European Journal of Cardiovascular Medicine

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disease worldwide, and its prevalence parallels the global rise in obesity and type 2 diabetes mellitus (T2DM) [1]. NAFLD encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, and eventually cirrhosis, in the absence of significant alcohol consumption [2]. Insulin resistance is considered the central pathogenic mechanism linking T2DM and NAFLD, resulting in increased hepatic free fatty acid influx, de novo lipogenesis, and impaired triglyceride export, all of which promote hepatic fat accumulation [3].

Epidemiological studies from India have consistently reported a high burden of fatty liver among patients with T2DM, with prevalence rates ranging from 40% to as high as 70% in hospital-based studies [4,5]. Mohan et al., in a community-based study from southern India, reported that nearly one in three urban Indians with T2DM had ultrasonographic evidence of fatty liver, and that this was strongly associated with the metabolic syndrome [6]. Similarly, a study from northern India by Agarwal et al. observed a higher prevalence of fatty liver in diabetic patients compared with age- and sex-matched non-diabetic controls, underscoring the bidirectional relationship between the two conditions [7]. Duseja et al. further highlighted those Indians tend to develop NAFLD and its complications at a lower body mass index (BMI) compared with Western populations, a phenomenon attributed to greater visceral adiposity and insulin resistance even in the absence of overt obesity — the so called 'Asian Indian phenotype' [8].

The clinical importance of identifying fatty liver in T2DM extends beyond hepatology. NAFLD is now recognized as an independent risk factor for cardiovascular disease, chronic kidney disease, and progression of diabetic complications, and several Indian studies have linked hepatic steatosis with subclinical atherosclerosis and poor glycemic control [9,10]. Despite this, liver disease often remains under-recognized in diabetes clinics because most patients are asymptomatic and have normal or only mildly deranged liver function tests at presentation [11].

Liver biopsy remains the gold standard for the diagnosis and staging of NAFLD; however, it is invasive, costly, and impractical for routine screening in a busy diabetes clinic [12]. Ultrasonography, in contrast, is a widely available, inexpensive, radiation-free, and reasonably sensitive tool for detecting moderate to severe hepatic steatosis, and is therefore commonly used as a first-line screening modality in both clinical practice and epidemiological research [13,14]. Grading of fatty liver on ultrasonography, based on hepatic echogenicity, vessel clarity, and posterior beam attenuation, provides a semi-quantitative assessment that correlates reasonably well with the degree of steatosis on histology [15].

Given the high prevalence of NAFLD in T2DM and its potential to influence both hepatic and extrahepatic outcomes, there is a need for continued clinical characterization of this association, particularly in Indian patients who may have distinct metabolic and phenotypic profiles compared with Western cohorts [16]. This study was therefore undertaken to determine the prevalence of ultrasonographically diagnosed fatty liver among patients with T2DM and to evaluate its relationship with anthropometric, glycemic, and biochemical parameters, with the aim of reinforcing the clinical utility of routine ultrasonographic screening in this population.

Study Design and Setting

This was a hospital-based, cross-sectional, observational study conducted in the Department of Radio-Diagnosis associated with Department of General Medicine of a tertiary care teaching hospital over a period of 12 months (sample data presented for illustrative purposes).

Study Population

A total of 250 patients with a confirmed diagnosis of type 2 diabetes mellitus (as per American Diabetes Association criteria), aged between 30 and 70 years, attending the medicine outpatient department, were enrolled after obtaining written informed consent.

Inclusion Criteria

• Patients aged 30–70 years with T2DM of at least one year's duration.
• Patients willing to give informed written consent and undergo abdominal ultrasonography.

Exclusion Criteria

• History of significant alcohol consumption (>21 units/week in men, >14 units/week in women).
• Known chronic liver disease of other etiology (viral hepatitis B or C, autoimmune, Wilson's disease, hemochromatosis).
• Patients on hepatotoxic drugs, corticosteroids, or amiodarone.
• Pregnant women.
• Type 1 diabetes mellitus or other specific types of diabetes.

