Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the most prevalent chronic liver disorders worldwide and represents an important interface between hepatic disease and systemic metabolic dysfunction. It encompasses a spectrum ranging from simple hepatic steatosis to steatohepatitis, progressive fibrosis, cirrhosis and hepatocellular carcinoma. Contemporary epidemiological evidence demonstrates that the burden of NAFLD has increased substantially during recent decades, largely in parallel with rising rates of obesity, type 2 diabetes mellitus and other components of metabolic syndrome.[1] A large systematic review reported a global prevalence of approximately 30%, with a marked increase in prevalence during the most recent periods analysed, indicating that fatty liver disease is becoming an increasingly important public-health concern.[1] The nomenclature of fatty liver disease has undergone a major transition. In 2023, a multisociety Delphi consensus introduced the overarching term steatotic liver disease (SLD) and proposed metabolic dysfunction-associated steatotic liver disease (MASLD) to replace NAFLD in individuals with hepatic steatosis accompanied by at least one cardiometabolic risk factor.[2] This change was intended to provide a more affirmative disease definition and to emphasize its metabolic basis. Nevertheless, the term NAFLD remains relevant for studies designed and conducted using the established exclusion-based diagnostic framework, particularly those involving exclusion of significant alcohol consumption and other recognized causes of hepatic steatosis. The magnitude of the disease burden is also substantial in India. A systematic review and meta-analysis of Indian studies demonstrated an overall adult NAFLD prevalence of approximately 38.6%, with substantially higher prevalence among high-risk populations.[3] Hospital-based populations are particularly likely to contain individuals with obesity, diabetes, hypertension and dyslipidaemia, and consequently may demonstrate prevalence estimates considerably higher than those reported in community screening programmes. Recent Indian evidence continues to identify obesity, diabetes mellitus, hypertension and abnormalities in lipid metabolism as important factors associated with fatty liver disease.[4] These findings underline the importance of evaluating locally encountered patient populations rather than extrapolating exclusively from Western epidemiological estimates. The pathogenesis of NAFLD is closely linked to metabolic dysfunction. Insulin resistance, increased adipose-tissue lipolysis, enhanced delivery of free fatty acids to the liver, increased hepatic de novo lipogenesis and altered lipid export collectively contribute to accumulation of triglycerides within hepatocytes. Excess adiposity further promotes chronic low-grade inflammation, adipokine dysregulation and metabolic stress. Current AASLD guidance identifies obesity, insulin resistance, type 2 diabetes and dyslipidaemia as central clinical and metabolic determinants of NAFLD development and progression.[5] Consequently, assessment of fatty liver cannot be separated from evaluation of the broader cardiometabolic phenotype. Obesity is among the most consistently recognized risk factors for hepatic steatosis. Increased body mass index and central adiposity are associated with greater hepatic fat accumulation and a higher probability of progressive metabolic liver disease. Nevertheless, NAFLD may also occur in individuals without overt obesity, particularly in Asian populations, highlighting the contribution of visceral adiposity, body composition, genetic susceptibility and metabolic health beyond BMI alone.[5] This makes simultaneous assessment of anthropometric and biochemical variables important when evaluating patients with ultrasonographically detected fatty liver. Abnormal glucose metabolism represents another major component of the disease. NAFLD and type 2 diabetes have a bidirectional relationship, with insulin resistance acting as a central mechanistic link. A recent systematic review and meta-analysis evaluating type 2 diabetes in patients with NAFLD or related metabolic fatty liver phenotypes demonstrated a substantial coexistence of the two disorders.[6] Patients with impaired glucose metabolism may develop increased hepatic lipid accumulation, while fatty liver itself may aggravate hepatic insulin resistance and contribute to deterioration of systemic glycaemic control. This interaction provides a rationale for evaluating fasting blood glucose in patients with hepatic steatosis. Dyslipidaemia is similarly common in NAFLD. Increased triglycerides, increased LDL cholesterol and reduced HDL cholesterol frequently accompany hepatic fat accumulation. Recent Indian meta-analytic evidence has also demonstrated a positive association between serum triglyceride levels and NAFLD.[4] These lipid abnormalities are clinically important because they reflect altered hepatic lipid handling and contribute to the broader cardiovascular risk profile of affected individuals. The systemic consequences of NAFLD extend beyond the liver. Cardiovascular disease is an important cause of morbidity among patients with fatty liver disease. An updated systematic review and meta-analysis involving more than 5.8 million participants demonstrated that NAFLD was associated with an increased risk of fatal and non-fatal cardiovascular events, with the risk increasing with more advanced liver disease.