Abstract

Background: Diabetes mellitus (DM) is a metabolic disorder in which hyperglycemia is a characteristic feature due to impairment in insulin secretion, defective insulin action, or both reasons. One long-term complication is the ischemic heart disease (IHD) which is a major cause of morbidity and mortality. Insulin and fetuin-A are hormones that play a role in glucose metabolism regulation. Insulin is responsible for regulating glucose passage to the cells, while fetuin-A blocks insulin binding to its receptor, which is linked to insulin resistance in metabolic syndrome. Higher fetuin-A level patients have 4 times greater risk of developing IHD compared to patients with lower fetuin-A levels. Studies found that both hormones participate in the development of T2DM and IHD, beside their role in the pathophysiology of metabolic syndrome. Aim of the study: Evaluate serum fetuin-A concentrations in type2 diabetic (T2D) patients with and without IHD and compare them with healthy individuals. Assess serum glucose, insulin levels, and HOMA-IR in T2D patients and IHD and compare them with healthy individuals. Subjects and Methods: A case control study, that included 120 patients (60 have T2DM with IHD and 60 having T2DM without IHD age ranged from 30 to 70 years patient, who attended Al-Yarmouk Teaching Hospital and Iraqi Center for Myocardial Infarction, Medical City Hospital, Baghdad during the period from November 2020 until February 2021 and compare result with 60 healthy control which age ranged from 30 to 70 years. Female: male ratio is almost 1:1 in the three studied groups. The diagnosis of MI is based on medical reports, laboratory, and clinical tests for heart disease. Patients with neuropathy, retinopathy, thyroid dysfunction and liver diseases were excluded from the study. BMI, FBS, serum insulin, HOMA-IR, and fetuin-A were measured or calculated for each participant. Result: a statistical difference in BMI between participants is found; 46.70% of T2DM in the IHD group are obese. No significant association between disease duration and development of IHD is found. All the included markers showed statistical differences in mean ± SD between the diabetic and control group; fetuin-a mean ± SD level was 27.63 13.31, 12.39 ± 5.61 and 9.93 ± 5.1 in T2DM with IHD, T2DM without IHD and control group, respectively. There was no statistical association between the markers and fetuin-A except a moderate positive correlation with insulin. Conclusion: Fetuin-A can be used as a predictor of IHD development in diabetic patients.

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