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Type 1 Diabetics (type 1 + diabetic)
Terms modified by Type 1 Diabetics Selected AbstractsComparison of vasodilator effects of substance P in human forearm vessels of normoalbuminuric Type 1 diabetic and non-diabetic subjectsDIABETIC MEDICINE, Issue 3 2000D. R. Meeking Summary Aims To compare the vasodilatory responses to substance P in human forearm vessels in Type 1 normoalbuminuric diabetic and non-diabetic subjects. Methods Forearm blood flow (FBF) was measured using a plethysmography technique in 12 normoalbuminuric Type 1 diabetic subjects (six males, six females) (HbA1C 8.2 ± 0.3% (mean ±,sem)) and 12 non-diabetic healthy control subjects in response to the infusion of the vasodilators substance P (SP), acetylcholine (ACh) and nitroprusside. Results There was no significant difference in baseline FBF between the two groups (2.80 ± 0.29 ml/min per 100 ml forearm tissue (diabetic group) vs. 2.85 ± 0.37 ml/min per 100 ml (non-diabetic group), P = 0.45). Infusion of SP was associated with an incremental increase in FBF in the diabetic (0.6, 2 and 6 ng/min , 6.08 ± 1.07, 7.82 ± 1.08 and 9.48 ± 1.14 ml/min per 100 ml, respectively) and the non-diabetic group (0.6, 2 and 6 ng/min , 5.41 ± 0.80, 6.93 ± 0.96 and 9.25 ± 1.11 ml/min per 100 ml, respectively). Similarly, an incremental rise in FBF was observed during infusion of ACh (diabetic group: 7.5, 15 and 30 ,g/min , 7.14 ± 1.22, 8.91 ± 1.40 and 11.67 ± 1.93 ml/min per 100 ml, respectively; non-diabetic group: 7.5, 15 and 30 ,g/min , 5.87 ± 0.81, 7.49 ± 0.96 and 10.74 ± 1.29 ml/min per 100 ml, respectively). When FBF was expressed as percentage change from baseline, there was no significant difference in vasodilatory responses between the two groups for SP (0.6 ng/min, P = 0.21; 2 ng/min, P = 0.19; 6 ng/min, P = 0.19) or ACh (7.5 ,g/min, P = 0.20; 15 ,g/min, P = 0.20; 30 ,g/min, P = 0.35). Conclusions This study suggests that endothelium-dependent vasodilatory responses to SP (and ACh) are not impaired in Type 1 diabetic subjects with normal urinary albumin excretion. [source] Quantifying hepatic glycogen synthesis by direct and indirect pathways in rats under normal ad libitum feeding conditionsMAGNETIC RESONANCE IN MEDICINE, Issue 1 2009Ana F. Soares Abstract Hepatic glycogen synthesis from intact hexose (direct pathway) relative to that from gluconeogenic precursors (indirect pathway) was quantified in ad libitum-fed rats. Following 2H2O administration and overnight feeding, the livers were removed and glycogen 2H-enrichment was measured by 2H NMR. Six controls and six rats rendered hyperglycemic by streptozotocin (STZ; fasting blood glucose = 385 ± 31 mg/dl) were studied. The indirect pathway contribution, estimated as glycogen hydrogen 5 relative to hydrogen 2 enrichment, was 54% ± 4% for control rats,similar to values from healthy, meal-fed humans. In STZ-treated rats, the indirect pathway contribution was significantly higher (68% ± 4%, P < 0.05 vs. controls), similar to that of Type 1 diabetic (T1D) patients. In conclusion, sources of hepatic glycogen synthesis in rats during ad libitum nocturnal feeding were quantified by analysis of glycogen enrichment from 2H2O. STZ caused alterations resembling the pathophysiology of hepatic glycogen synthesis in T1D patients. Magn Reson Med 61:1,5, 2009. © 2008 Wiley-Liss, Inc. [source] Decreased cortisol production in male type 1 diabetic patientsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2003M. N. Kerstens Abstract Background It is unclear whether cortisol production and the 11,HSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects. Materials and methods Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8·5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11,HSD activity. Results Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7·4 ± 2·5 vs. 7·7 ± 2·3 nmol min,1 m,2 (NS) in diabetic patients and 9·7 ± 2·1 vs. 11·2 ± 4·1 nmol min,1 m,2 (NS) in healthy subjects, respectively (P < 0·05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0·05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading. Conclusions The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5, reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11,HSD setpoint is not affected by physiological variations in sodium intake. [source] Case Report: Combined Pancreas and En Bloc Kidney Transplantation Using a Bladder Patch Technique From Very Small Pediatric DonorsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2010J. Sageshima Very small pediatric donors are underutilized for pancreas and kidney transplantation for the fear of inadequate islet mass and higher incidence of technical complications, and the lower age limit for such donors is not well defined. We present here two cases of combined pancreas and en bloc kidney transplantation from very small pediatric donors (14 and 18 months old) to adult type 1 diabetic and uremic patients. The conventional surgical procedure for simultaneous pancreas and kidney transplantation with systemic venous and bladder exocrine drainage was successfully applied to very small organs. For both, we utilized the recently described bladder patch technique for ureteral reconstruction. One patient developed venous thrombosis (partial thrombosis of the splenic and mesenteric veins) and the other urine leak (from a midportion of the medial ureter without compromising the bladder patch) after the transplants; both were