European Journal of Cardiovascular Medicine

Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver conditions characterized by excessive hepatic fat accumulation in the absence of significant alcohol intake, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma [1]. As the global prevalence of obesity and type 2 diabetes mellitus (T2DM) has escalated, NAFLD has emerged as the most common chronic liver disease worldwide, affecting approximately one-quarter of the general adult population [2]. Among individuals with T2DM, the prevalence of NAFLD is substantially higher due to shared pathophysiological mechanisms, with insulin resistance serving as a central driver of hepatic lipid accumulation through increased lipolysis, de novo lipogenesis, and impaired fatty acid oxidation [3].

The coexistence of NAFLD and T2DM is bidirectional and synergistic: NAFLD independently increases the risk of incident T2DM by nearly two-fold, while T2DM accelerates NAFLD progression to NASH and advanced fibrosis, thereby exacerbating both hepatic and extra-hepatic complications [4,5]. Mechanistic links include chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and dysregulated adipokine secretion, which collectively promote hepatic injury, fibrogenesis, and cardiovascular risk [6]. Genetic predispositions, notably polymorphisms in PNPLA3, TM6SF2, and GCKR, further modulate individual susceptibility to NAFLD development and severity in diabetic patients [7].

Epidemiological studies underscore a global NAFLD prevalence of approximately 65% among T2DM patients, with substantial regional variability: Latin America reports the highest rates (~70%), followed by the Middle East, South Asia, and North America, whereas East Asia shows comparatively lower—but still significant—prevalence [8]. In this high-risk population, up to one-third develop NASH and over one-third exhibit clinically significant fibrosis, with nearly 15% progressing to advanced fibrosis [1]. These figures highlight the imperative for proactive screening strategies utilizing non-invasive tools—such as the Fibrosis-4 (FIB-4) index, NAFLD Fibrosis Score, transient elastography, and MRI-based modalities—to stratify risk, monitor progression, and guide timely interventions [9].

Early identification of NAFLD in T2DM patients enables implementation of lifestyle modifications—especially weight reduction through hypocaloric diets and increased physical activity—which have demonstrated histological improvements in steatosis, inflammation, and fibrosis at weight loss thresholds of 7–10%[10]. Pharmacotherapies targeting both glycemic control and hepatic pathology—such as pioglitazone, GLP-1 receptor agonists, and SGLT-2 inhibitors—have shown efficacy in reducing hepatic fat content, improving insulin sensitivity, and attenuating fibrotic progression [11]. Furthermore, bariatric surgery in eligible patients yields substantial and sustained improvements in NAFLD and metabolic comorbidities [12].

Given the high burden and progressive nature of NAFLD in T2DM, integration of liver health into diabetes management is essential. Consensus guidelines recommend routine NAFLD screening in all T2DM patients, irrespective of transaminase levels, followed by a stepwise evaluation—non-invasive scores first, imaging or elastography for indeterminate cases, and biopsy reserved for diagnostic clarification or clinical trials [9]. Multidisciplinary care involving hepatologists, endocrinologists, nutritionists, and exercise specialists can optimize outcomes by addressing metabolic risk factors, comorbidities, and patient adherence.

Study Design and Setting

This was a cross-sectional observational study conducted at a tertiary care hospital in Central India over a period of 12 months. The study aimed to assess the prevalence and risk factors associated with Non-Alcoholic Fatty Liver Disease (NAFLD) in patients diagnosed with Type 2 Diabetes Mellitus. The study was approved by the institutional ethics committee, and informed consent was obtained from all participants before enrollment.

Study Population

The study included adult patients aged 40-70 years, diagnosed with Type 2 Diabetes Mellitus, attending the outpatient department of the hospital. A total of 100 patients were recruited into the study, with inclusion and exclusion criteria outlined as follows:

Inclusion Criteria

• Adults aged 40-70 years.
• Diagnosed with Type 2 Diabetes Mellitus for at least 1 year.
• Willing to provide informed consent for participation in the study.

