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      Effect of Short-Term rHuEPO Treatment on Insulin Resistance in Haemodialysis Patients

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          Background/Aim: Decreased sensitivity to the hypoglycaemic action of insulin is an almost universal phenomenon in uraemic patients, and it is attributed either to uraemic toxins or to anaemia or even to secondary hyperparathyroidism. Considering the conflicting data of few existing studies, we examined the influence of erythropoietin (EPO) treatment on insulin resistance and tested the probable correlation of this influence with sympathetic nervous system (SNS) activity. Methods: We studied 8 non-obese, non-diabetic, stable dialysis patients using the euglycaemic insulin clamp technique before administration of EPO (phase A), 10 days after (phase B), and after the correction of the haematocrit level, at least 8 weeks later (phase C). We estimated the indices (glucose infusion rate, mg/kg/min), M/G (glucose clearance), and M/I (tissue sensitivity to insulin), and we measured haematocrit, haemoglobin, triglyceride, ferritin, EPO, and fasting insulin levels in each phase. During each phase, we tested the SNS activity using the response of blood pressure to persistent handgrip and the response of blood pressure to the standing position. Results: Our patients appeared to have an increased insulin resistance in phase A (M<sub>A</sub> = 6.24 ± 1.01) which was significantly improved 10 days after the beginning of EPO treatment and before the rise of haematocrit (M<sub>B</sub> = 7.71 ± 1.54, p < 0.05). There was no further improvement in phase C. Indices M/G and M/I behaved similarly. The serum triglyceride levels decreased in response to the increased insulin sensitivity. The patients studied did not demonstrate fasting hyperinsulinaemia, while the SNS activity was abnormal and remained unchanged throughout the study period in spite of some individual improvement. Conclusions: Our study proves the beneficial effect of EPO treatment on insulin resistance in dialysis patients which could be attributed to the EPO itself and not to the correction of anaemia and is accompanied by improvement in triglyceride levels. Amelioration of insulin resistance did not influence the SNS activity, making the association between EPO treatment and SNS-derived changes in blood pressure quite improbable.

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          Insulin resistance and hypertension.

           James Sowers (1990)
          A common mechanism which may be involved in the development of hypertension in both type I and type II diabetes mellitus is a deficiency of insulin at the cellular level. Observations from a number of laboratories suggest that impaired cellular response to insulin rather than hyperinsulinemia predisposes to increased vascular smooth muscle tone (the hallmark of hypertension in the diabetic state). This review presents some of the data which suggest that there is a relationship between impaired cellular action of insulin, altered cellular calcium metabolism and the development of hypertension.

            Author and article information

            S. Karger AG
            April 2000
            30 March 2000
            : 84
            : 4
            : 320-325
            aRenal Department, Second Hospital of IKA, Thessaloniki, and bSecond Department of Internal Medicine, Papanikolaou Hospital, Thessaloniki, Greece
            45606 Nephron 2000;84:320–325
            © 2000 S. Karger AG, Basel

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            Tables: 3, References: 18, Pages: 6
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