successfully managed and the patients demonstrated immediate and sustained pancreas and kidney graft functions for 12 and 2 months posttransplantation. These cases illustrate the feasibility of combined pancreas and en bloc kidney transplantation from very small pediatric donors using a bladder patch technique to avoid small ureteral anastomosis. [source] Balancing needs and means: the dilemma of the ,-cell in the modern worldDIABETES OBESITY & METABOLISM, Issue 2009G. Leibowitz The insulin resistance of type 2 diabetes mellitus (T2DM), although important for its pathophysiology, is not sufficient to establish the disease unless major deficiency of ,-cell function coexists. This is demonstrated by the fact that near-physiological administration of insulin (CSII) achieved excellent blood glucose control with doses similar to those used in insulin-deficient type 1 diabetics. The normal ,-cell adapts well to the demands of insulin resistance. Also in hyperglycaemic states some degree of adaptation does exist and helps limit the severity of disease. We demonstrate here that the mammalian target of rapamycin (mTOR) system might play an important role in this adaptation, because blocking mTORC1 (complex 1) by rapamycin in the nutritional diabetes model Psammomys obesus caused severe impairment of ,-cell function, increased ,-cell apoptosis and progression of diabetes. On the other hand, under exposure to high glucose and FFA (gluco-lipotoxicity), blocking mTORC1 in vitro reduced endoplasmic reticulum (ER) stress and ,-cell death. Thus, according to the conditions of stress, mTOR may have beneficial or deleterious effects on the ,-cell. ,-Cell function in man can be reduced without T2DM/impaired glucose tolerance (IGT). Prospective studies have shown subjects with reduced insulin response to present, several decades later, an increased incidence of IGT/T2DM. From these and other studies we conclude that T2DM develops on the grounds of ,-cells whose adaptation capacity to increased nutrient intake and/or insulin resistance is in the lower end of the normal variation. Inborn and acquired factors that limit ,-cell function are diabetogenic only in a nutritional/metabolic environment that requires high functional capabilities from the ,-cell. [source] Multiple mealtime administration of biphasic insulin aspart 30 versus traditional basal-bolus human insulin treatment in patients with type 1 diabetesDIABETES OBESITY & METABOLISM, Issue 6 2006J. -W. Aim:, The aim of this study was to compare the effect of multiple mealtime injections of biphasic insulin aspart 30 (30% fast-acting insulin aspart in the formulation, BIAsp30) to traditional basal-bolus human insulin regimen (HI) on glycaemic control in patients with type 1 diabetes. Methods:, Twenty-three patients (eight women and 15 men) aged 44.8 (20.6,62.5) years (median and range) with a diabetes duration of 19.5 (1.6,44.6) years completed the study. All eligible patients were randomly assigned to BIAsp30 thrice daily supplied with bedtime NPH insulin when necessary, or basal-bolus HI for 12 weeks and then switched to the alternative regimen for another 12 weeks. The insulin dose adjustments were made by patients on the basis of advice from a diabetes nurse. At end of each treatment period, the patients attended two profile days, 1 week apart for pharmacodynamic and pharmacokinetic assessments. HbA1C was measured at baseline and at the end of each treatment period. A seven-point self-monitored blood glucose (SMBG) was obtained twice weekly. Results:, In comparison with HI, multiple mealtime injections of BIAsp30 resulted in a significant reduction in HbA1C[HI vs. BIAsp30 (%, geometric mean and range): 8.6 (7.4,11.4) vs. 8.3 (6.7,9.8), p = 0.013]. During treatment with BIAsp30, nighttime glycaemic control was significantly improved. Day-to-day variation in pharmacodynamics and pharmacokinetics and the rate of hypoglycaemia were not increased with BIAsp30 compared with HI. Conclusions:, In type 1 diabetics, multiple mealtime administration of BIAsp30 compared with traditional basal-bolus human insulin treatment significantly improves long-term glycaemic control without increasing the risk of hypoglycaemia. Despite a higher proportion of intermediate-acting insulin, thrice-daily injections with BIAsp30 do not increase the day-to-day variations in insulin pharmacokinetics and pharmacodynamics. [source] IL-6,174 genotype associated with the extent of periodontal disease in type 1 diabetic subjectsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2009Taina Raunio Abstract Aim: The aim of this study was to investigate whether genetic polymorphism in certain cytokine and receptor molecule genes and diabetic status associate with the extent of periodontal disease in type 1 diabetes mellitus (DM). Material and Methods: Eighty patients with type 1 DM participated. Visible plaque, bleeding on probing (BOP), probing pocket depth (PD) and attachment level (AL) were examined clinically and glycosylated haemoglobin (HbA1c) levels were used to assess the glycemic control of DM. CD-14, IL-6, TNF- ,, IL-10, IL-1,, IL-1, and TLR-4 gene polymorphisms were studied using the polymerase chain reaction (PCR). Results: The 3-year HbA1c was good (<7.5%) in 16%, acceptable (7.5,8.5%) in 36% and poor (>8.5%) in 48% of the subjects. IL-6,174 genotype and 3-year GHbA1c associated significantly with BOP and PD4 mm, subjects with the GG genotype of the IL-6,174 exhibiting more severe periodontal