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Correlation of Adipokines (Omentin-1 and Chemerin) in Type 2 Diabetes Mellitus with Metabolic Syndrome Patients: A
1Department of Biochemistry, Pacific Institute of Medical Sciences, Sai Tirupati University, Udaipur, Rajasthan, India.
Context:
Type 2 diabetes mellitus (T2DM) is characterized by peripheral insulin resistance, largely due to downregulation of insulin receptors. Altered secretion of adipokines is frequently observed in diabetic individuals thought to contribute to impaired glucose metabolism. Nonetheless, the regulatory mechanisms that oversee adipokine expression and function are still under discussion.
Aim:
This study aims to compare serum adipokines (omentin-1 and chemerin) in T2DM patients with metabolic syndrome (MetS) and healthy controls and to examine their relationship with metabolic parameters.
Settings And Design:
A case-control study was performed involving 294 individuals aged 25-75 years, comprising 147 patients with T2DM and 147 healthy controls matched for age and sex.
Subjects And Methods:
Participants underwent detailed history taking, clinical examination, anthropometric assessment, blood pressure measurement, and laboratory investigations, including diabetic markers, lipid profile, and serum omentin-1 and chemerin levels.
Statistical Analysis Used:
Data were analyzed using SPSS version 20.0. Student's t-test and correlation coefficient analysis were applied, with P < 0.05 considered statistically significant.
Results:
Mean serum omentin-1 levels were significantly lower in T2DM cases compared to controls (22.8 ± 6.3 vs. 38.4 ± 7.1 ng/mL, P < 0.001). Conversely, serum chemerin levels were significantly higher in cases than controls (178.5 ± 25.6 vs. 129.2 ± 21.4 ng/mL, P < 0.001). Chemerin showed positive correlation with body mass index, waist-hip ratio, fasting glucose, glycated hemoglobin, and triglycerides, while omentin-1 showed inverse correlations with these parameters.
Conclusions:
Decreased omentin-1 and increased chemerin are strongly associated with insulin resistance and may contribute to the pathogenesis of T2DM with MetS.
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