[7] Recognition of NAFLD on routine imaging should therefore prompt consideration not only of liver-related complications but also of accompanying metabolic and cardiovascular abnormalities. Serum alanine aminotransferase and aspartate aminotransferase are commonly measured when evaluating patients with suspected liver disease. Elevated aminotransferase levels may reflect hepatocellular injury and metabolic stress; however, normal values do not exclude clinically significant NAFLD or fibrosis. Current practice guidance therefore recommends that liver enzyme levels should not be used in isolation to exclude important disease.[5] Their relationship with ultrasonographic severity nevertheless remains clinically relevant and can provide useful information when interpreted together with metabolic and imaging findings. Although liver biopsy remains the reference standard for histological characterization of steatosis, inflammation and fibrosis, its invasive nature limits its suitability for routine screening. Ultrasonography is widely used because it is accessible, non-invasive, relatively inexpensive and capable of identifying characteristic features of hepatic steatosis. A landmark meta-analysis demonstrated that conventional ultrasonography has good diagnostic accuracy for moderate-to-severe fatty liver when compared with histology.[8] More recent meta-analyses of ultrasound-based attenuation methods have further demonstrated the potential of quantitative ultrasonographic techniques for assessment of hepatic steatosis.[9] However, conventional ultrasonography has limitations. Its sensitivity decreases in mild steatosis, image interpretation may be operator-dependent, and conventional sonography cannot reliably characterize inflammation or stage hepatic fibrosis. Current European clinical practice guidelines therefore advocate a broader assessment incorporating cardiometabolic risk factors and, where appropriate, non-invasive fibrosis assessment in patients with hepatic steatosis, particularly those with obesity, type 2 diabetes or abnormal liver enzymes.[10] Against this background, evaluation of the relationship between ultrasonographic grades of fatty liver and readily measurable metabolic parameters may provide clinically useful information, particularly in settings where advanced imaging techniques are not routinely available. Assessment of BMI, fasting blood glucose, serum lipids and aminotransferases alongside ultrasonography may facilitate identification of individuals with a greater burden of metabolic dysfunction and help guide further risk stratification. The present study was therefore undertaken to determine the prevalence and ultrasonographic severity of NAFLD among adult participants and to examine its relationship with anthropometric and biochemical parameters, including BMI, fasting blood glucose, lipid profile, ALT and AST. AIM To assess the occurrence and ultrasonographic severity of non-alcoholic fatty liver disease and evaluate its association with selected anthropometric, glycaemic, lipid and hepatic biochemical parameters among adult participants. OBJECTIVES 1. To determine the prevalence and ultrasonographic grades of non-alcoholic fatty liver disease among the study participants. 2. To evaluate the association and correlation of ultrasonographic severity of non-alcoholic fatty liver disease with body mass index, fasting blood glucose, lipid profile and serum aminotransferase levels, and to identify independent metabolic factors associated with NAFLD.

Study Design and Setting This hospital-based, cross-sectional observational study was conducted in the Department of Radiodiagnosis in collaboration with the Department of General Medicine at Mahavir Institue of Medical Sciences, Vikarabad, Telangana.The study was conducted over a period of one year from April 2025 to March 2026. Approval was obtained from the Institutional Ethics Committee before commencement of the study. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki. Written informed consent was obtained from all participants before enrollment. Study Population A total of 250 adult participants undergoing abdominal ultrasonographic evaluation were included in the study. Participants were recruited consecutively from eligible patients attending outpatient and inpatient clinical services during the study period. Adults aged 18 years or older who underwent ultrasonographic examination of the liver and fulfilled the predefined eligibility criteria were considered for participation. Inclusion Criteria 1. Adults aged ≥18 years. 2. Individuals undergoing abdominal ultrasonography for routine health assessment or clinical indications. 3. Participants who underwent adequate ultrasonographic assessment of hepatic parenchyma. 4. Participants willing to provide written informed consent. 5. Individuals for whom relevant anthropometric and biochemical information was available. Exclusion Criteria 1. History of significant alcohol consumption, defined as >20 g/day in women and >30 g/day in men. 2. Known chronic viral hepatitis. 3. Autoimmune or inherited chronic liver disease. 4. Wilson disease, hemochromatosis, or other established metabolic liver disorders. 5. Drug-induced liver injury or chronic use of medications known to produce hepatic steatosis. 6. Known hepatic malignancy or metastatic liver disease. 7. Pregnancy. 8. Inadequate ultrasonographic visualization of the liver. 