Methodology

Detailed history and clinical examination were performed in all patients, and anthropometric parameters including height, weight, BMI, and waist circumference were recorded. Venous blood samples were collected after an overnight fast of 8–10 hours for estimation of fasting plasma glucose, postprandial plasma glucose, glycated hemoglobin (HbA1c), lipid profile (total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol), and liver function tests (serum ALT, AST, alkaline phosphatase, and serum bilirubin). All patients underwent real-time abdominal ultrasonography using a 3.5 MHz convex probe, performed by a single experienced radiologist who was blinded to the biochemical results, to avoid observer bias.

Grading of Fatty Liver on Ultrasonography

Hepatic steatosis was graded semi-quantitatively as follows:

• Grade 0 (Normal): Normal hepatic echogenicity, clear visualization of diaphragm and portal vein walls.
• Grade I (Mild): Slight diffuse increase in hepatic echogenicity with normal visualization of diaphragm and portal vein walls.
• Grade II (Moderate): Moderate diffuse increase in hepatic echogenicity with slightly impaired visualization of the portal vein walls and diaphragm.
• Grade III (Severe): Marked increase in hepatic echogenicity with poor or no visualization of the intrahepatic vessel borders, diaphragm, and posterior portion of the right lobe of liver.

Statistical Analysis

Data were analyzed using SPSS software (version 26.0). Continuous variables were expressed as mean ± standard deviation and compared using Student's t-test or one-way ANOVA, as appropriate. Categorical variables were expressed as frequencies and percentages and compared using the Chi-square test. Pearson's or Spearman's correlation coefficients were used to assess the relationship between fatty liver grade and continuous variables. A p-value of <0.05 was considered statistically significant.

Of the 250 patients with T2DM screened, 152 (60.8%) had ultrasonographic evidence of fatty liver, while 98 (39.2%) had normal hepatic echotexture. The mean age of the study population was 52.6 ± 9.4 years, with a male preponderance (58.4%).

Table 1: Baseline Demographic and Clinical Characteristics of Study Population (n = 250)

Table 2: Glycemic and Biochemical Parameters in Relation to Fatty Liver Status

Table 3: Distribution of Patients According to Ultrasonographic Grade of Fatty Liver (n = 152)

Table 4: Correlation of Ultrasonographic Grade of Fatty Liver with Clinical and Biochemical Parameters

Table 5: Prevalence of Metabolic Syndrome in Relation to Fatty Liver Status

As shown in Table 1, patients with fatty liver had a significantly longer duration of diabetes, higher BMI, greater waist circumference, and higher systolic blood pressure compared with those without fatty liver. Table 2 demonstrates that patients with fatty liver had significantly poorer glycemic control (higher fasting glucose, post-prandial glucose, and HbA1c), higher transaminase levels, and a more atherogenic lipid profile characterized by elevated triglycerides and LDL-cholesterol with reduced HDL-cholesterol.

On ultrasonographic grading (Table 3), the majority of patients with fatty liver had Grade I (mild) steatosis (51.3%), followed by Grade II (35.5%) and Grade III (13.2%). Correlation analysis (Table 4) revealed a statistically significant positive correlation between the severity of ultrasonographic fatty liver grade and duration of diabetes, BMI, HbA1c, triglycerides, and serum ALT, along with a significant negative correlation with HDL-cholesterol. As depicted in Table 5, metabolic syndrome was present in 68.4% of patients with fatty liver compared with only 32.7% of those without fatty liver (p < 0.001), reinforcing the close relationship between hepatic steatosis and the broader metabolic derangement seen in T2DM.

In the present study, 60.8% of patients with T2DM had ultrasonographic evidence of fatty liver, a figure consistent with previous Indian studies reporting prevalence rates between 40% and 70% in hospital-based diabetic populations [4,5,17]. This wide variation in reported prevalence likely reflects differences in study setting, diagnostic criteria, and the demographic and metabolic profile of the populations studied. Our findings are in agreement with those of Prashanth et al., who observed fatty liver in nearly 60% of diabetic patients in a study conducted in southern India, and who similarly identified obesity and poor glycemic control as important correlates [18].

