Tip 1 diyabetik hasta eritrositlerinde, azalmış glikoz metabolizması
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Abstract
İstanbul Üniversitesi, İstanbul Tıp Fakültesi, Endokrinoloji, Diyabet ve Metabolizma Anabilim dalında, Tip 1 Diyabetik teşhisi ile tedavi altına alınan hastalardan izole edilen kırmızı kan hücrelerinde, fizyolojik glikoz konsantrasyonlarında Ashcroft yöntemiyle ölçülen eritrosit içi glikoz metabolizmasında, kontrol guruba nazaran azalma tespit edildi. İnsülin hormonu etkisinde, in vivo koşullarda canlı eritrositlerde; hem normal, hem Tip 1 Diyabetik eritrositlerde glikoz kullanımında normal artış saptandı. Ancak Tip 1 Diyabetik grupta insüline normal cevap ile eklenen glikoz kullanımı, fizyolojik konsantrasyonlarda çalışıldığında, mutlak glikoz kullanımındaki yetersizliği gidermeye yetmedi. Kısacası, Tip 1 Diyabetik hasta eritrositlerinde, insülinin eritrositlere etkisinden bağımsız bir glikoz metabolizma bozukluğu saptandı. Impaired glucose utilization as measured by H20 production in erythrocytes of patients with type I Diabetes Mellitus. Type 1 Diabetes is an important health problem in the world that has not yet been fully resolved. Metabolic measurements related to the disease will help to understand the disease and identify the problems and develop appropriate treatments.The radioactive physics and chemistry industry, which has advanced in recent years, has helped to develop new methods in in vitro experimental medicine. The Aschroft method is based on the principle that the industrial radioactive glucose molecules can be broken down into water molecules as nutrients, just like non-radioactive D-Glucose.When the red blood cells lose their vitality, their ability to break down glucose into water is lost. The more glucose molecules break down into water molecules, the more glucose they have utilized. In this radioactive labeling method; if more radioactive molecules (D-[5-3H] glucose) break down into the radioactive water molecule (3HOH), means that more cells are alive or their metabolism is high.In the study, the described radioactive labeling method is employed to quantify Glucose Utilization in live erythrocytes isolated from healthy subjects and from patients diagnosed with Type 1 Diabetes. According to measurements, Type 1 Diabetes erythrocytes is normal in response to the insulin hormone, there is no abnormality in insulin induced incremental glucose utilization rates (%); but in comparison to healthy group erythrocytes, the glucose utilization rate of erythrocytes isolated from Type 1 Diabetic group, fed in vitro, at 2.8, 5.6, 11.2 and 16.8 mM glucose intensities respectively, is decreased. Especially when fed with a high glucose amount (16.8 millimolar of Glucose; both in the presence and absence of Insulin) that increases the osmotic pressure; the erythrocytes of Type 1 Diabetic group found to be inadequate in comparison to healthy group. In summary, the measurements in the erythrocytes of Type 1 Diabetic (n=20) and Kontrol (n=25) groups performed at increasing amounts of glucose, both in the presence (insulin; 2.10-9 mol.Lt-1) and absence of Insulin indicated that the rate of glucose utilization in the diabetic group was decreased on the average by 17±6 % (statistically significant; students t-test). The glycolytic pathway abnormality we have detected may not only be indicative of erythrocyte but may be indicative of the inadequate anaerobic Glucose Utilization in other cells of the body; the underlying cause of vascular malformations in Type 1 Diabetes patients, particularly eye retinopathy, may be due to such metabolic insufficiency. In conclusion, Glucose Utilization rate in erythrocytes from Type 1 Diabetes is below the normal range.
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