Current Issue : April - June Volume : 2012 Issue Number : 2 Articles : 7 Articles
Diabetes is one of the leading life threatening diseases in the world. Diabetes is more common in South Asian, African and African-Caribbean origin. In India there has been sharp rise in the prevalence of diabetes among the urban as well as rural population due to environmental and lifestyle changes. In general, diabetes can be divided into two major categories (Insulin dependent and non insulin dependent). Other categories commonly accrued in female during pregnancy called Gestational Diabetes Mellitus (GDM) and more than 56 specific types of diabetics were recorded. Lifestyle changes are the cornerstone of diabetic management and can easily managed, the patient can live a long healthy life. Diabetes associated disease and mortality rate may reduce through proper evaluation of diabetes in the primary care setting with targeted application of suitable screening methods. Hence, the present study, we have taken to assess the appropriate diabetic screening and its importance to manage the diabetic in holistic way of approach....
Objective: Axon reflex-mediated neurogenic vasodilatation in response to cutaneous heating may reflect early, pre-clinical\nsmall fibre dysfunction. We aimed to evaluate the distribution of the vascular flare area measured by laser doppler imaging\n(ââ?¬Ë?ââ?¬Ë?LDIFLARE areaââ?¬â?¢Ã¢â?¬â?¢) in type 1 diabetes and in healthy volunteers.\nResearch and Methods: Concurrent with clinical and electrophysiological examination to classify diabetic sensorimotor\npolyneuropathy (DSP), LDIFLARE area (cm2) was determined in 89 type 1 diabetes subjects matched to 64 healthy volunteers.\nWe examined the association and diagnostic performance of LDI with clinical and subclinical measures of DSP and its\nseverity.\nResults: Compared to the 64 healthy volunteers, the 56 diabetes controls without DSP had significantly lower LDIFLARE area\n(p = 0.006). The 33 diabetes cases with DSP had substantially lower LDIFLARE area as compared to controls without DSP\n(p = 0.002). There was considerable overlap in LDIFLARE area between all groups such that the ROC curve had an AUC of 0.72\nand optimal sensitivity of 70% for the detection of clinical DSP. Use of a subclinical definition for DSP, according to\nsubclinical sural nerve impairment, was associated with improved AUC of 0.75 and sensitivity of 79%. In multivariate analysis\nhigher HbA1c and body mass index had independent associations with smaller LDIFLARE area.\nConclusions: Axon reflex-mediated neurogenic vasodilatation in response to cutaneous heating is a biomarker of early\nnerve dysfunction in DSP. Its independent association with glycemic exposure in diabetes subjects and both glycemic\nexposure and BMI in healthy volunteers highlights the existence of small-fibre dysfunction in the natural history of DSP....
Heart failure with preserved ejection fraction (HFpEF) constitutes approximately 50% of heart failure patients. The prevalence of\ndiabetes mellitus in HFpEF is high at 30-40%. The paper provides a systematic review of the pathophysiological features\nunderlying HFpEF in diabetes mellitus. The importance of mechanisms other than left ventricular diastolic dysfunction underlying\nthis important condition is emphasised. Thus, ventricular-arterial coupling & vascular dysfunction together with chronotropic\nincompetence & cardiovascular reserve dysfunction play an important role. The various morphologic and molecular features\noccurring in the myocardium and vasculature in diabetes secondary to hyperglycaemia and other metabolic disturbances are also\ndiscussed. These include microangiopathy, myocardial fibrosis, increased oxidative stress, impaired calcium homeostasis,\nactivation of the cardiac renin-angiotensin system, autonomic neuropathy, endothelial dysfunction, re-expression of foetal gene\nresponse as well as stem cell involvement. Nonetheless, a lot is still unknown and further studies are needed to establish the\nunderlying pathophysiological mechanisms with the hope that novel pharmacotherapies targeting this disease will be\ndeveloped. In the meantime, cardiometabolic factors, including hyperglycaemia, hypertension and dyslipidaemia should be\ntargeted and aggressively treated....
