Type-2 diabetes mellitus (T2DM) is a major contributor to atherosclerotic cardiovascular disease (ASCVD), and dyslipidemia represents one of the most consistent metabolic links between chronic hyperglycemia and vascular injury [1]. The characteristic lipid abnormalities in T2DM include elevated triglycerides (TG), increased triglyceride-rich lipoproteins such as very-low-density lipoproteins (VLDL) and their remnants, reduced high-density lipoprotein cholesterol (HDL-C), and a predominance of small, dense low-density lipoprotein (LDL) particles with enhanced atherogenic potential [2,3]. Even in the absence of markedly elevated fasting LDL-C levels, these qualitative lipoprotein alterations associated with insulin resistance promote arterial lipid retention, oxidative stress, inflammation, and endothelial dysfunction, thereby accelerating atherogenesis [3,4]. These lipid disturbances are frequently intensified by coexisting obesity and poor glycemic control, both of which are common among adults with T2DM [4].

Traditionally, lipid assessment has been performed in the fasting state to minimize post-meal variability. However, individuals spend most hours of the day in a fed or post-prandial state, and contemporary evidence increasingly recognizes atherosclerosis as a process influenced by repeated post-prandial surges of triglyceride-rich lipoproteins and remnant cholesterol [5]. Post-prandial hypertriglyceridemia is closely associated with coronary risk and reflects impaired clearance and/or increased production of triglyceride-rich lipoproteins, abnormalities that are particularly pronounced in insulin-resistant states and T2DM [5,6]. In addition, post-prandial hyperglycemia and hyperlipidemia frequently coexist and act synergistically, amplifying oxidative stress and pro-inflammatory signaling in the post-meal period, thereby enhancing vascular injury [6].

In routine clinical practice, reliance solely on fasting lipid parameters can underestimate the true atherogenic burden, especially in individuals who exhibit exaggerated post-prandial triglyceride and VLDL responses, a pattern commonly observed in patients with T2DM. Measurement of lipid parameters in the post-prandial state therefore provides additional clinically relevant information, improving recognition of residual cardiovascular risk and facilitating more comprehensive risk stratification and management strategies. Despite growing international evidence, data from Indian tertiary care settings directly comparing fasting and post-prandial lipid profiles in patients with T2DM and matched healthy controls remain limited, underscoring the need for further evaluation.

Accordingly, the objectives of the present study were: (i) to compare fasting lipid profile parameters between patients with type-2 diabetes mellitus and healthy controls; (ii) to compare post-prandial lipid profile parameters between the two groups; and (iii) to assess within-group differences between fasting and post-prandial lipid parameters among patients with type-2 diabetes mellitus.

Study design and setting:

This case–control study was carried out in the Department of Biochemistry in collaboration with the Department of General Medicine at Government Siddhartha Medical College and Government General Hospital, Vijayawada, Andhra Pradesh, a tertiary care teaching hospital. The study period was one year, from June 2023 to May 2024.

Participants:

A total of 100 adults aged 40–65 years were enrolled by consecutive sampling. The case group included 50 patients with established T2DM diagnosed as per standard clinical criteria and on follow‑up at the hospital. The control group included 50 apparently healthy volunteers without known diabetes or major systemic illness. Both sexes were included.

Inclusion and exclusion criteria:

Cases were included if they had T2DM and provided informed consent. Controls were included if fasting plasma glucose was within the normal range and there was no history of diabetes. Participants with acute infections, pregnancy, chronic liver disease, chronic kidney disease, thyroid disorders, use of drugs known to markedly alter lipid levels (e.g., systemic steroids), or recent hospitalization were excluded. Participants on stable lipid‑lowering therapy were recorded and analyzed as part of real‑world practice, while those with recent dose changes were excluded to avoid short‑term confounding.

Clinical evaluation and anthropometry:

Demographic details and clinical history were documented. Body mass index (BMI) was calculated as weight (kg)/height (m²). Routine investigations, including fasting blood sugar (FBS), renal function tests (RFT), liver function tests (LFT), and urine routine examination, were performed to screen for major organ dysfunction.

Biochemical measurements:After an overnight fast of 10–12 hours, venous blood samples were collected for estimation of fasting lipid profile and glycemic parameters. Post-prandial blood sampling was performed 2 hours after consumption of a usual mixed meal, thereby reflecting real-life exposure to post-meal lipemia and aligning with current clinical recommendations that support routine non-fasting lipid assessment [1,2]. Serum total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C) were measured using standard enzymatic methods on an automated analyzer. Low-density lipoprotein cholesterol (LDL-C) was calculated using the Friedewald formula when serum triglyceride levels were below 400 mg/dL, while very-low-density lipoprotein cholesterol (VLDL-C) was estimated as triglycerides divided by five. Glycated hemoglobin (HbA1c) was estimated using an NGSP-traceable standardized method.

Ethical considerations: The study was conducted in accordance with institutional ethical guidelines and the principles outlined in the Declaration of Helsinki. Written informed consent was obtained from all participants prior to enrollment in the study.

Statistical analysis: Data were entered in Microsoft Excel and analyzed using standard statistical software. Continuous variables were expressed as mean ± standard deviation and categorical variables as frequency and percentage. Comparisons between cases and controls were performed using the independent samples t‑test for continuous variables and chi‑square test for categorical variables. Within‑group comparison of fasting versus post‑prandial lipid parameters among cases was carried out using the paired t‑test. A p‑value <0.05 was considered statistically significant.

A total of 100 participants were evaluated in the present study, comprising 50 patients with type-2 diabetes mellitus (T2DM) and 50 healthy controls. The two groups were comparable with respect to mean age and sex distribution. However, body mass index (BMI) was significantly higher among patients with T2DM, indicating greater adiposity in the diabetic group (Table 1).