Exclusion Criteria

• Patients with a history of significant alcohol consumption (>30 g/day for males, >20 g/day for females).
• Patients with viral hepatitis (hepatitis B, C), cirrhosis, or other liver diseases.
• Patients with known cardiovascular disease, chronic kidney disease, or other severe comorbidities.
• Patients who were pregnant or lactating.
• Patients with acute infections or other acute illnesses.

Data Collection

A structured questionnaire was used to collect demographic information, medical history, and lifestyle factors. The following parameters were assessed:

1. Demographic Data: Age, gender, education, occupation, and family history of NAFLD or metabolic disorders.
2. Medical History: Duration of Type 2 Diabetes Mellitus, presence of comorbidities (hypertension, dyslipidemia, obesity), and use of medications.
3. Lifestyle Factors: Physical activity levels, dietary habits, and alcohol consumption.

Clinical and Laboratory Assessment

1. Physical Examination:
• Body Mass Index (BMI): BMI was calculated as weight (kg) divided by the square of height (m²).
• Waist Circumference (WC): Measured at the midpoint between the lower rib and iliac crest using a non-stretchable measuring tape.
• Blood Pressure: Blood pressure was measured in both arms after the patient rested for at least 5 minutes. The average of two readings was recorded.
2. Biochemical Investigations:
• Liver Function Tests (LFTs): Serum ALT (alanine aminotransferase), AST (aspartate aminotransferase), and bilirubin levels were measured.
• Fasting Blood Glucose (FBG): Fasting blood glucose was measured using the glucose oxidase method after a 12-hour overnight fast.
• Lipid Profile: Total cholesterol, triglycerides, HDL (high-density lipoprotein), and LDL (low-density lipoprotein) cholesterol levels were determined using standard enzymatic methods.
3. Ultrasound Examination:
• Liver Ultrasound: All participants underwent abdominal ultrasound to assess liver echogenicity. NAFLD diagnosis was confirmed based on the findings of increased liver echogenicity without any significant alcohol consumption or other liver diseases.
• NAFLD Severity: The severity of NAFLD was categorized based on the ultrasound findings into mild, moderate, or severe based on liver fat content.
4. Diagnosis of NAFLD:
• NAFLD was diagnosed based on the presence of abnormal liver ultrasound findings (increased echogenicity) and exclusion of other causes of liver disease such as alcohol consumption, viral hepatitis, or cirrhosis.

Data Analysis

Data was analyzed free software available online. Descriptive statistics, including mean, standard deviation, and percentages, were used to summarize the demographic characteristics, biochemical parameters, and ultrasound findings. The chi-square test was used to assess the association between categorical variables, while t-tests were applied to compare the means between groups. A p-value of <0.05 was considered statistically significant.

Table 1: Prevalence of NAFLD in Type 2 Diabetic Patients

This table presents the prevalence of Non-Alcoholic Fatty Liver Disease (NAFLD) among Type 2 diabetic patients. The data shows that 65% of the participants were found to have NAFLD, indicating a high prevalence of this liver condition in the diabetic population. This emphasizes the importance of early detection and management of NAFLD in diabetic patients.

Table 2: Risk Factors Associated with NAFLD in Type 2 Diabetic Patients

This table shows the risk factors associated with the presence of NAFLD in Type 2 diabetic patients. Significant associations were found between NAFLD and several risk factors, including age, gender (more males in the NAFLD group), obesity, hypertension, dyslipidemia, family history of NAFLD, and the duration of diabetes. Obesity (BMI ≥30 kg/m²) and a longer duration of diabetes were particularly strong indicators of NAFLD.