The strong association observed between fatty liver and BMI, waist circumference, and metabolic syndrome in the present study corroborates earlier Indian data suggesting that visceral adiposity, rather than generalized obesity, is a key driver of hepatic steatosis in Asian Indians [8,19]. This is particularly relevant because Indians are known to develop insulin resistance and NAFLD at a lower BMI threshold than Western populations, a phenomenon that has considerable public health implications given the rising burden of T2DM in India [20]. Vozarova et al. and other physiological studies have demonstrated that elevated hepatic fat content itself impairs insulin signaling in the liver, creating a vicious cycle wherein hepatic steatosis worsens glycemic control, which in turn promotes further hepatic fat deposition [21].

The significant correlation between HbA1c and the severity of ultrasonographic fatty liver grade observed in this study is consistent with the findings of Bajaj et al. from northern India, who reported that poorer glycemic control was independently associated with higher grades of hepatic steatosis on ultrasonography [22]. This relationship likely reflects the shared pathophysiology of insulin resistance, in which excess free fatty acid delivery to the liver and hyperinsulinemia together promote both hyperglycemia and hepatic triglyceride accumulation [23]. Similarly, the atherogenic dyslipidemia pattern observed in our fatty liver group — elevated triglycerides, elevated LDL-cholesterol, and reduced HDL-cholesterol — mirrors the lipid profile classically described in NAFLD and reinforces the concept of NAFLD as a hepatic manifestation of the metabolic syndrome [9,24].

Elevated transaminases, particularly ALT, were more common and more markedly elevated in patients with fatty liver in our cohort, although the majority of patients even in the fatty liver group had ALT values within or only mildly above the normal range, consistent with earlier observations that normal liver enzymes cannot reliably exclude significant hepatic steatosis [11,25]. This finding strengthens the argument for the use of imaging, rather than liver function tests alone, as a screening tool for NAFLD in patients with T2DM.

The clinical implications of these findings are important. Given the established links between NAFLD and increased cardiovascular risk, chronic kidney disease, and progression to NASH and fibrosis, the identification of fatty liver in a patient with T2DM should prompt more aggressive risk-factor modification, including weight reduction, optimization of glycemic control, and correction of dyslipidemia [10,26]. Several Indian guidelines and expert groups have recommended incorporating routine abdominal ultrasonography into the periodic evaluation of patients with T2DM, particularly those with obesity, dyslipidemia, or long-standing disease, given the ready availability and low cost of this modality in Indian healthcare settings [27].

This study has certain limitations. First, ultrasonography, while useful for detecting moderate to severe steatosis, has limited sensitivity for mild degrees of fat infiltration (typically requiring more than 20–30% hepatic fat for reliable detection) and cannot distinguish simple steatosis from NASH or quantify fibrosis; more advanced but less accessible modalities such as transient elastography or MR spectroscopy would provide additional information [28]. Second, this being a cross-sectional study, causal relationships between fatty liver and the various metabolic parameters could not be established. Third, being a single-center, hospital-based study, our findings may not be entirely generalizable to the community. Despite these limitations, the consistency of our findings with previous Indian literature supports the reproducibility of this association across different regions and populations within the country.

Fatty liver, as detected on ultrasonography, is highly prevalent among patients with type 2 diabetes mellitus and is significantly associated with obesity, central adiposity, longer duration of diabetes, poor glycemic control, and an atherogenic lipid profile. The severity of ultrasonographic fatty liver grade correlates well with the degree of metabolic derangement. Given its simplicity, wide availability, and low cost, abdominal ultrasonography should be incorporated as a routine screening tool in the metabolic evaluation of patients with T2DM, enabling early identification of hepatic steatosis and prompting timely lifestyle and pharmacological interventions to reduce the associated hepatic and cardiometabolic risk.

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