholic fatty liver disease (NAFLD), but underlying mechanism remains unclear. This study aims to explore the role of chronic inflammation in the association between sodium and NAFLD. We also observed whether β-carotene, which had a strong anti-inflammatory effect, lowers the odds of NAFLD. Methods We performed mediation analyses to assess the mediating effects of C-reactive protein (CRP) and red cell distribution width (RDW) on the relationship between dietary sodium and NAFLD defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI), respectively. Results A total of 6725 participants were included in this study. Compared with the high sodium-low carotene group, participants in the high sodium-high carotene group had 16% and 26% lower odds for HSI and FLI-defined NAFLD, respectively. There were positive indirect effects of dietary sodium intake on the HSI-defined NAFLD (indirect effect: 0.0057, 95% CI: 0.0021–0.0091, P < 0.0001), as well as the FLI defined NAFLD (indirect effect: 0.0081, 95% CI: 0.0024–0.0162, P < 0.0001) when C-reactive protein (CRP) was considered as a mediator. The mediating effects were somewhat attenuated after further adjusting for dietary β-carotene intake. Similar results were found when RDW was considered as a mediator in the HSI-defined NAFLD analysis. Conclusions Higher sodium intake increases the odds of NAFLD by upregulating inflammation. Dietary β-carotene may attenuate this association by down regulating inflammation.

Fruit and vegetable intake and the risk of non-alcoholic fatty liver disease: a meta-analysis of observational studies

“…Furthermore, dietary fiber also enhances satiety, thus promoting calorie restriction (36). Additionally, fruits and vegetables are rich in antioxidants, including vitamin C, vitamin E, beta-carotene, polyphenols, which neutralize free radicals and mitigate the detrimental effects of oxidative stress on the liver (37)(38)(39)(40)(41). It should also be noted that NAFLD is frequently accompanied by an inflammatory response.…”

Association between carotenoid intake and metabolic dysfunction-associated fatty liver disease among US adults: A cross-sectional study

“…[ 33 ] A mediation analysis study using data from the NHANES 2007 to 2010 revealed that dietary β-carotene may decrease the likelihood of NAFLD by suppressing inflammation. [ 34 ] Another case-control study, which recruited 24 control participants and 62 biopsy-proven NAFLD patients, revealed a notable decrease in serum β-carotene levels among NAFLD patients compared to the control group. [ 35 ] Furthermore, serum β-carotene levels gradually decreased with increasing histological severity of NAFLD, implying a potential protective effect of β-carotene on liver pathology.…”

In Silico and In Vitro Methods in the Characterization of Beta-Carotene as Pharmaceutical Material via Acetylcholine Esterase Inhibitory Actions

“…However, an extreme level of BC intake can cause changes in skin tone along with itching, abdominal cramps, exhaustion, and weight loss. Indeed, the higher dose of β-carotene supplementation also enhances hepatic damage in alcoholic patients [30][31][32]. The pathological mechanism of BC is converting it to vitamin A, which leads to abundant accumulation of vitamin A stored in hepatic stellate cells, causing cellular hypertrophy, excessive biosynthesis of collagen, fibrosis, and hepatic damage [33].…”