Abstract Background: Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic disease characterized by impaired glucose homeostasis, insulin resistance, and progressive β-cell dysfunction, leading to significant multisystem complications and high global prevalence.
Objectives: This study was conducted to (I) measure and compare concentrations of ghrelin, leptin, and insulin in individuals with T2DM and non-diabetic controls; (II) analyze differences in metabolic profiles between the two groups; and (III) explore potential associations among insulin levels, BMI, and other hormonal and metabolic parameters assessed in the study.
Methods: A case-control study was conducted, comprising 80 individuals diagnosed with T2DM (cases) and 80 non-diabetic controls matched for age, sex, and body mass index (BMI). Clinical data were collected via standardized interviews, and venous blood samples were obtained to assess serum concentrations of ghrelin, leptin, insulin, glucose, lipid profile components, urea, and creatinine.
Results: Compared with the control group, participants with T2DM exhibited significantly higher insulin levels (28.8 ± 23.9 vs. 18.8 ± 13.5 μIU/ml; P = 0.025) and slightly elevated leptin concentrations (7.1 ± 2.7 vs. 5.9 ± 2.2 ng/ml; P = 0.081). Conversely, ghrelin concentrations were significantly lower among cases compared with controls (1189 ± 580 vs. 1531 ± 822 pg/ml; P = 0.038). Glucose (187.4 ± 74.1 vs. 98.3 ± 17.0 mg/dl; P<0.001) and triglyceride levels (212.5 ± 78.9 vs. 143.2 ± 50.4 mg/dl; P<0.001) were also markedly elevated in the cases group. Significant positive correlations were observed between insulin and both glucose (P = 0.011) and triglycerides (P = 0.049), whereas a weak, non-significant inverse correlation was identified between ghrelin and insulin levels (r = -0.213, P = 0.057).
Conclusion: Individuals with T2DM display distinct metabolic and hormonal alterations compared to non-diabetic controls, reflecting a complex endocrine interplay. The presence of both positive and inverse associations among insulin, leptin, and ghrelin highlights the multifaceted regulatory mechanisms underlying the pathophysiology of T2DM.