Table 3: Distribution of NAFLD Severity Based on Liver Ultrasound Findings

This table illustrates the severity of NAFLD as assessed by liver ultrasound in Type 2 diabetic patients. It shows that the majority of patients with NAFLD (46.2%) had mild disease, while 30.8% had moderate NAFLD, and 23.1% had severe NAFLD. This distribution suggests that while most diabetic patients with NAFLD have a mild form, a significant proportion also exhibit moderate to severe liver damage.

Table 4: Correlation Between NAFLD and Biochemical Markers in Type 2 Diabetic Patients

This table shows the correlation between NAFLD and various biochemical markers in Type 2 diabetic patients. Patients with NAFLD had significantly higher levels of liver enzymes (ALT, AST) and serum bilirubin compared to those without NAFLD, indicating liver dysfunction. Furthermore, patients with NAFLD had higher fasting blood glucose levels, which could suggest a more advanced stage of diabetes associated with liver damage.

Table 5: Treatment and Management Approaches for NAFLD in Type 2 Diabetic Patients

This table highlights the treatment and management strategies used for Type 2 diabetic patients with NAFLD. The majority of patients (92.3%) undergo regular monitoring of liver function, while lifestyle modifications such as diet and exercise are recommended for 69.2% of patients. Additionally, 61.5% of patients were advised to achieve weight loss of at least 5%, and 38.5% were treated with medications like insulin sensitizers or statins to manage both diabetes and NAFLD.

The prevalence of NAFLD among Type 2 diabetic patients in our study (65%) closely mirrors global estimates, with meta-analyses reporting pooled rates of 55.5% and 65.0% in T2DM populations, underscoring a consistently high burden of disease worldwide [13,14]. Age, obesity, hypertension, dyslipidemia, family history, and diabetes duration emerge repeatedly as key risk factors, aligning with findings that metabolic syndrome components and longer T2DM duration independently elevate NAFLD risk [13,15,16]. Our observed mean age difference (58.3 vs. 50.1 years) parallels reports showing older patients have higher NAFLD prevalence, likely reflecting cumulative metabolic insult over time [13]. Obesity (BMI >30 kg/m²) was present in 69.2% of NAFLD cases, consistent with studies where obesity rates ranged from 60% to 70% among diabetic NAFLD cohorts [15]. Likewise, hypertension and dyslipidemia prevalence among NAFLD patients in our work (76.9% and 73.8%, respectively) concurs with epidemiological data linking these conditions to hepatic steatosis in T2DM [15,16].

Regarding severity, our distribution of mild (46.2%), moderate (30.8%), and severe (23.1%) NAFLD cases corresponds with biopsy and imaging studies reporting that nearly one-quarter to one-third of T2DM patients present with advanced disease or fibrosis [14,15]. Elevated liver enzymes (ALT, AST) and bilirubin levels in our NAFLD group reflect biochemical profiles described in previous research, where transaminases and bilirubin serve as practical screening markers in diabetic populations [15,17].

Treatment approaches emphasizing lifestyle modification, weight reduction (>5%), and pharmacotherapy (insulin sensitizers, statins) are congruent with guideline-driven strategies reported in the literature, which recommend comprehensive metabolic management to mitigate liver fat and slow disease progression [17,18]. High rates of regular liver function monitoring (92.3%) in our cohort exceed those in many real-world studies, highlighting proactive surveillance practices that may improve early detection and intervention [16].

Common limitations—modest sample sizes, cross-sectional design, and reliance on ultrasound—are shared across studies and justify calls for longitudinal cohorts and advanced diagnostics (biopsy, elastography) to better characterize NAFLD trajectories in diabetes [13,15].

This study highlights the high prevalence of NAFLD in Type 2 diabetic patients and identifies several key risk factors, including obesity, hypertension, dyslipidemia, and a family history of NAFLD. The findings emphasize the importance of early detection and regular monitoring of liver function in diabetic patients, as well as the need for effective lifestyle interventions to prevent or slow the progression of NAFLD. With appropriate management, the adverse effects of NAFLD can be mitigated, improving long-term outcomes for Type 2 diabetic patients.

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