Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the most common chronic liver disorders worldwide and represents a growing public health concern. It is characterized by excessive accumulation of fat in hepatocytes in individuals who consume little or no alcohol. NAFLD encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and even hepatocellular carcinoma [1]. The rising prevalence of NAFLD parallels the increasing incidence of metabolic disorders such as obesity, type 2 diabetes mellitus, dyslipidemia, and hypertension. These conditions collectively form the basis of metabolic syndrome, a cluster of interrelated risk factors that significantly increase the risk of cardiovascular disease and type 2 diabetes. NAFLD is now considered the hepatic manifestation of metabolic syndrome, reflecting the underlying metabolic dysfunction [2]. Metabolic syndrome is defined by the presence of central obesity, insulin resistance, elevated blood pressure, and abnormal lipid profile. Insulin resistance plays a key role in the pathogenesis of NAFLD by promoting increased lipolysis, hepatic fat accumulation, and oxidative stress, which contribute to liver injury and inflammation [3]. The close association between NAFLD and metabolic syndrome underscores the importance of early detection and comprehensive evaluation. Ultrasonography is widely used as the first-line imaging modality for the detection of fatty liver due to its non-invasive nature, affordability, and availability. It detects hepatic steatosis based on increased echogenicity of liver parenchyma compared to the renal cortex, along with attenuation of the ultrasound beam and poor visualization of intrahepatic structures. Ultrasonography also allows grading of fatty liver into mild, moderate, and severe categories, which can provide an estimate of disease severity [4]. Although liver biopsy remains the gold standard for diagnosis of NAFLD, it is invasive, costly, and not feasible for routine screening. In contrast, ultrasonography offers a practical alternative for large-scale screening and follow-up of patients, particularly in resource-limited settings [5]. The association between fatty liver and metabolic syndrome has been widely reported, with studies showing that individuals with NAFLD have a significantly higher prevalence of metabolic abnormalities compared to those without fatty liver. This relationship is bidirectional, as metabolic syndrome predisposes to NAFLD, and NAFLD itself increases the risk of developing metabolic syndrome and cardiovascular disease [6]. Early identification of fatty liver and its correlation with metabolic syndrome is essential for implementing preventive and therapeutic strategies to reduce disease progression and associated complications. Therefore, this study aims to evaluate fatty liver using ultrasonography and assess its association with metabolic syndrome in patients attending a tertiary care centre.

Study Design and Setting This study was a prospective observational study conducted in a tertiary care teaching hospital. The study involved collaboration between the Department of General Medicine and the Department of Radiology. The Department of General Medicine was responsible for clinical evaluation and assessment of metabolic syndrome, while the Department of Radiology performed and interpreted ultrasonographic examinations. Study Duration The study was conducted over a period of 6 months. Study Population The study included patients attending the outpatient and inpatient services who were referred for abdominal ultrasonography during the study period. Sample Size A total of 120 patients who fulfilled the inclusion criteria were enrolled consecutively during the study period. Inclusion Criteria • Patients aged ≥18 years • Patients undergoing abdominal ultrasonography • Patients willing to participate and provide informed consent Exclusion Criteria • History of significant alcohol consumption • Known cases of chronic liver disease or cirrhosis • Patients with hepatitis B or hepatitis C infection • Pregnant women • Patients on hepatotoxic drugs Data Collection Procedure Data were collected using a structured proforma. Each participant underwent detailed clinical, biochemical, and radiological evaluation. Clinical Assessment: • Demographic details: age, gender • Anthropometric measurements: body mass index (BMI), waist circumference • Blood pressure measurement • Medical history including diabetes, hypertension, and dyslipidemia Biochemical Assessment • Fasting blood glucose • Lipid profile (total cholesterol, triglycerides, HDL, LDL) Ultrasonographic Assessment; Abdominal ultrasonography was performed using a standard ultrasound machine with a convex probe. Fatty liver was diagnosed based on: • Increased echogenicity of liver parenchyma • Hepatorenal contrast • Attenuation of ultrasound beam • Poor visualization of intrahepatic vessels Grading of Fatty Liver • Grade I (Mild): Slight increase in echogenicity with normal visualization of diaphragm and vessels • Grade II (Moderate): Moderate increase in echogenicity with slightly impaired visualization • Grade III (Severe): Marked increase in echogenicity with poor visualization of diaphragm and vessels Definition of Metabolic Syndrome Metabolic syndrome was diagnosed based on standard criteria (e.g., ATP III), requiring the presence of three or more of the following: • Central obesity (increased waist circumference) • Elevated fasting blood glucose • Hypertension • Elevated triglycerides • Reduced HDL cholesterol Outcome Measures Primary Outcome • Detection and grading of fatty liver by ultrasonography Secondary Outcomes • Prevalence of metabolic syndrome • Association between fatty liver and metabolic syndrome • Correlation between fatty liver grade and metabolic parameters Statistical Analysis Data were entered into Microsoft Excel and analyzed using Statistical Package for Social Sciences (SPSS) version 20.0. Continuous variables were expressed as mean ± standard deviation (SD).Categorical variables were expressed as frequency and percentage. Chi-square test was used to assess association between categorical variables. A p-value < 0.05 was considered statistically significant Ethical Considerations Approval was obtained from the Institutional Ethics Committee (IEC).Written informed consent was obtained from all participants

