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Aims: To determine if access to mobile phone support for sick-day management is associated with reduced hospital admissions with diabetic ketoacidosis in young adults aged 15-25 with Type 1 diabetes., Methods: This was an observational study with data collected prospectively from January 2005 to December 2008. A mobile phone support service for sick-day management began in May 2005. Data from clinic attendees (group 1), including age, sex, diabetes duration, referral age, insulin therapy delivery, clinic attendance and HbA(1c) , were compared with clinic attendees with diabetic ketosis accessing sick-day management phone support (group 2), clinic attendees not accessing phone support and admitted with diabetic ketoacidosis (group 3) and non-clinic attendees admitted with diabetic ketoacidosis (group 4)., Results: Age was similar in all groups. Patients in group 3 had significantly shorter duration of diabetes (6.8 ± 3.1 years) than groups 1 or 2 (10.1 and 9.8 years, respectively). Diabetes control was poor in all presentations of diabetic ketoacidosis (groups 2-4, HbA(1c) > 97 mmol/mol, > 11%) and was significantly higher than clinic attendees without ketosis (HbA(1c) 70 mmol/mol, 8.6%; P < 0.001). There was similar attendance at the clinic across all three groups, 2.9 compared with 2.4 compared with 2.1 visits/year, respectively. Thirty-one patients accessed phone support on 83 occasions for sick-day management (mean 2.7 contacts/episode); two patients progressed to admission with diabetic ketoacidosis. Diabetic ketoacidosis admission rates in the clinic population fell significantly from baseline, 0.10 to 0.05 admissions per patient per year (P < 0.05) in the third year., Conclusion: Mobile phone support is associated with reduced progression of ketosis to diabetic ketoacidosis in young adults despite poor diabetes control., (© 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK.)

Aims: To determine if a transition support programme for young adults with diabetes could maintain attendance at a specialist clinic, improve diabetes control and reduce acute hospital admissions with diabetic ketoacidosis (DKA) in 15-25-year-olds with Type 1 diabetes., Methods: A transition coordinator/diabetes educator arranged booking and rebooking of appointments for a young adult diabetes clinic based in an adult hospital between July 2001 and March 2006. An after-hours phone support service was initiated. Data collected included source of referral, frequency of clinic attendance and HbA1c at each visit. Numbers of admissions and readmissions with DKA, length of stay and HbA1c on admission were recorded., Results: One hundred and ninety-one young adults were referred. HbA1c at initial referral was 9.3 +/- 2.17%. HbA1c significantly improved to 8.8 +/- 1.9% (P < 0.001) after a median of five visits with a statistically significant fall in HbA1c of 0.13% per visit (P = 0.01). The greatest improvements were seen in those with starting HbA1c > 11% (-2.5 +/- 2.3%, P < 0.001). Eighty-two percent had attended appointments in the last 6 months. There was a significant reduction in DKA admissions falling by 1/3 (P = 0.05), and in readmissions a significant reduction in length of stay (-3.6 days, P = 0.02), over 3.5 years., Conclusions: If young adults are appropriately supported in adult services, clinic attendance is maintained, diabetes control is improved and hospital admission rates with DKA are reduced. The cost savings from reduced admissions covered the costs of the programme.

Background: The pathophysiological mechanism of diabetes mellitus in the presence of the 3243 A-G tRNALEU(UR) mitochondrial DNA mutation is thought to result from deficient insulin secretion. However, few subjects with normal glucose tolerance have been studied to determine the sequence of events resulting in the development of diabetes mellitus., Aim: To determine whether abnormalities of insulin sensitivity, insulin secretion or glucose effectiveness are present in non-diabetic subjects with the 3243 A-G tRNALEU(UUR) mitochondrial DNA mutation., Methods: Twelve non-diabetic subjects with the mutation were compared with 12 controls, matched for age and anthropometric parameters, using both oral and intravenous glucose tolerance tests, the latter with Minimal Model analysis., Results: Following an oral glucose load we found significantly higher blood glucose levels at 90 min and 120 min and significantly higher insulin levels at 120 min and 180 min in non-diabetic subjects with the mutation but no difference in the insulinogenic indices at 30 min and 180 min. From the intravenous glucose tolerance test there was no difference in overall glucose tolerance, insulin sensitivity, first- or second-phase insulin secretion, proinsulin secretion or glucose effectiveness. Insulin-independent glucose disposal was increased in subjects with lower insulin sensitivity and declined with increasing age in subjects with the mutation but not in controls., Conclusions: While there appear to be subtle defects of glucose handling in non-diabetic subjects with the 3243 mutation, these could not be explained by differences in insulin sensitivity or secretion.

Two types of retinopathy, diabetic and pigmentary, may be seen in subjects with maternal inheritance diabetes and deafness. The potential for interactions between the two retinopathies has not been explored. The mitochondrial mutation may affect development of diabetic retinopathy in subjects with MIDD by altering normal pathways of glucose metabolism. We identified five unrelated MIDD kindreds with 61 living maternal line family members. Twenty-three of the family members, 12 with diabetes mellitus and 11 without volunteered to be studied. Subjects were graded for severity of diabetic retinopathy and presence or absence of pigmentary retinopathy after slit lamp biomicroscopy, retinal photography of seven standard fields and fluorescein angiography. Blood was taken, in the fasted state, from MIDD subjects (duration of diabetes 17.0+/-6.9 yr) and non-diabetic subjects with the mutation, for assay of sorbitol and glucose and values compared with diabetic and non-diabetic control subjects without the mutation. Diabetic retinopathy was absent in 9/12 subjects (75%), with 3 having mild non-proliferative retinopathy. No one had cataract. Red blood cell sorbitol levels, adjusted for ambient blood glucose, were significantly lower in MIDD subjects compared with diabetic subjects (1.16+/-0.5 cf. 2.03+/-1.1, x 10(-3) g mmol(-1), p=0.04). Pigmentary retinopathy was present in 15 of 23 subjects, of whom 13 had some abnormality of glucose tolerance. Abnormal glucose tolerance was strongly associated with the development of pigmentary retinopathy (odds ratio 19.5, p=0.008). In conclusion, there appears to be a decreased prevalence of diabetic retinopathy and cataract in MIDD, which we propose is due to reduced glucose metabolism by the polyol pathway. Abnormal glucose tolerance increases the clinical expression of pigmentary retinopathy in subjects with a mitochondrial genome mutation. A greater understanding of the metabolic effects of mitochondrial DNA mutations has the potential to give insight into the mechanisms of diabetic retinopathy and other complications of diabetes mellitus.