9. Incomplete clinical, anthropometric, or biochemical data. Clinical Assessment A structured data collection form was used to document demographic and clinical characteristics, including age, sex, relevant medical history, presence of diabetes mellitus, hypertension, and other metabolic risk factors. Blood pressure was measured after the participant had rested in the seated position for at least five minutes using a standardized sphygmomanometer. Two readings were obtained when necessary, and an appropriate representative measurement was documented. Anthropometric Assessment Body weight was measured using a calibrated digital weighing scale with participants wearing light clothing and without footwear. Height was measured using a standard stadiometer. Body mass index was calculated using the formula: BMI = Weight in kilograms / Height in metres² Waist circumference was measured using a non-stretchable measuring tape at the midpoint between the inferior margin of the lowest palpable rib and the upper border of the iliac crest. BMI and central adiposity were evaluated as metabolic risk indicators. Biochemical Investigations After an overnight fasting period of approximately 8–12 hours, venous blood samples were collected under aseptic precautions. The following biochemical parameters were evaluated: • Fasting blood glucose • Total cholesterol • Serum triglycerides • High-density lipoprotein cholesterol • Low-density lipoprotein cholesterol • Alanine aminotransferase • Aspartate aminotransferase Biochemical investigations were performed in the central clinical laboratory using standardized automated analytical systems. Internal quality-control procedures were followed according to the laboratory's established protocols. Ultrasonographic Assessment Abdominal ultrasonography was performed using a high-resolution ultrasound system equipped with an appropriate convex abdominal transducer. Participants were examined by experienced radiologists using standardized ultrasonographic criteria. Assessment of hepatic steatosis was based principally on: 1. Increased echogenicity of hepatic parenchyma compared with the renal cortex. 2. Posterior attenuation of the ultrasound beam. 3. Reduced visualization of intrahepatic vascular structures. 4. Reduced definition of the diaphragm. 5. Alteration in visualization of deeper portions of the liver. Where feasible, radiologists interpreting ultrasonographic findings were unaware of the biochemical results at the time of imaging assessment. Ultrasonographic Grading of Hepatic Steatosis Hepatic steatosis was classified into three grades. Grade I — Mild Steatosis A mild diffuse increase in hepatic echogenicity with preservation of visualization of the diaphragm and intrahepatic vascular margins. Grade II — Moderate Steatosis A moderate increase in hepatic echogenicity accompanied by partial reduction in visualization of intrahepatic vessels and the diaphragm. Grade III — Severe Steatosis Marked hepatic echogenicity with substantial posterior attenuation and poor visualization of intrahepatic vessels, deeper hepatic segments, and the diaphragm. Based on these findings, participants were categorized as having ultrasonographically detectable fatty liver or no evidence of fatty liver. Outcome Measures Primary Outcome The primary outcome was the proportion of study participants demonstrating ultrasonographic evidence of NAFLD and the distribution of disease according to ultrasonographic grade. Secondary Outcomes Secondary outcomes included evaluation of the relationships between ultrasonographic severity of hepatic steatosis and: • BMI • Fasting blood glucose • Total cholesterol • Triglycerides • HDL-C • LDL-C • ALT • AST Independent metabolic factors associated with the presence of NAFLD were additionally evaluated. Statistical Analysis Data were entered into Microsoft Excel and analyzed using an appropriate statistical software package.Continuous variables were summarized as mean ± standard deviation when approximately normally distributed and as median with interquartile range where appropriate.Categorical variables were expressed as frequencies and percentages.Normality of continuous variables was evaluated using the Shapiro–Wilk test together with graphical assessment where required. For comparison between participants with and without NAFLD: • Independent-samples Student's t-test was used for normally distributed continuous variables. • Mann–Whitney U test was used for non-normally distributed continuous variables. • Chi-square test or Fisher's exact test was applied for categorical variables. Differences in continuous metabolic parameters across Grade I, Grade II, and Grade III hepatic steatosis were assessed using one-way analysis of variance followed by appropriate post-hoc testing. Where parametric assumptions were not satisfied, corresponding non-parametric tests were considered.The relationship between ultrasonographic grade and metabolic parameters was examined using Pearson's or Spearman's correlation coefficient according to the nature and distribution of the variables.Multivariable binary logistic regression analysis was performed to determine factors independently associated with the presence of NAFLD after adjustment for potential confounding variables.Adjusted odds ratios were reported together with their 95% confidence intervals.All statistical tests were two-tailed, and a p-value <0.05 was considered statistically significant.