Fatty liver was detected in a majority of patients, indicating a high prevalence in the study population. Table 1: Prevalence of Fatty Liver (n = 120) Category Number (n) Percentage (%) Fatty liver present 78 65% Normal liver 42 35% Among patients with fatty liver, Grade I was the most common, followed by Grade II and Grade III. Table 2: Grading of Fatty Liver (n = 78) Grade Number (n) Percentage (%) Grade I (Mild) 40 51% Grade II (Moderate) 25 32% Grade III (Severe) 13 17% A statistically significant association was observed between fatty liver and metabolic syndrome (p < 0.001). Patients with fatty liver had a higher prevalence of metabolic syndrome compared to those with normal liver. Table 3: Association of Fatty Liver with Metabolic Syndrome Category Metabolic Syndrome Present Absent Total p-value Fatty liver (n=78) 52 26 78 < 0.001 Normal liver (n=42) 10 32 42 The prevalence of metabolic syndrome increased with the severity of fatty liver, indicating a positive correlation between fatty liver grade and metabolic risk. Table 4: Fatty Liver Grade vs Metabolic Syndrome Grade Metabolic Syndrome Present Percentage (%) p-value Grade I 22 55% < 0.001 Grade II 18 72% Grade III 12 92%

Non-alcoholic fatty liver disease (NAFLD) has become a significant global health concern, paralleling the increasing prevalence of metabolic syndrome and its components. In the present study, fatty liver was detected in 65% of patients, indicating a high burden of hepatic steatosis in the study population. This prevalence is comparable to previous studies that have reported NAFLD prevalence ranging from 25% to 70%, depending on population characteristics and diagnostic methods [7]. Ultrasonography proved to be a reliable and effective modality for the detection and grading of fatty liver in this study. Its non-invasive nature, accessibility, and cost-effectiveness make it an ideal screening tool, particularly in resource-limited settings. Similar studies have demonstrated that ultrasonography has good sensitivity for detecting moderate to severe steatosis, supporting its role in routine clinical practice [8]. In the present study, Grade I fatty liver was the most common (51%), followed by Grade II and Grade III. This distribution suggests that a majority of patients were identified at an early stage of the disease, which is important for timely intervention. Comparable findings have been reported in previous studies, where mild steatosis constituted the largest proportion of cases [9]. A key finding of this study was the significant association between fatty liver and metabolic syndrome (p < 0.001). Patients with fatty liver had a markedly higher prevalence of metabolic syndrome compared to those with normal liver. This observation reinforces the concept that NAFLD is the hepatic manifestation of metabolic syndrome. Similar associations have been reported in earlier studies, highlighting the strong link between hepatic steatosis and metabolic abnormalities such as obesity, diabetes, and dyslipidemia [10]. Furthermore, the present study demonstrated a progressive increase in the prevalence of metabolic syndrome with increasing grades of fatty liver, with the highest prevalence observed in Grade III (92%). This finding indicates a clear dose–response relationship between the severity of hepatic steatosis and metabolic risk factors. Previous studies have also reported that higher grades of fatty liver are associated with increased insulin resistance and greater cardiovascular risk [11]. The pathophysiological link between NAFLD and metabolic syndrome is largely mediated by insulin resistance, which leads to increased lipolysis, elevated free fatty acids, and hepatic fat accumulation. Additionally, oxidative stress and inflammatory pathways contribute to liver injury and progression of disease. These mechanisms explain the close association observed between fatty liver and metabolic abnormalities in this study [12].

Fatty liver is highly prevalent and shows a strong and statistically significant association with metabolic syndrome. Ultrasonography is a reliable, non-invasive tool for the detection and grading of fatty liver. The severity of hepatic steatosis demonstrates a clear dose–response relationship with metabolic risk factors, with higher grades associated with increased prevalence of metabolic syndrome. Early identification of fatty liver through ultrasonography can serve as an important marker for underlying metabolic abnormalities, enabling timely intervention to prevent disease progression and associated cardiovascular complications.

1. Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of NAFLD. Hepatology. 2012;55(6):2005–2023. 2. Lonardo A, Bellentani S, Argo CK, et al. Epidemiological modifiers of NAFLD. Dig Liver Dis. 2015;47(12):997–1006. 3. Alberti KG, Zimmet P, Shaw J. The metabolic syndrome. Lancet. 2005;366(9491):1059–1062. 4. Hernaez R, Lazo M, Bonekamp S, et al. Diagnostic accuracy of ultrasonography for fatty liver. Hepatology. 2011;54(3):1082–1090. 5. Bedossa P. Current histological classification of NAFLD. Gastroenterol Clin Biol. 2007;31(1):4–7. 6. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver and metabolic syndrome. Hepatology. 2003;37(4):917–923. 7. Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of NAFLD. Hepatology. 2016;64(1):73–84. 8. Hernaez R, Lazo M, Bonekamp S, et al. Diagnostic accuracy of ultrasonography for fatty liver. Hepatology. 2011;54(3):1082–1090. 9. Das K, Das K, Mukherjee PS, et al. Nonobese population in NAFLD. Hepatology. 2010;51(5):1593–1602. 10. Marchesini G, Brizi M, Bianchi G, et al. NAFLD as a feature of metabolic syndrome. Diabetes. 2001;50(8):1844–1850. 11. Targher G, Bertolini L, Padovani R, et al. NAFLD and cardiovascular risk. Diabetes Care. 2005;28(10):2499–2504. 12. Buzzetti E, Pinzani M, Tsochatzis EA. Pathogenesis of NAFLD. Metabolism. 2016;65(8):1038–1048.