Abstract
BackgroundPrevious studies have shown that metabolic dysfunction associated fatty liver disease (MAFLD) is associated with thyroid hormones (THs), immunity, and inflammation status, but few studies involved thyroid autoimmunity. This study aimed to evaluate the role of THs, thyroid autoantibodies, inflammatory biomarkers in MAFLD, its cofactors, and other possible determinants.Materials and MethodsIn the study, a total of 424 Chinese patients were selected and categorized as non-MAFLD and MAFLD. Serum thyroid hormone, thyroid autoantibody and high-sensitive C-reactive protein (hsCRP) levels were measured. The data of blood pressure, the serum lipid profile, glucose and liver enzymes were collected. The differences and association between research findings were examined and analyzed by Wilcoxon Signed Rank Test, One-Way ANOVA test and Multiple Logistic Regression models.ResultsThe study showed significant increase in the prevalence of MAFLD with high thyroid stimulating hormone (TSH) levels (P < 0.01) and abnormal high-sensitive C-reactive protein (hsCRP) levels (P < 0.01). The proportion of MAFLD patients decreased significantly with the rise of free thyroxine (FT4) (P = 0.04), thyrotropin receptor antibodies (TRAb) (P < 0.01), anti-thyroglobulin antibodies (TgAb) (P < 0.01), and thyroid peroxidase antibodies (TPOAb) levels (P < 0.01). Based on logistic regression analysis, MAFLD was significantly associated with lower levels of TgAb (P < 0.01), TPOAb (P < 0.01), and higher levels of hsCRP (P < 0.01) in male. In female, elevated TgAb (P < 0.01) may be a protective factor, while higher levels of hsCRP (P < 0.01) showed increased risk of MAFLD. Logistic models were adjusted for age, BMI, SBP, DBP, FBG, ALT, AST, TC, TG, LDL, HDL.ConclusionsTaken together, TgAb may be a potential protective factor for MAFLD and elevated hsCRP level should be considered as an independent risk factor for MAFLD in both genders. TPOAb also demonstrated protective effect, but only in male. The prevalence of MAFLD increased with higher TSH levels and lower FT4, TRAb levels, but no significant association were found. However, Our findings provide a new insight into the pathogenesis of MAFLD by further investigating the impact of THs, thyroid autoimmunity, and inflammation on MAFLD patients.
Highlights
Nonalcoholic fatty liver disease (NAFLD) has been renamed as metabolic dysfunction associated fatty liver disease (MAFLD), underlining the association of fatty liver disease with metabolic dysfunction [1, 2]
Other studies have suggested that the association between MAFLD and thyroid stimulating hormone (TSH) is mediated by the characteristics of metabolic syndrome (MetS), TSH levels cannot be used as independent risk factors for nonalcoholic fatty liver disease (NAFLD) [11]
We explored that patients with elevated anti-thyroglobulin antibodies (TgAb) had lower diastolic blood pressure (DBP) volume, lower fasting blood glucose (FBG) levels, lower TG levels and higher high density lipoprotein (HDL) levels compared to the normal TgAb group
Summary
Nonalcoholic fatty liver disease (NAFLD) has been renamed as metabolic dysfunction associated fatty liver disease (MAFLD), underlining the association of fatty liver disease with metabolic dysfunction [1, 2]. THs targets the liver to regulate body weight, lipogenesis, lipid metabolism, and insulin resistance (IR) Many liver diseases, such as liver fibrosis and cirrhosis hepatocellular carcinoma [9] are affected by THs. Recently, the association between MAFLD and THs has been discussed and is considered controversial. Some studies have shown that the prevalence of MAFLD is positively correlated with thyroid stimulating hormone (TSH), and TSH level may be an important risk factor for MAFLD [10]. Other THs, including free triiodothyronine (FT3), free thyroxine (FT4), and FT3/FT4 ratio have proven to be associated with MAFLD [12, 13] This association of MAFLD with FT3 and FT4 levels are heterogeneous among population [10, 11]. This study aimed to evaluate the role of THs, thyroid autoantibodies, inflammatory biomarkers in MAFLD, its cofactors, and other possible determinants
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