Baseline Characteristics A total of 250 participants fulfilled the eligibility criteria and were included in the final analysis. The mean age of the study population was 47.1 ± 11.8 years, with an age range of 18–77 years. Of the 250 participants, 135 (54.0%) were males and 115 (46.0%) were females. Ultrasonography demonstrated fatty liver in 150 participants (60.0%), whereas 100 participants (40.0%) showed no ultrasonographic evidence of hepatic steatosis. Table 1. Demographic and Ultrasonographic Characteristics of the Study Population (N = 250) Characteristic Frequency Percentage Male 135 54.0 Female 115 46.0 Age 18–30 years 37 14.8 Age 31–45 years 81 32.4 Age 46–60 years 89 35.6 Age >60 years 43 17.2 NAFLD present 150 60.0 NAFLD absent 100 40.0 Participants aged 46–60 years represented the largest proportion of the study population, accounting for 35.6%, followed by those aged 31–45 years at 32.4%. The overall prevalence of ultrasonographically detected NAFLD was 60.0%. Distribution of Ultrasonographic Grades of NAFLD Among the 150 participants diagnosed with NAFLD, Grade I hepatic steatosis was most frequent, followed by Grade II and Grade III disease. Table 2. Distribution of Ultrasonographic Grades of NAFLD (n = 150) Ultrasonographic Grade Frequency Percentage Grade I 72 48.0 Grade II 51 34.0 Grade III 27 18.0 Total 150 100.0 Grade I fatty liver constituted nearly half of all NAFLD cases. Moderate steatosis was identified in approximately one-third of affected participants, while Grade III disease constituted the smallest subgroup. The distribution therefore demonstrated a progressive reduction in frequency with increasing severity of hepatic steatosis. Comparison of Metabolic Parameters Between NAFLD and Non-NAFLD Groups Table 3. Anthropometric and Biochemical Parameters According to NAFLD Status Variable NAFLD (n = 150) Mean ± SD Non-NAFLD (n = 100) Mean ± SD p-value BMI (kg/m²) 29.5 ± 4.1 24.3 ± 3.4 <0.001 Fasting blood glucose (mg/dL) 116.8 ± 27.9 94.5 ± 17.6 <0.001 Total cholesterol (mg/dL) 210.7 ± 37.4 183.6 ± 29.8 <0.001 Triglycerides (mg/dL) 188.6 ± 57.8 126.9 ± 40.7 <0.001 HDL-C (mg/dL) 40.2 ± 7.4 47.1 ± 8.1 <0.001 LDL-C (mg/dL) 133.8 ± 30.9 113.7 ± 26.8 <0.001 ALT (U/L) 52.8 ± 19.1 30.4 ± 10.8 <0.001 AST (U/L) 40.7 ± 15.6 26.7 ± 9.2 <0.001 Participants with NAFLD demonstrated significantly higher BMI, fasting blood glucose, total cholesterol, triglycerides, LDL-C, ALT, and AST compared with participants without NAFLD. HDL-C showed the opposite pattern, with significantly lower concentrations among participants with NAFLD. Relationship Between Metabolic Parameters and Severity of Fatty Liver Table 4. Selected Metabolic Parameters According to Ultrasonographic Grade Variable Grade I (n = 72) Grade II (n = 51) Grade III (n = 27) p-value BMI (kg/m²) 27.4 ± 3.3 30.2 ± 3.7 33.0 ± 4.0 <0.001 FBG (mg/dL) 106.7 ± 21.4 119.1 ± 26.2 134.8 ± 32.7 <0.001 Triglycerides (mg/dL) 159.8 ± 40.5 195.7 ± 52.8 240.9 ± 67.4 <0.001 ALT (U/L) 44.1 ± 14.6 56.2 ± 17.5 71.9 ± 22.8 <0.001 A progressive increase in BMI, fasting blood glucose, triglycerides, and ALT was observed with increasing ultrasonographic severity of hepatic steatosis. The differences across the three grades were statistically significant. Correlation Between NAFLD Grade and Metabolic Variables Table 5. Correlation of Ultrasonographic Grade With Metabolic Parameters Variable Correlation coefficient (r) p-value BMI 0.598 <0.001 Fasting blood glucose 0.472 <0.001 Total cholesterol 0.404 <0.001 Triglycerides 0.631 <0.001 ALT 0.568 <0.001 AST 0.511 <0.001 Ultrasonographic severity of NAFLD demonstrated significant positive correlations with all evaluated metabolic variables. The strongest relationship was observed with serum triglycerides (r = 0.631), followed by BMI (r = 0.598) and ALT (r = 0.568). These findings indicate that increasing severity of hepatic steatosis was associated with worsening adiposity, dyslipidemia, glycemic status, and hepatic enzyme abnormalities. Independent Factors Associated With NAFLD Table 6. Multivariable Logistic Regression Analysis Variable Adjusted OR 95% CI p-value BMI ≥25 kg/m² 3.54 1.89–6.63 <0.001 Diabetes mellitus 2.49 1.31–4.72 0.005 Triglycerides ≥150 mg/dL 3.11 1.72–5.62 <0.001 Elevated ALT 2.06 1.12–3.79 0.020 After adjustment for potential confounding variables, elevated BMI, diabetes mellitus, hypertriglyceridemia, and elevated ALT remained independently associated with NAFLD. Participants with BMI ≥25 kg/m² had approximately 3.5-fold higher adjusted odds of having NAFLD, while triglyceride levels ≥150 mg/dL were associated with approximately 3.1-fold higher odds. Thus, obesity and hypertriglyceridemia emerged as particularly important independent metabolic correlates of ultrasonographically detected NAFLD.

