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Chronic Hyperglycaemia (chronic + hyperglycaemia)
Selected AbstractsEffects of hyperglycaemia on ocular development in rabbit: refraction and biometric changesOPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 2 2005Peter Herse Abstract Aim:, To determine the effect of acute and chronic hyperglycaemia on the refraction and development of the rabbit eye. Methods:, Ocular dimensions of five alloxan-induced hyperglycaemic and six control rabbits were measured over 9 weeks using A scan biometry. Refraction was measured using retinoscopy. The animals were 10 weeks of age at the start of the experiment. Results:, The acute onset of hyperglycaemia was associated with a fast and stable 2 D hyperopic shift in refraction. Lens thickness increased during the first 2 weeks of hyperglycaemia, returned to near normal thickness after 3,5 weeks of hyperglycaemia and then decreased in thickness in the last 4 weeks of the study. The hyperopic refraction remained unchanged during changes in lens thickness. Nine weeks of hyperglycaemia was associated with a 25% reduction in the growth of both the globe and the lens and a 17% decrease in body mass compared with the controls. Conclusion:, The hyperopic refraction change of acute hyperglycaemia is likely to be because of a change in the refractive index of the cortical fibres of the lens and is the probable source of the fluctuating refraction seen in diabetic patients. Chronic hyperglycaemia reduced the axial development of the eye and is the probable source of the chronic hyperopic refraction seen in children with Type I diabetes. [source] Glycaemic status and cardiovascular disease in type 2 diabetes mellitus: re-visiting glycated haemoglobin targets for cardiovascular disease preventionDIABETES OBESITY & METABOLISM, Issue 6 2007Sherita H. Golden Cardiovascular disease (CVD) is the leading cause of death among people with type 2 diabetes. Recent attention has focused on chronic hyperglycaemia as an additional risk factor in people with diabetes since their excess CVD risk is not entirely explained by traditional cardiovascular risk factors. Clinical trials of intensive glucose control to reduce CVD events have been equivocal, but recent epidemiological studies have shown that HbAlc, a measure of chronic hyperglycaemia, predicts incident cardiovascular events. This review, which focuses on type 2 diabetes, summarizes (i) the epidemiological literature examining the relation between glycaemic status, as assessed by glycated haemoglobin (HbAlc) and CVD, (ii) the controversy regarding treatment goals for HbAlc in terms of preventing microvascular disease vs. macrovascular disease and (iii) on-going clinical trials of intensive glycaemic control for CVD prevention. [source] ,-cell preservation: a potential role for thiazolidinediones to improve clinical care in Type 2 diabetesDIABETIC MEDICINE, Issue 8 2005L. A. Leiter Abstract Type 2 diabetes is caused by progressively increasing insulin resistance coupled with deteriorating ,-cell function, and there is a growing body of evidence to suggest that both of these defects precede hyperglycaemia by many years. Several studies have demonstrated the importance of maintaining ,-cell function in patients with Type 2 diabetes. This review explores parameters used to indicate ,-cell dysfunction, in Type 2 diabetes and in individuals with a predisposition to the disease. A genetic element undoubtedly underlies ,-cell dysfunction; however, a number of modifiable components are also associated with ,-cell deterioration, such as chronic hyperglycaemia and elevated free fatty acids. There is also evidence for a link between pro-inflammatory cytokines and impairment of insulin-signalling pathways in the ,-cell, and the potential role of islet amyloid deposition in ,-cell deterioration continues to be a subject for debate. The thiazolidinediones are a class of agents that have demonstrated clinical improvements in indices of ,-cell dysfunction and have the potential to improve ,-cell function. Data are accumulating to show that this therapeutic group offers a number of advantages over traditionally employed oral agents, and these data demonstrate the growing importance of thiazolidinediones in Type 2 diabetes management. [source] Autoantibodies to the islet cell antigen SOX-13 are associated with duration but not type of diabetesDIABETIC MEDICINE, Issue 3 2003T. M. E. Davis Abstract Aims The autoantigen SOX-13 of the SRY-related high mobility group box is a low-frequency reactant in sera from patients with Type 1 diabetes. We further investigated the potential diagnostic role of anti-SOX-13, and in particular its ability to distinguish Type 1 from Type 2 diabetes, in two large, well-characterized cohorts. Methods SOX-13 autoantibody status was ascertained using a radioimmunoprecipitation assay in (i) a random sample of 546 participants in an Australian community-based study (the Fremantle Diabetes Study; FDS) of whom 119 had Type 1 and 427 Type 2 diabetes, and (ii) a sample of 333 subjects with Type 2 diabetes from the United Kingdom Prospective Diabetes Study (UKPDS) stratified by age, anti-glutamic acid decarboxylase (GAD) and islet cell antibody (ICA) status, and requirement for insulin therapy within 6 years of diagnosis. Results The frequencies of anti-SOX-13 in the FDS subjects were 16.0% and 14.8% for Type 1 and Type 2 patients, respectively, and levels were similar. In the UKPDS subjects, the frequency was 4.5%. In a logistic regression model involving demographic, anthropometric and metabolic variables, only diabetes duration was significantly associated with anti-SOX-13 positivity, especially for duration > 