Table 1. Demographic and Anthropometric Profile of Study Participants

Glycemic parameters differed markedly between the two groups. Patients with T2DM had significantly higher fasting blood sugar and HbA1c levels compared with controls, confirming poor glycemic control among cases (Table 2).

Table 2. Glycemic Parameters in Cases and Controls

Figure 1:Glycemic Parameters in T2DM Cases and Controls

Comparison of fasting lipid profiles revealed a distinctly atherogenic pattern in the T2DM group. Fasting total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein cholesterol (VLDL-C) were significantly higher in patients with T2DM, while high-density lipoprotein cholesterol (HDL-C) levels were significantly lower when compared with healthy controls (Table 3).

Table 3. Comparison of Fasting Lipid Profile Between Cases and Controls

Figure 2:Comparison of Fasting Lipid Profile Between T2DM Cases and Controls

A similar but more pronounced pattern was observed in the post-prandial state. Post-prandial total cholesterol, triglycerides, LDL-C, and VLDL-C levels were significantly elevated in the T2DM group compared with controls, whereas HDL-C levels remained significantly lower (Table 4).

Table 4. Comparison of Post‑prandial Lipid Profile Between Cases and Controls

When fasting and post-prandial lipid parameters were compared within the T2DM group, post-prandial levels of total cholesterol, triglycerides, LDL-C, and VLDL-C showed a statistically significant increase relative to fasting values. In contrast, HDL-C levels did not demonstrate a significant change between the two states (Table 5).

Table 5. Fasting vs Post‑prandial Lipid Profile in T2DM Cases (n = 50)

Other routine biochemical parameters, including serum creatinine, serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), and urine routine examination findings, were within normal limits in both groups and did not show statistically significant differences (Table 6).

Table 6. Other Biochemical Parameters in Study Groups

This study demonstrated a consistent atherogenic lipid profile in adults with T2DM compared with healthy controls in both fasting and post‑prandial states. The observed phenotype—higher TG, higher VLDL‑C, higher LDL‑C, and lower HDL‑C—aligns with established descriptions of diabetic dyslipidemia driven by insulin resistance, increased hepatic VLDL production, and delayed clearance of TG‑rich lipoproteins [6–8]. Importantly, the post‑prandial state accentuated dyslipidemia in T2DM, particularly for TG and VLDL‑C, suggesting a greater burden of circulating remnants after meals.

Mechanistically, post‑prandial lipemia reflects the accumulation of chylomicrons, VLDL, and their remnant particles, which can penetrate the arterial intima and contribute disproportionately to cholesterol deposition and inflammation [9,14]. Reviews have emphasized that repeated post‑meal excursions in both glucose and lipids constitute “post‑prandial dysmetabolism,” a milieu linked to oxidative stress, endothelial dysfunction, and higher cardiovascular risk [10]. In individuals with T2DM, impaired lipoprotein lipase activity, increased apolipoprotein C‑III, and competition for clearance pathways between intestinal and hepatic TG‑rich particles can prolong post‑meal hypertriglyceridemia [11,13]. Our finding of a significant rise in post‑prandial TG and VLDL‑C within T2DM cases is consistent with this pathophysiology [11,13].

The clinical relevance of post‑prandial lipid testing has grown. A joint European consensus statement concluded that fasting is not routinely required for determination of a standard lipid profile, and highlighted practical laboratory cut‑points for flagging elevated non‑fasting triglycerides [1]. Complementary perspectives have further argued that routine lipid panels can be effectively interpreted in the non‑fasting state in most patients, improving convenience and potentially increasing screening uptake [2]. For T2DM, where remnant lipoproteins and post‑meal TG elevations are common, non‑fasting measures can provide incremental risk information beyond fasting values [3,4,12]. Our data support this approach by showing that post‑prandial values were consistently higher than fasting values for TC, TG, LDL‑C, and VLDL‑C in T2DM, while HDL‑C remained low across both states.

From a management viewpoint, identification of post‑prandial dyslipidemia reinforces the need for intensive lifestyle modification (weight reduction, dietary quality, and physical activity) and evidence‑based lipid‑lowering therapy as appropriate for overall ASCVD risk [6–8]. Current reviews on post‑prandial hyperlipidemia in T2DM highlight that targeting TG‑rich lipoproteins and remnants can be a rational strategy alongside LDL‑C reduction, especially when non‑fasting TG remains elevated [4,14]. In resource‑limited settings, incorporating post‑prandial lipid assessment into routine evaluation can be a practical step toward earlier recognition of residual atherogenic risk in T2DM.

Limitations

This study used a single‑center, hospital‑based sample, which limits external generalizability to the broader community. Post‑prandial sampling followed a usual mixed meal rather than a standardized fat‑load, introducing inter‑individual variation in meal composition. The analysis did not stratify participants by duration of diabetes, medication classes, or lipid‑lowering therapy intensity, which influences lipid levels and post‑meal responses

In this case–control study, adults with T2DM demonstrated a distinctly atherogenic lipid pattern compared with healthy controls in both fasting and post‑prandial states. Total cholesterol, triglycerides, LDL‑C and VLDL‑C were consistently higher, while HDL‑C remained significantly lower among cases. Within T2DM, the post‑prandial period produced additional rises in total cholesterol and triglyceride‑rich fractions, underscoring that clinically relevant lipid burden persists beyond fasting measurements. Routine assessment of post‑prandial (non‑fasting) lipids, alongside glycemic control and anthropometry, strengthens risk recognition and supports earlier, targeted interventions to reduce cardiovascular morbidity and mortality in T2DM.

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