The present study evaluated ultrasonographically detected non-alcoholic fatty liver disease (NAFLD) and its relationship with anthropometric and biochemical parameters among 250 adults. Hepatic steatosis was identified in 150 participants, representing 60.0% of the study population. Among participants with NAFLD, Grade I steatosis was observed in 48.0%, Grade II in 34.0%, and Grade III in 18.0%. Participants with NAFLD demonstrated higher body mass index (BMI), fasting blood glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), together with lower high-density lipoprotein cholesterol (HDL-C), compared with participants without NAFLD. Furthermore, BMI, fasting blood glucose, triglycerides, and ALT increased progressively across increasing ultrasonographic grades. These findings demonstrate a consistent relationship between increasing sonographic hepatic steatosis and an adverse metabolic profile. The frequency of NAFLD observed in the present study should be interpreted in the context of its hospital-based sampling framework rather than as an estimate of prevalence in the general population. Participants undergoing abdominal ultrasonography for clinical indications or health assessment may have a greater burden of obesity, dysglycaemia, dyslipidaemia, and other metabolic abnormalities than an unselected community population. Therefore, the principal significance of the present findings lies not only in the frequency of steatosis but also in its relationship with metabolic abnormalities and their progressive increase across ultrasonographic grades. Grade I steatosis was the most frequent ultrasonographic category, accounting for 48.0% of affected participants. Nevertheless, Grade II and Grade III disease together constituted 52.0% of NAFLD cases. Conventional B-mode ultrasonography remains clinically useful for identifying hepatic steatosis, particularly because of its accessibility, safety, and relatively low cost. However, visual ultrasonographic grading represents an estimate of hepatic fat accumulation and should not be interpreted as a direct measure of steatohepatitis or hepatic fibrosis. Contemporary literature has increasingly emphasized the complementary roles of conventional ultrasonography, quantitative ultrasound, and elastography in the assessment of steatotic liver disease.[11] Obesity demonstrated a prominent relationship with hepatic steatosis in the present study. Mean BMI was 29.5 ± 4.1 kg/m² among participants with NAFLD compared with 24.3 ± 3.4 kg/m² among those without NAFLD. BMI also increased progressively from 27.4 ± 3.3 kg/m² in Grade I to 30.2 ± 3.7 kg/m² in Grade II and 33.0 ± 4.0 kg/m² in Grade III steatosis. The reported correlation coefficient between BMI and ultrasonographic grade was 0.598. These observations indicate that increasing adiposity accompanied increasing sonographic hepatic fat burden in the study population. Recent ultrasound-based evidence indicates that the relationship between adiposity and hepatic steatosis extends beyond BMI. Flagiello et al. evaluated metabolically at-risk individuals and demonstrated that ultrasound-derived visceral adipose tissue was associated with hepatic fat and multiple metabolic abnormalities. Visceral adiposity also demonstrated stronger relationships with several metabolic variables than conventional anthropometric measures.[12] These observations suggest that future studies may improve metabolic characterization by incorporating waist circumference or direct measures of visceral adiposity in addition to BMI. Abnormal glucose metabolism was another important feature of NAFLD in the present study. Mean fasting blood glucose was 116.8 ± 27.9 mg/dL among participants with NAFLD compared with 94.5 ± 17.6 mg/dL among those without NAFLD. Fasting blood glucose increased progressively from 106.7 ± 21.4 mg/dL in Grade I to 119.1 ± 26.2 mg/dL in Grade II and 134.8 ± 32.7 mg/dL in Grade III steatosis. The reported correlation coefficient between fasting glucose and ultrasonographic grade was 0.472. Diabetes mellitus also remained associated with NAFLD in the reported multivariable model. These observations support the close coexistence of hepatic steatosis and impaired glucose metabolism. Dyslipidaemia was similarly prominent. Participants with NAFLD had higher mean triglyceride, total cholesterol, and LDL-C concentrations and lower HDL-C concentrations than participants without NAFLD. The relationship with triglycerides was particularly marked. Mean triglyceride concentrations increased from 159.8 ± 40.5 mg/dL in Grade I to 195.7 ± 52.8 mg/dL in Grade II and 240.9 ± 67.4 mg/dL in Grade III disease. Among the evaluated metabolic variables, triglycerides demonstrated the highest reported correlation coefficient with ultrasonographic grade (0.631). The relationship between triglycerides and hepatic fat accumulation is supported by recent quantitative ultrasound research. Tavaglione et al. evaluated individuals at high risk for metabolic dysfunction-associated steatotic liver disease (MASLD) using ultrasound-derived fat fraction (UDFF). Their study demonstrated significant relationships among quantitatively assessed hepatic fat, triglycerides, ALT, and visceral adipose tissue. Triglycerides, ALT, and visceral adipose tissue were independently associated with UDFF.