5 years (P < 0.002). When the coexistence of autoantibodies was assessed in the two study samples, there were no significant associations between anti-SOX-13 and ICA, anti-GAD or ICA512/IA-2. Conclusions Whilst the frequency of anti-SOX-13 may be increased in some populations of diabetic patients, this reactivity does not usefully distinguish Type 1 from Type 2 diabetes. However, the association with diabetes duration suggests that anti-SOX-13 may be a non-specific marker of tissue damage associated with chronic hyperglycaemia. Diabet. Med. 20, 198,204 (2003) [source] Forearm vasoconstrictor response in uncomplicated type 1 diabetes mellitusEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006P. J. Van Gurp Abstract Background, According to the ,haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM). Materials and methods, In 15 DM patients (DM duration 6·3 ± 3·8 year; HbA1c 7·9 ± 1·3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular ,- and ,-adrenergic receptor blockade. Results, At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (,FVR: 12 ± 4 vs. 19 ± 3 arbitrary units, P < 0·05). The responses of plasma NA and heart rate variability did not differ. Conclusions,, Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness. [source] Liraglutide: can it make a difference in the treatment of type 2 diabetes?INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2010J. Unger Summary Despite advances in the management of type 2 diabetes, glycaemic control remains suboptimal for many patients because of the complexities of disease progression and the need to balance improved glycaemic control against adverse treatment effects, particularly weight gain and hypoglycaemia. Thus, the development of new antidiabetes therapies continues in earnest. Incretin hormones have been the recent focus of research, as they account for up to 70% of the insulin response following a meal. There is also a high concordance between the physiological actions of one hormone, glucagon-like peptide-1 (GLP-1), and the therapeutic needs of patients. As native human GLP-1 has a half life of only approximately 2 min, researchers have developed molecules that act as GLP-1 receptor agonists or inhibit the enzyme responsible for GLP-1 degradation (dipeptidyl peptidase-4). Liraglutide, a human GLP-1 analogue sharing 97% of its amino acid sequence identity with native GLP-1, has been approved for use as monotherapy (not in Europe) and in combination with selected oral agents. In this supplement, we summarise key liraglutide data, offer practical insight into what we might expect of liraglutide in clinical use and examine selected case studies. For reasons of the safety and efficacy of GLP-1 receptor agonists, many thought leaders believe that these will become background therapy for majority of patients in the coming years. This supplement will serve as a resource from which readers can extract information concerning the potential benefits for patients who are overweight, losing pancreatic beta-cell function and drifting towards the ravaging effects of chronic hyperglycaemia. [source] Effects of hyperglycaemia on ocular development in rabbit: refraction and biometric changesOPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 2 2005Peter Herse Abstract Aim:, To determine the effect of acute and chronic hyperglycaemia on the refraction and development of the rabbit eye. Methods:, Ocular dimensions of five alloxan-induced hyperglycaemic and six control rabbits were measured over 9 weeks using A scan biometry. Refraction was measured using retinoscopy. The animals were 10 weeks of age at the start of the experiment. Results:, The acute onset of hyperglycaemia was associated with a fast and stable 2 D hyperopic shift in refraction. Lens thickness increased during the first 2 weeks of hyperglycaemia, returned to near normal thickness after 3,5 weeks of hyperglycaemia and then decreased in thickness in the last 4 weeks of the study. The hyperopic refraction remained unchanged during changes in lens thickness. Nine weeks of hyperglycaemia was associated with a 25% reduction in the growth of both the globe and the lens and a 17% decrease in body mass compared with the controls. Conclusion:, The hyperopic refraction change of acute hyperglycaemia is likely to be because of a change in the refractive index of the cortical fibres of the lens and is the probable source of the fluctuating refraction seen in diabetic patients. Chronic hyperglycaemia reduced the axial development of the eye and is the probable source of the chronic hyperopic refraction seen in children with Type I diabetes. [source] Pathogenesis of diabetic retinopathy and the renin-angiotensin systemOPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 6 2003Hideharu Funatsu Abstract Despite the beneficial effects of good glycaemic control, loss of vision because of diabetic retinopathy (DR) still occurs. Recent studies have suggested that hypertension is a risk factor for the development and progression of DR and that blood pressure reduction can delay the progression of retinopathy. The renin-angiotensin system is activated by chronic hyperglycaemia, and the vitreous fluid level of angiotensin II (AII) is elevated in patients with proliferative diabetic retinopathy and diabetic macular oedema. AII increases vascular permeability and promotes neovascularization. It has been suggested that an autocrine-paracrine relationship may exist between AII and vascular endothelial growth factor in the ocular tissues. Accordingly, angiotensin-converting enzyme inhibitors or AII Type 1 (AT1) receptor blockers may be useful therapeutic agents for preventing the progression of DR. [source] | ||||||||||||||||||||||