Evaluation Of Fasting And Postprandial Dysglycemia, Hyperinsulinemia, And Blood Pressure Combination In An Adult Health Check-Up Cohort: A Cross-Sectional Observational Study

Abstract

Introduction
Hyperinsulinemia and dysglycemia represent key precursors to type 2 diabetes mellitus and cardiovascular disease. However, the simultaneous coupling of glycemic, insulinemic, and hemodynamic metrics in real-world clinical screening settings remains insufficiently characterized.
Objectives
To evaluate baseline demographic, glycemic, hyperinsulinemic, and blood pressure profiles in an adult clinical cohort, investigating intra-domain physiological coupling, postprandial metabolic reactivity, and potential sex-based variances.
Methods
A retrospective descriptive cross-sectional study was conducted at a tertiary care hospital in Pondicherry, India, following institutional review board approval. From an eligible registry of 356 health check-up records (participants aged 30–75 years), a sample size of N = 61 (male n = 37, female n = 24) was systematically selected using a fixed sampling interval (k = 6). Standardized clinical evaluations included mean resting blood pressure from three seated readings. Biochemical assays following a 10–12 hour fast measured fasting blood sugar (FBS) and fasting insulin; postprandial blood sugar (PPBS) and postprandial insulin were evaluated 2 hours after a 75g glucose load or standardized meal. Systemic insulin resistance was estimated via HOMA-IR. Data were analyzed using IBM SPSS version 26, employing non-parametric inferential tests including Spearman rank correlation (rs), Wilcoxon signed-rank test ( Z) , and Mann-Whitney U test (U),to assess physiological coupling, postprandial reactivity, and sex-based differences ( p < 0.05 ).
Results
The cohort (mean age 56.89 ± 11.96 years) demonstrated high baseline burdens of dysglycemia (fasting blood glucose 132.07 ± 49.55mg/dL; postprandial blood glucose 212.77 ±114.91 mg/dL), hyperinsulinemia (fasting insulin 43.13 ± 48.24IU/mL; postprandial insulin 74.65 ± 75.94IU/mL), and systemic hypertension (mean systolic blood pressure 150.59 ± 13.89 mmHg; mean diastolic blood pressure 88.67 ±8.57 mmHg). Spearman rank correlation revealed strong intra-domain coupling between fasting and postprandial glucose (rs = 0.877, p < 0.001) as well as fasting and postprandial insulin (rs = 0.900, p < 0.001). Cross-domain correlations between glycemic, insulinemic, and hemodynamic variables were statistically non-significant (p > 0.05). Wilcoxon signed-rank tests confirmed significant postprandial increases in glucose ( Z = -6.727, p < 0.001 ) and insulin ( Z = -6.360, p < 0.001 ), with 96.7% (n = 59) of participants showing positive rank increases. Mann-Whitney U tests showed no significant sex-based differences across glycemic, postprandial insulinemic, or blood pressure profiles (p > 0.05).
Conclusion
The findings highlight pronounced compensatory hyperinsulinemia and severe postprandial metabolic excursions, reflecting blunted tissue sensitivity and near-exhaustion of pancreatic β-cell reserve. The physiological independence between metabolic and hemodynamic axes suggests that while these risk factors co-occur in metabolic syndrome, their individual severity follows distinct pathophysiological trajectories. The absence of sex-based variance underscores a shared cardiometabolic disease burden across both sexes in this clinical setting, supporting the routine inclusion of hyperinsulinemia screening alongside standard glycemic and blood pressure metrics.