[13] These findings support the close relationship between dyslipidaemia and hepatic fat accumulation observed in the present study. Serum aminotransferases were also higher among participants with NAFLD. Mean ALT was 52.8 ± 19.1 U/L in participants with NAFLD compared with 30.4 ± 10.8 U/L in those without NAFLD, while the corresponding AST concentrations were 40.7 ± 15.6 U/L and 26.7 ± 9.2 U/L, respectively. ALT increased progressively across ultrasonographic grades and demonstrated a reported correlation coefficient of 0.568 with steatosis grade. Elevated ALT also remained associated with NAFLD in the reported multivariable analysis. The association between ALT and quantitatively assessed hepatic fat has also been demonstrated in recent ultrasound studies.[13] Nevertheless, serum aminotransferases should not be considered direct measures of hepatic fat or fibrosis. Biochemical and imaging parameters provide different information and should be interpreted together. Normal aminotransferase concentrations do not exclude clinically important steatotic liver disease, while elevated aminotransferases alone cannot establish steatohepatitis or fibrosis. The reported multivariable analysis identified BMI ≥25 kg/m², diabetes mellitus, triglycerides ≥150 mg/dL, and elevated ALT as factors independently associated with NAFLD. The adjusted odds ratios were 3.54 for BMI ≥25 kg/m², 2.49 for diabetes mellitus, 3.11 for triglycerides ≥150 mg/dL, and 2.06 for elevated ALT. This pattern demonstrates clustering of adiposity, dysglycaemia, dyslipidaemia, and hepatic biochemical abnormalities among participants with ultrasonographically detected steatosis. These associations should, however, be interpreted within the cross-sectional design of the study and should not be regarded as evidence of causality. The contemporary transition from NAFLD to MASLD provides an important framework for interpreting these findings. The newer terminology places cardiometabolic dysfunction within the disease definition and reflects the close relationship between hepatic steatosis and metabolic risk factors. Jin et al. reviewed the role of ultrasound and elastography in the context of the new MASLD definition and emphasized the increasing importance of non-invasive imaging for assessment of hepatic steatosis and fibrosis.[11] Although the present study retains the term NAFLD because participants were evaluated using conventional NAFLD criteria, the clustering of obesity, abnormal glucose metabolism, dyslipidaemia, and hepatic steatosis observed in the present study is consistent with the metabolic phenotype emphasized by the MASLD framework. An important limitation of conventional B-mode ultrasonography is that visual assessment of hepatic echogenicity remains partly subjective and does not directly quantify hepatic fat. Diagnostic performance may also be influenced by the degree of steatosis, patient habitus, equipment characteristics, and operator experience. Contemporary research has therefore increasingly focused on quantitative ultrasound techniques capable of estimating hepatic fat content more objectively. Tavaglione et al. demonstrated that UDFF correlated with established non-invasive measures of hepatic steatosis in individuals at high risk for MASLD.[13] More recently, Jin et al. evaluated UDFF against magnetic resonance imaging-derived proton density fat fraction (MRI-PDFF). UDFF demonstrated a strong correlation with MRI-PDFF and high diagnostic performance for detecting hepatic steatosis.[14] These findings indicate that quantitative ultrasound may provide a reproducible extension of conventional B-mode assessment. Additional evidence has emerged from prospective international investigation. Huang et al. evaluated quantitative ultrasonographic techniques in patients with MASLD using histopathology as the reference standard. Tissue attenuation imaging and tissue scatter-distribution imaging were independently associated with hepatic steatosis, while two-dimensional shear-wave elastography was associated with hepatic fibrosis.