Background: Diabetic nephropathy (DN) affects about 30% of patients with type 1 diabetes (T1D) and contributes to serious\r\nmorbidity and mortality. So far only the 3q21ââ?¬â??q25 region has repeatedly been indicated as a susceptibility region for DN.\r\nThe aim of this study was to search for new DN susceptibility loci in Finnish, Danish and French T1D families.\r\nMethods and Results: We performed a genome-wide linkage study using 384 microsatellite markers. A total of 175 T1D\r\nfamilies were studied, of which 94 originated from Finland, 46 from Denmark and 35 from France. The whole sample set\r\nconsisted of 556 individuals including 42 sib-pairs concordant and 84 sib-pairs discordant for DN. Two-point and multi-point\r\nnon-parametric linkage analyses were performed using the Analyze package and the MERLIN software. A novel DN locus on\r\n22q11 was identified in the joint analysis of the Finnish, Danish and French families by genome-wide multipoint nonparametric\r\nlinkage analysis using the Kong and Cox linear model (NPLpairs LOD score 3.58). Nominal or suggestive evidence\r\nof linkage to this locus was also detected when the three populations were analyzed separately. Suggestive evidence of\r\nlinkage was found to six additional loci in the Finnish and French sample sets.\r\nConclusions: This study identified a novel DN locus at chromosome 22q11 with significant evidence of linkage to DN. Our\r\nresults suggest that this locus may be of importance in European populations. In addition, this study supports previously\r\nindicated DN loci on 3q21ââ?¬â??q25 and 19q13....
Hyperglycaemia occurring in diabetes is responsible for accelerated arterial remodeling and atherosclerosis, affecting the macroand\r\nthe microcirculatory system. Vessel injury is mainly related to deregulation of glucose homeostasis and insulin/insulinprecursors\r\nproduction, generation of advanced glycation end-products, reduction in nitric oxide synthesis, and oxidative and\r\nreductive stress. It occurs both at extracellular level with increased calcium and matrix proteins deposition and at intracellular\r\nlevel, with abnormalities of intracellular pathways and increased cell death. Peripheral arterial disease, coronary heart disease, and\r\nischemic stroke are the main causes of morbidity/mortality in diabetic patients representing a major clinical and economic issue.\r\nPharmacological therapies, administration of growth factors, and stem cellular strategies are the most effective approaches and\r\nwill be discussed in depth in this comprehensive review covering the regenerative therapies of diabetic microangiopathy....
Intensive insulin therapy and protein restriction delay the development of nephropathy in a variety of conditions, but few\ninterventions are known to reverse nephropathy. Having recently observed that the ketone 3-beta-hydroxybutyric acid (3-\nOHB) reduces molecular responses to glucose, we hypothesized that a ketogenic diet, which produces prolonged elevation\nof 3-OHB, may reverse pathological processes caused by diabetes. To address this hypothesis, we assessed if prolonged\nmaintenance on a ketogenic diet would reverse nephropathy produced by diabetes. In mouse models for both Type 1\n(Akita) and Type 2 (db/db) diabetes, diabetic nephropathy (as indicated by albuminuria) was allowed to develop, then half\nthe mice were switched to a ketogenic diet. After 8 weeks on the diet, mice were sacrificed to assess gene expression and\nhistology. Diabetic nephropathy, as indicated by albumin/creatinine ratios as well as expression of stress-induced genes,\nwas completely reversed by 2 months maintenance on a ketogenic diet. However, histological evidence of nephropathy was\nonly partly reversed. These studies demonstrate that diabetic nephropathy can be reversed by a relatively simple dietary\nintervention. Whether reduced glucose metabolism mediates the protective effects of the ketogenic diet remains to be\ndetermined....
Type 2 diabetes (T2D) and ageing have well documented effects on every organ in the body. In T2D the autonomic nervous system\r\nis impaired due to damage to neurons, sensory receptors, synapses and the blood vessels. This paper will concentrate on how\r\nautonomic impairment alters normal daily activities. Impairments include the response of the blood vessels to heat, sweating, heat\r\ntransfer, whole body heating, orthostatic intolerance, balance, and gait. Because diabetes is more prevalent in older individuals,\r\nthe effects of ageing will be examined. Beginning with endothelial dysfunction, blood vessels have impairment in their ability to\r\nvasodilate. With this and synaptic damage, the autonomic nervous system cannot compensate for effectors such as pressure on\r\nand heating of the skin. This and reduced ability of the heart to respond to stress, reduces autonomic orthostatic compensation.\r\nDiminished sweating causes the skin and core temperature to be high during whole body heating. Impaired orthostatic tolerance,\r\nimpaired vision and vestibular sensing, causes poor balance and impaired gait. Overall, people with T2D must be made aware and\r\ncounseled relative to the potential consequence of these impairments....
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