[Is insulin resistance a contributor risk factor for diabetic retinopathy in type 2 diabetes?]

Retinopathy is the most common long-term complication of diabetes mellitus, and diabetic retinopathy is a complex disease, in which that inflammation plays a critical role. The aim of this study was to evaluate the association between insulin resistance as a known inflammatory marker and diabetic retinopathy in type 2 diabetes. In this study 342 patients with type 2 diabetes were enrolled, and their demographic data were recorded. HbA1c, FBS, lipid profiles and insulin levels were measured for all patients. Insulin resistance was calculated by the homeostatic model assessment of insulin resistance[HOMA-IR] formula. Following ophthalmologic examination [fundoscopy] patients were divided according to retinal involvement. The relation between HOMA-IR with diabetic retinopathy was evaluated. Mean age of patients was 55.05 +/- 9.8 years, and 30.4% of all patients had diabetic retinopathy. This analysis showed that HbA1c and duration of diabetes are the only independent predictive factors for diabetic retinopathy. Insulin resistance was not significantly different between patients with and without retinopathy but median level of HOMA-IR was significantly higher in patients with diabetic proliferative retinopathy compared with patients with non proliferative diabetic retinopathy [2.1[0.7- 6.6] Vs 1.2[0.5-2.8], P=0.021]. This data suggests that the insulin resistance may play a role in diabetic retinopathy in type 2 diabetes

[Prevalance of anemia in type 2 diabetic patients and the role of nephropathy]

Anemia is a common problem in diabetic patients, who usually suffer from a greater degree and severity of anemia based on their level of renal impairment, compared to non diabetic patients. This study investigates the prevalence of anemia in type 2 diabetic patients and aims to determine the role of different stages of nephropathy in development of anemia in these patients. For this study, 1962 outpatients, with type 2 diabetes were selected. A full blood count and iron indices were obtained for all patients. Anemia was defined as Hemoglobin<13g/lit in males and <12 g/lit in females. The correlation of anemia with other variables including sex, age, duration of diabetes, fasting blood sugar, glycosylated hemoglobin, glumerolar filtration rate, albuminuria, uric acid and metabolic syndrome was identified with multivariate logistic regression analysis. In males 9.2% and among females 10.4% of patients had anemia. The prevalence of elevated albuminuria [micro or macroalbuminuria] was 38. 1%. of our patients, 8.1% had moderate [creatinine clearance <60 ml/min/1. 73 m2] and 31. 4% had mild [CCr= 60-90] renal impairment. Patients with moderate renal impairment had significantly higher levels of anemia than patients with mild renal failure [30% Vs. 9%, p<0.001]. Patients with diabetes and macroalbuminuria were also likely to have more anemia than patients with microalbuminuria [32.4% Vs. 8.4%, p<0.001]; also patients with microalbuminuria were also more likely to have anemia than patients without elevated albuminuria [8. 4% vs. 5. 7%, p<0. 001]. Anemia has a high prevalence in type 2 diabetic patients. Any degree of renal impairment and albuminuria are risk factors for anemia in such patients

[Effects of calcitriol [1,25[OH]2D3 treatment on control of glucose intolerance in hemodialysis patients]

Impaired carbohydrate metabolism is a common finding in patients with chronic renal failure. Although intermittent hemodialysis results in a significant improvement of impaired glucose metabolism of uremia, complete normalization did not occur. Vitamin D[3] deficiency, it seems is linked with disturbance of glucose metabolism. A role of vit D in endocrine pancreatic function has been suggested. The aim of this study was to determine the effects of 1,25 [OH]2D3 treatment on glucose tolerance, insulin resistance and beta cell function in hemodialysis patients. Of sixty-five patients with uremia on hemodialysis, twenty -seven who had never been treated with vitamin D or related drugs and without history of diabetes were selected for this study. These patients were randomly divided to two groups, group I were treated with oral calcitriol [0.5 mcg/day] for 8 weeks and group it received placebo for the 8 weeks. In all cases, before and 8 weeks after treatment fasting glucose, insulin, total cholesterol, triglycerides, HDL, LDL, calcium, phosphorous, PTH, HbA1C and blood sugar after 75 gr load of glucose were measured. Insulin resistance [homostatic model assessment-insulin resistance = HOMA-IR] and beta cell function [homostatic model assessment- insulin secretion =HOMA-SECR] were calculated and results of these measurements, before and after 8 weeks, in both groups were compared. In group I, after calcitriol treatment, blood sugar after 75 gr load of glucose [p= 0.045], HOMA -IR [p= 0.035], HbA1C [p=0.00], total cholesterol [p=0.037], and triglycerides [p=0.036] decreased, whereas calcium levels increased, significantly [0.014]; changes in other parameters were not significant. In group II [without treatment] after 8 weeks of observation, fasting blood sugar [p=0.002], HbA1C [p=0.004], HOMA -IR [p=0.036] significantly increased and beta cell function decreased significantly [p= 0.032]; again alterations in other parameters were not significant. These results seem to confirm that the active form of vitamin D influences glucose and lipid metabolism, by the improvement of insulin resistance