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Summary and conclusionSummaryMetabolic syndrome is the association of central obesity, hypertension, dyslipidemia, IGT/IFG and atherosclerosis. Several studies using standard diagnostic criteria have shown that both insulin resistance and impaired first-phase insulin secretion are independent determinants of progression from NGT to IGT and from IGT to diabetes and consequently endothelial dysfunction.Endothelial dysfunction has been demonstrated in type 2 diabetes, and it is detectable very early in the course of the disease, even before overt hyperglycemia. Studies have suggested that serum von Willebrand factor concentration is an indicator of generalized endothelial damage and contributes to platelet aggregation to the vascular endothelium, the first step in thrombosis.Adipocytes express and secrete numerous peptide hormones and cytokines, CRP concentrations elevated in subjects with severe metabolic syndrome may reflect cytokine production by adipocytes, and it can predict the inflammatory process of atherosclerosis.Resistin hormone is a new hormone that has been identified linking obesity to type 2 diabetes. It has been called resistin (for ”resistance to insulin) and it can explain a mechanism linking obesity and insulin resistance.The aim of this study is to study endothelial dysfunction in obese with or without glucose intolerance, and to study resistin hormone in relation to insulin resistance and endothelial dysfunction.This study was carried out in the department of Internal Medicine, Diabetes and Endocrinology out patient clinic and Biochemistry department faculty of Medicine Zagazig University. It included 60 subjects, 10 were lean subjects served as control, 10 obese non diabetic, 10 diabetic and 30 patients with IGT/IFG all subjects were subjected to complete physical examination, full clinical examination, body mass index, waist circumference and waist hip ratio measurement laboratory investigations (Fasting and 2hour postprandial blood glucose level, serum insulin level, C- reactive protein, serum von willebrand factor as a marker of endothelial dysfunction and Real time polymerase chain reaction (PCR) for RESISTIN hormone mRNA gene expression in a sub samples. Insulin resistance and cell function was calculated using HOMA model.The results showed:Cardiovascular complications are present in 30% of obese non diabetic group and IFG/IGT group, and in 60% of diabetic patients.Insulin resistance, CRP mg/l level and von willebrand factor U/L increase as patients progressed to IGT/IFG then to overt diabetes.CRP was higher in diabetic and IGT/IFG patients compared to lean control (p<0.001), and also higher when compared to obese non diabetic group (p<0.01), but there was no statistical significant difference between obese diabetic and obese with IGT/IFG (p NS), also von willebrand factor level is significantly higher in both (IGT/IFG, diabetic) groups compared to either control and or the obese non diabetic (p<0.001).40% of obese non diabetic group have insulin resistance, compared to 90% of both IGT/IFG and obese diabetic.Beta cell function % is more in obese non diabetic group compared to IGT/IFG group and with the development of diabetes beta cell function decreased.Resistin gene expression (pgrm) was higher in lean control (23.08±5.27), than diabetic patients (18.7± 10.59) then obese non diabetic group (14.58±7.42), and lastly IFG/IGT (7.4±1.45).There was a positive correlation between insulin resistance and BMI, waist FBG, PPBG, CRP, and vWf in the three obese groups.There were no correlations between resistin gene expression and studied parameters in lean and obese groups.Conclusion Insulin resistance is present in obese patients even before diabetes, so endothelial dysfunction can start in obese patients even without overt hyperglycemia. Plasma vWf and CRP can be useful tools to assess endothelial dysfunction in diabetes and pre-diabetic states. The role of the recently discovered resistin hormone in relation to insulin resistance, inflammation and endothelial dysfunction is not clearly identified.Recommendations Screening for all obese and overweight subjects above 40 years must be performed to detect impaired glucose tolerance and impaired fasting glucose (pre-diabetic states). Life style modifications, weight reduction and even drug treatment will prevent and /or delay complications in these pre-diabetic states. Resistin hormone is what we can say an innocent bystander and, its role in humans needs further future evaluation using different methods of detection.
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