[15] These findings are important because they demonstrate that different ultrasonographic parameters can provide complementary information regarding hepatic fat accumulation and fibrotic change. This distinction between steatosis and fibrosis is clinically important when interpreting the present findings. Increasing conventional ultrasonographic steatosis grade cannot independently establish the presence or severity of hepatic fibrosis. A patient with severe steatosis does not necessarily have advanced fibrosis, while clinically important fibrosis may occur without marked steatosis. Therefore, ultrasonographic steatosis grade should not be regarded as a surrogate for the complete histopathological spectrum of steatotic liver disease. Recent quantitative ultrasound studies have also demonstrated the potential for more objective assessment of hepatic fat. Jin et al. reported a strong correlation between UDFF and MRI-PDFF, supporting the ability of ultrasound-based fat quantification to approximate an established quantitative imaging reference.[14] However, differences between methods at higher hepatic fat fractions indicate that quantitative ultrasound techniques should be interpreted within their validated ranges and should not automatically be considered interchangeable with MRI-based measurements. Another emerging approach is quantitative measurement of ultrasound attenuation. Huang et al. prospectively evaluated an ultrasound-guided attenuation parameter for identifying MASLD and demonstrated the feasibility of attenuation-based assessment of hepatic steatosis.[16] Together with UDFF, tissue attenuation imaging, tissue scatter-distribution imaging, and elastography, these developments represent a transition from subjective visual assessment toward quantitative multiparametric ultrasonography. These advances do not diminish the clinical utility of conventional ultrasonography. B-mode ultrasonography remains widely available, non-invasive, relatively inexpensive, and suitable for initial recognition of hepatic steatosis, particularly in settings where advanced imaging is unavailable. Quantitative ultrasound and elastography should instead be considered complementary technologies that may improve characterization of hepatic fat and fibrosis where clinically indicated.[11,15,16] The findings of the present study therefore support a broader interpretation of fatty liver identified during abdominal ultrasonography. Hepatic steatosis should not be considered an isolated radiological finding. In this study, increasing sonographic severity was accompanied by progressively higher BMI, fasting blood glucose, triglycerides, and ALT, while participants with NAFLD demonstrated an overall adverse metabolic profile. Identification of hepatic steatosis provides an opportunity to evaluate accompanying obesity, glucose abnormalities, dyslipidaemia, blood pressure, and other cardiometabolic risk factors. From a clinical perspective, conventional ultrasonography can serve as an accessible first-line method for identifying hepatic steatosis. Patients with associated metabolic abnormalities may subsequently require further risk stratification according to clinical context. Non-invasive fibrosis assessment, including validated blood-based scores and elastographic techniques, may provide additional information that conventional steatosis grading cannot supply. The purpose of such assessment is not simply to quantify hepatic fat but to identify individuals at increased risk of progressive liver disease.

Ultrasonographically detected NAFLD was frequent in this hospital-based study population and was associated with an adverse metabolic profile characterized by higher BMI, fasting blood glucose, triglycerides, total cholesterol, LDL-C, ALT, and AST and lower HDL-C. Increasing ultrasonographic steatosis grade was accompanied by progressively higher BMI, fasting blood glucose, triglycerides, and ALT, demonstrating a consistent relationship between increasing sonographic hepatic fat burden and metabolic abnormalities. The findings support the clinical importance of evaluating metabolic risk factors when hepatic steatosis is identified on routine ultrasonography. Conventional B-mode ultrasonography remains a useful and accessible initial imaging modality but does not independently quantify hepatic fat, establish steatohepatitis, or determine fibrosis stage. Quantitative ultrasound and elastographic techniques may provide complementary information where further characterization is clinically indicated. Because of the cross-sectional and hospital-based design, the findings should not be interpreted as evidence of causality or as an estimate of NAFLD prevalence in the general population. Prospective studies integrating quantitative assessment of hepatic steatosis, metabolic risk factors, and non-invasive fibrosis evaluation are warranted.

