European Journal of Cardiovascular Medicine

Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, hyperglycemia, and progressive β-cell dysfunction. It is a major global health concern, contributing to increased morbidity and mortality due to vascular complications, which can be categorized into microvascular (diabetic retinopathy, nephropathy, and neuropathy) and macrovascular (coronary artery disease, peripheral arterial disease, and cerebrovascular disease) complications (1,2). Obesity is a well-established risk factor for T2DM and is often associated with a higher prevalence of vascular complications due to systemic inflammation, dyslipidemia, and endothelial dysfunction (3). However, non-obese individuals with T2DM also develop significant vascular complications, suggesting that mechanisms beyond adiposity contribute to disease pathogenesis (4,5).

Obesity-related metabolic disturbances, such as increased levels of pro-inflammatory cytokines and insulin resistance, accelerate vascular damage in diabetic patients (6). However, in non-obese T2DM patients, genetic predisposition, ectopic fat deposition, and low-grade inflammation may also play a role in vascular complications (7). Several studies have reported that non-obese individuals with T2DM exhibit a comparable risk of cardiovascular disease due to poor glycemic control, altered lipid metabolism, and endothelial dysfunction (8,9). Despite similar HbA1c levels, variations in inflammatory markers and lipid profiles between obese and non-obese T2DM patients could contribute to differences in vascular outcomes (10).

Understanding the role of obesity in vascular complications among T2DM patients is crucial for individualized management strategies. Identifying risk factors beyond BMI can help optimize preventive and therapeutic approaches. This study aims to evaluate and compare vascular complications in non-obese and obese T2DM patients to better understand their pathophysiology and clinical implications.

Study Design and Population

This cross-sectional study was conducted in a tertiary care hospital, involving 200 patients diagnosed with Type 2 Diabetes Mellitus (T2DM). The study population was divided into two groups: 100 obese T2DM patients (Body Mass Index [BMI] ≥ 30 kg/m²) and 100 non-obese T2DM patients (BMI < 25 kg/m²). Patients with a history of Type 1 Diabetes Mellitus, secondary diabetes, chronic inflammatory conditions, or those on immunosuppressive therapy were excluded from the study.

Clinical and Biochemical Assessments

A detailed medical history was obtained from all participants, including disease duration, medication history, and lifestyle factors. A thorough physical examination was conducted to record BMI, blood pressure, and waist-to-hip ratio.

Fasting blood samples were collected to assess glycemic control (HbA1c), lipid profile (total cholesterol, LDL, HDL, and triglycerides), and inflammatory markers (C-reactive protein [CRP] and interleukin-6 [IL-6]). Kidney function was evaluated using the estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).

Vascular Complication Assessment

• Peripheral Arterial Disease (PAD): Ankle-Brachial Index (ABI) was measured using Doppler ultrasonography, with an ABI < 0.9 indicating PAD.
• Diabetic Retinopathy: All participants underwent a fundoscopic examination by an ophthalmologist to assess retinal changes.
• Diabetic Nephropathy: Defined by an elevated UACR (>30 mg/g) and reduced eGFR (<60 mL/min/1.73 m²).

Statistical Analysis

Data were analyzed using SPSS software (version 26.0). Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables were presented as frequencies and percentages. The Student’s t-test was used to compare continuous variables, while the Chi-square test assessed categorical variables. A p-value of less than 0.05 was considered statistically significant.

Baseline Characteristics

The study included 200 T2DM patients, with 100 categorized as obese and 100 as non-obese. The mean age of the obese group was 55.2 ± 6.8 years, while that of the non-obese group was 53.5 ± 7.2 years (p = 0.08). The obese group had a significantly higher BMI (32.8 ± 2.6 kg/m²) compared to the non-obese group (23.4 ± 1.9 kg/m², p < 0.001). Systolic and diastolic blood pressure levels were also higher in obese patients (p < 0.05) (Table 1).

Glycemic and Lipid Profile

HbA1c levels were slightly higher in the obese group (8.2% ± 1.3) compared to the non-obese group (7.9% ± 1.1), but the difference was not statistically significant (p = 0.08). However, lipid abnormalities were more pronounced in the obese group, with significantly higher total cholesterol, LDL, and triglycerides, while HDL levels were lower compared to non-obese patients (p < 0.05) (Table 2).

Inflammatory Markers and Kidney Function

C-reactive protein (CRP) and interleukin-6 (IL-6) levels were significantly elevated in obese patients compared to non-obese patients (p < 0.05). Kidney function, assessed by estimated glomerular filtration rate (eGFR), was lower in the obese group (58.2 ± 8.6 mL/min/1.73 m²) compared to the non-obese group (64.7 ± 7.9 mL/min/1.73 m², p < 0.05), and albuminuria was more prevalent in obese individuals (Table 3).

