Metabolic dysfunction-associated fatty liver disease (MAFLD) is highly prevalent among patients with type 2 diabetes mellitus (T2DM) and closely linked to metabolic disturbances such as insulin resistance and dyslipidemia. Thyroid hormones are central regulators of hepatic lipid metabolism and systemic energy homeostasis. Despite biological plausibility for a relationship between thyroid function and fatty liver in diabetes, the specific pattern of thyroid hormone alterations associated with MAFLD in T2DM populations has not been fully clarified. This case-control study aimed to evaluate thyroid function parameters in patients with T2DM with and without MAFLD.
This was a case-control study that enrolled a total of 150 patients with T2DM. The study population was split evenly into two groups: 75 patients with MAFLD (cases) and 75 patients with T2DM but without MAFLD (controls). Detailed inclusion and exclusion criteria, recruitment setting, and participant demographics beyond group counts are not reported in the provided source excerpt.
Hepatic steatosis was assessed and confirmed using transient elastography with the controlled attenuation parameter (CAP), a noninvasive imaging-based method for detecting hepatic fat. Thyroid status was evaluated by measuring serum free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) using chemiluminescent immunoassays. Clinical, anthropometric, and routine biochemical parameters were also assessed, including lipid profile components.
In comparisons between the MAFLD and non-MAFLD groups, the study reports:
Significantly lower FT3 levels in patients with MAFLD compared with diabetic controls without MAFLD (p = 0.016).
Significantly higher TSH levels in the MAFLD group (p < 0.001).
FT4 levels were comparable between groups.
The MAFLD group exhibited an adverse metabolic lipid profile: higher triglycerides, higher total cholesterol, higher low-density lipoprotein cholesterol (LDL-C), and lower high-density lipoprotein cholesterol (HDL-C); all reported with p < 0.001.
The abstract states that liver enzymes were significantly different between groups, but the specific enzymes (e.g., ALT, AST), their numerical values, and statistical details were not available in the provided excerpt.
These results indicate an association between altered thyroid function—specifically reduced FT3 and elevated TSH—and the presence of MAFLD in people with T2DM, coinciding with a more atherogenic lipid profile.
The investigators performed multivariate logistic regression analysis to identify independent predictors of MAFLD among the assessed variables. The abstract indicates that such modeling was completed but truncates before listing which factors remained statistically significant in multivariate analysis and the magnitude of their associations (odds ratios, confidence intervals). Therefore, the specific independent predictors from the multivariate model are not reported in the available source text.
The reported pattern—lower FT3 and higher TSH in MAFLD cases—supports a link between altered thyroid function and hepatic steatosis in the context of T2DM. Because thyroid hormones influence hepatic lipid handling and systemic metabolism, these findings are biologically plausible and suggest that thyroid status may contribute to or reflect risk for MAFLD in diabetic patients. The concurrent adverse lipid profile in MAFLD cases underscores the clustering of cardiometabolic risk factors in this subgroup. Clinicians managing patients with T2DM and hepatic steatosis may consider that altered thyroid parameters, particularly FT3 and TSH, are associated with MAFLD, but causality and utility for screening or management are not established by this observational study.
The provided source excerpt is an abstract that is truncated in places. Several important details are missing or not reported in the excerpt, including: exact numerical values for thyroid and liver enzyme measures, full lipid panel numbers, participant demographic breakdown, inclusion/exclusion criteria, and specifics of the multivariate model (which variables were adjusted for, effect sizes, and confidence intervals).
The abstract mentions that liver enzymes were significantly different between groups but does not state which enzymes or give data.
Because the regression outputs are not available in the provided text, it is not possible to determine which variables were independent predictors of MAFLD after adjustment.
As an observational case-control design, the study can identify associations but cannot establish causation.
In this case-control cohort of 150 patients with T2DM (75 with MAFLD and 75 without), MAFLD was associated with lower FT3 and higher TSH levels, while FT4 did not differ between groups. MAFLD cases also had a more adverse lipid profile (higher triglycerides, total cholesterol, LDL-C, and lower HDL-C). Multivariate logistic regression was performed to identify independent predictors, but the provided abstract does not present the multivariable results. Several methodological and numerical details were not reported in the available excerpt, limiting appraisal of effect sizes and the independent contribution of thyroid measures to MAFLD risk.