1. Younossi ZM, Golabi P, Paik JM, Henry A, Van Dongen C, Henry L. The global epidemiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among patients with type 2 diabetes. Clin Gastroenterol Hepatol. 2023;21(5):1197-1209.e5. doi:10.1016/j.cgh.2022.07.052. 2. Rinella ME, Lazarus JV, Ratziu V, Francque SM, Sanyal AJ, Kanwal F, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol. 2023;79(6):1542-1556. doi:10.1016/j.jhep.2023.06.003. 3. Shalimar, Elhence A, Bansal B, Gupta H, Anand A, Singh TP, et al. Prevalence of non-alcoholic fatty liver disease in India: a systematic review and meta-analysis. J Clin Exp Hepatol. 2022;12(3):818-829. doi:10.1016/j.jceh.2021.11.010. 4. Kannan S, Surendran S, Ravindran R, George K, Koshy M, Prasad JH. Prevalence of non-alcoholic fatty liver disease and its associated factors among adults in rural South India. Indian J Public Health. 2022;66(4):444-449. doi:10.4103/ijph.ijph_532_22. 5. Powell EE, Wong VWS, Rinella M. Non-alcoholic fatty liver disease. Lancet. 2021;397(10290):2212-2224. doi:10.1016/S0140-6736(20)32511-3. 6. Targher G, Corey KE, Byrne CD, Roden M. The complex link between NAFLD and type 2 diabetes mellitus-mechanisms and treatments. Nat Rev Gastroenterol Hepatol. 2021;18(9):599-612. doi:10.1038/s41575-021-00448-y. 7. Mantovani A, Petracca G, Beatrice G, Csermely A, Lonardo A, Schattenberg JM, et al. Non-alcoholic fatty liver disease and risk of incident diabetes mellitus: an updated meta-analysis of 501,022 adult individuals. Gut. 2021;70(5):962-969. doi:10.1136/gutjnl-2020-322572. 8. Cusi K, Isaacs S, Barb D, Basu R, Caprio S, Garvey WT, et al. American Association of Clinical Endocrinology clinical practice guideline for the diagnosis and management of nonalcoholic fatty liver disease in primary care and endocrinology clinical settings. Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010. 9. Muzurović E, Mikhailidis DP, Mantzoros C. Non-alcoholic fatty liver disease, insulin resistance, metabolic syndrome and their association with vascular risk. Metabolism. 2021;119:154770. doi:10.1016/j.metabol.2021.154770. 10. Zhou JH, Cai JJ, She ZG, Li HL. Noninvasive evaluation of nonalcoholic fatty liver disease: current evidence and practice. World J Gastroenterol. 2019;25(11):1307-1326. doi:10.3748/wjg.v25.i11.1307. 11. Jin X, Yip TCF, Wong GLH, Wong VWS, Lai JCT. The new definition of metabolic dysfunction-associated steatotic liver disease: the role of ultrasound and elastography. Ultrasonography. 2025;44(3):189-201. doi:10.14366/usg.24219. 12. Flagiello V, Gallo P, Terracciani F, Falcomatà A, De Vincentis A, Di Pasquale G, et al. Ultrasound-derived visceral adipose tissue as a reliable marker of hepato-metabolic risk in patients with MASLD. Dig Liver Dis. 2026;58(1):113-118. doi:10.1016/j.dld.2025.11.008. 13. Tavaglione F, Flagiello V, Terracciani F, Gallo P, Capparelli E, Spiezia C, et al. Non-invasive assessment of hepatic steatosis by ultrasound-derived fat fraction in individuals at high-risk for metabolic dysfunction-associated steatotic liver disease. Diabetes Metab Res Rev. 2024;40(3):e3787. doi:10.1002/dmrr.3787. 14. Jin H, Jiao M, Yu C, Ren T, Chen Q, Dai Z, et al. Discovery of ultrasound-derived fat fraction as a non-invasive tool for MASLD diagnosis. J Transl Med. 2025;23:1014. doi:10.1186/s40001-025-03229-4. 15. Huang TY, Li ZY, Tian J, Xie XJ, Lee JM, Ren XP, et al. Metabolic dysfunction-associated steatotic liver disease at quantitative US: international prospective study. Radiology. 2025;316(1):e242564. doi:10.1148/radiol.242564. 16. Huang YL, Sun C, Wang Y, Cheng J, Wang SW, Wei L, et al. Ultrasound-guided attenuation parameter for identifying metabolic dysfunction-associated steatotic liver disease: a prospective study. Ultrasonography. 2025;44(2):134-144. doi:10.14366/usg.24204.