disease than those with the GC/CC genotype. After stratification by IL-6 genotype, associations between the extent of periodontal disease and 3-year HbA1c levels remained significant in subjects carrying the GC/CC but not the GG genotype. Conclusions: In addition to the HbA1c level, the IL-6,174 genotype is a significant susceptibility factor for periodontal disease among type 1 diabetics. [source] Interpreting incidence trends for treated end-stage renal disease: Implications for evaluating disease control in AustraliaNEPHROLOGY, Issue 4 2004JOHN H STEWART SUMMARY: Background: Five sources of change modify trends in incidence of treated end-stage renal disease (ESRD): (i) demography; (ii) disease control, comprising prevention and treatment of progressive kidney disease; (iii) competing risks, which encompass dying from untreated uraemia or non-renal comorbidity; (iv) lead-time bias; and (v) classification bias. Thus, rising crude incidence of treated ESRD may conceal effective disease control when there has been demographic change, lessening competing risks, or the introduction of bias. Methods: Age-specific incidences of treated ESRD in Australia were calculated from Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry data by indigenous/non-indigenous status (all causes) and by primary renal disease (non-indigenous only) for two successive decades, 1982,1991 and 1992,2001. Results: We postulate that less competing risks explained much of the increase in treated ESRD in the elderly and Indigenous Australians. The increase in glomerulonephritic ESRD in non-indigenous Australians could be ascribed mainly to immigration from non-European countries. There was no significant change in incidence of treated ESRD in Indigenous or non-indigenous persons aged less than 25 years, in non-indigenous persons aged 25,64 years for ESRD caused by hereditary polycystic disease or hypertension, or in type 1 diabetics aged over 55 years. End-stage renal disease from analgesic nephropathy had declined. The increase in treated ESRD caused by type 2 diabetic nephropathy appeared to be multifactorial. Lead-time/length bias and less competing risks may have concealed a small favourable trend in other primary renal diseases. Conclusion: Whether recent disease control measures have had an impact on incidence of treated ESRD is not yet certain, but seems more likely than implied by previous reports. [source] Impact of Medicare Coverage on Disparities in Access to Simultaneous Pancreas and Kidney TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2009J. K. Melancon In the setting of disparities in access to simultaneous pancreas and kidney transplantation (SPKT), Medicare coverage for this procedure was initiated July 1999. The impact of this change has not yet been studied. A national cohort of 22 190 type 1 diabetic candidates aged 18,55 for kidney transplantation (KT) alone or SPKT was analyzed. Before Medicare coverage, 57% of Caucasian, 36% of African American and 38% of Hispanic type 1 diabetics were registered for SPKT versus KT alone. After Medicare coverage, these proportions increased to 68%, 45% and 43%, respectively. The overall increase in SPKT registration rate was 27% (95% CI 1.16,1.38). As expected, the increase was more substantial in patients with Medicare primary insurance than those with private insurance (Relative Rate 1.18, 95% CI 1.09,1.28). However, racial disparities were unaffected by this policy change (African American vs. Caucasian: 0.97, 95% CI 0.87,1.09; Hispanic vs. Caucasian: 0.94, 95% CI 0.78,1.05). Even after Medicare coverage, African Americans and Hispanics had almost 30% lower SPKT registration rates than their Caucasian counterparts (95% CI 0.66,0.79 and 0.59,0.80, respectively). Medicare coverage for SPKT succeeded in increasing access for patients with Medicare, but did not affect the substantial racial disparities in access to this procedure. [source] Improved patient survival in recipients of simultaneous pancreas,kidney transplant compared with kidney transplant alone in patients with type 1 diabetes mellitus and end-stage renal disease,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 9 2003P. Mohan Background: There are emerging data that simultaneous pancreas,kidney transplant (SPK) prolongs life compared with kidney transplant alone (KTA) in type 1 diabetics with end-stage renal disease. This study was a retrospective comparison of SPK with KTA in patients with type 1 diabetes. Methods: Between 1 January 1992 and 30 April 2002, 101 patients with type 1 diabetes were transplanted. Fifty-one of these patients received a KTA and 50 had a SPK. All patients underwent coronary angiography with surgical correction of any coronary artery disease before being listed. All patients who underwent SPK received quadruple immunosuppressive therapy consisting of antilymphocyte globulin, calcineurin inhibitor (tacrolimus or cyclosporin), azathioprine and steroids. Those who underwent KTA received calcineurin inhibitor (tacrolimus or cyclosporin), azathioprine and steroids. Results: Patient survival at 1, 3, 5 and 8 years was 96, 93, 89 and 77 per cent respectively after SPK, and 93, 75, 57 and 47 per cent respectively after KTA (P = 0·018 at 8 years). Conclusion: The addition of pancreatic transplantation prolongs life in type 1 diabetic patients with renal failure compared with renal transplantation alone. Copyright © 2003 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | ||||||||||