Prevalence of Vascular Complications

Obese T2DM patients had a higher prevalence of vascular complications. Peripheral arterial disease (PAD) was observed in 45% of obese patients compared to 30% in the non-obese group (p = 0.02). Diabetic retinopathy was present in 50% of obese individuals versus 35% of non-obese individuals (p = 0.03). Nephropathy was detected in 40% of obese patients, whereas 25% of non-obese patients had this complication (p = 0.04) (Table 4).

Table 1: Baseline Characteristics of the Study Population

Table 2: Glycemic and Lipid Profile

Table 3: Inflammatory Markers and Kidney Function

Table 4: Prevalence of Vascular Complications

The findings indicate that obese T2DM patients are at a higher risk of vascular complications, with significantly elevated inflammatory markers and altered lipid profiles contributing to disease progression (Tables 2–4).

The present study evaluated vascular complications in obese and non-obese individuals with Type 2 Diabetes Mellitus (T2DM). Our findings indicate that obesity significantly contributes to an increased prevalence of vascular complications, as demonstrated by higher rates of peripheral arterial disease (PAD), diabetic retinopathy, and nephropathy among obese T2DM patients. These complications appear to be influenced by multiple factors, including metabolic dysregulation, systemic inflammation, and lipid abnormalities.

Obesity is widely recognized as a major risk factor for cardiovascular diseases and metabolic disorders (1). Adipose tissue dysfunction in obese individuals promotes insulin resistance, inflammation, and endothelial dysfunction, all of which accelerate vascular complications in diabetes (2,3). Elevated levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) in obese T2DM patients, as observed in our study, align with previous reports emphasizing the role of chronic low-grade inflammation in vascular impairment (4,5). Inflammatory cytokines contribute to atherogenesis and vascular remodeling, increasing susceptibility to atherosclerosis and PAD (6).

Despite the established role of obesity in vascular complications, non-obese T2DM patients also exhibited significant vascular risks, albeit at a lower prevalence than their obese counterparts. This suggests that factors beyond BMI, such as ectopic fat deposition, genetic predisposition, and endothelial dysfunction, play a crucial role in vascular complications among non-obese individuals (7,8). Some studies have reported that lean T2DM patients with visceral fat accumulation have similar cardiovascular risk profiles to obese individuals (9). Additionally, non-obese individuals with T2DM may develop vascular complications due to long-term glycemic variability, oxidative stress, and insulin resistance independent of adiposity (10,11).

Diabetic nephropathy was significantly more prevalent in obese T2DM patients in our study, which is consistent with earlier findings that obesity exacerbates renal dysfunction through glomerular hyperfiltration, increased proteinuria, and activation of the renin-angiotensin-aldosterone system (12,13). Similarly, lipid abnormalities, including elevated LDL and triglycerides and reduced HDL levels in obese individuals, are known to promote endothelial dysfunction and accelerate atherosclerosis, increasing the risk of nephropathy and cardiovascular disease (14,15).

Our study also found a higher prevalence of diabetic retinopathy in obese patients, which may be attributed to increased systemic inflammation and oxidative stress leading to microvascular damage (16). While glycemic control (as indicated by HbA1c levels) was similar between the two groups, the higher burden of vascular complications in obese individuals suggests that metabolic factors beyond glycemia, such as dyslipidemia and inflammation, significantly contribute to disease progression (17,18). However, non-obese T2DM patients also showed considerable rates of diabetic retinopathy, reinforcing the need for early screening and comprehensive risk assessment in all T2DM patients, irrespective of BMI (19).

One of the key strengths of this study is its direct comparison of vascular complications between obese and non-obese T2DM patients, providing insights into the differential risk factors contributing to disease progression. However, this study has some limitations. The cross-sectional design prevents establishing causality, and a longitudinal follow-up would be required to assess the progression of vascular complications over time. Additionally, the study did not consider the impact of medication use, dietary habits, or physical activity, which could influence vascular health outcomes.

Obese individuals with T2DM exhibit a significantly higher prevalence of vascular complications compared to their non-obese counterparts. The increased risk is likely driven by chronic inflammation, dyslipidemia, and metabolic disturbances. However, non-obese T2DM patients are not exempt from vascular complications, indicating the need for a broader assessment beyond BMI to identify at-risk individuals. Future research should focus on the underlying mechanisms contributing to vascular complications in lean diabetic patients and explore targeted prevention strategies.

Obese individuals with T2DM exhibit a significantly higher prevalence of vascular complications compared to their non-obese counterparts. The increased risk is likely driven by chronic inflammation, dyslipidemia, and metabolic disturbances. However, non-obese T2DM patients are not exempt from vascular complications, indicating the need for a broader assessment beyond BMI to identify at-risk individuals. Future research should focus on the underlying mechanisms contributing to vascular complications in lean diabetic patients and explore targeted prevention strategies.

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