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At least 73 records · Page 4Linked to original sources
PubMed2004

Hippocampal synaptic plasticity and glutamate receptor regulation: influences of diabetes mellitus.

Diabetes mellitus is an endocrine disorder of carbohydrate metabolism resulting primarily from inadequate insulin release (Type 1 insulin-dependent diabetes mellitus) or insulin insensitivity coupled with inadequate compensatory insulin release (Type 2 non-insulin-dependent diabetes mellitus). Previous studies involving behavioural and electrophysiological analysis indicate that diabetes mellitus induces cognitive impairment and defects of long-term potentiation in the hippocampus. Considered to be an important mechanism of learning and memory in mammals, long-term potentiation is known to require regulation of the glutamate receptor properties. According to many studies, defects of long-term potentiation in the hippocampus of diabetic animals are due to abnormal glutamate receptors. We review here the changes in glutamate receptors that may account for modifications of long-term potentiation in various models of diabetes mellitus. As glutamate receptors are also involved in the appearance of neurodegenerative states, we discuss the possibility that deficits in long-term potentiation during chronic diabetes might arise from dysfunction of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in early stages of the disease. This review addresses the possible role of hyperglycaemia and insulin in regulating these receptors.

Animals↗
PubMed1998

Serum levels of basic fibroblast growth factor and vascular endothelial growth factor in children and adolescents with type 1 diabetes mellitus.

Diabetes mellitus is characterized by microangiopathy and increased angiogenic response in various organs. Basic fibroblast growth factor (bFGF) as well as vascular endothelial growth factor (VEGF) are both angiogenic and are involved in vascular endothelial cell growth. The purpose of this study was to determine serum levels of bFGF and VEGF, in children and adolescents (youngsters) with type 1 diabetes mellitus, and correlate them with parameters reflecting the severity of the disease. Forty diabetic youngsters without clinical evidence of complications were compared with 30 healthy control subjects (mean age +/- SD, 14.3 +/- 3.6 and 13.8 +/- 3.6 y, respectively). Diabetes duration and metabolic control (expressed by glycosylated Hb) were (mean +/- SD) 6.2 +/- 3.8 y and 9.6 +/- 1.8%, respectively. bFGF and VEGF (pg/mL) were measured in serum samples by enzyme immunoassays, and both were not significantly different between the type 1 diabetes mellitus and the control group (p = 0.952 and p = 0.559, respectively). Restricting the analysis to the type 1 diabetes mellitus group, neither the duration nor the metabolic control of the disease showed any correlation with bFGF and VEGF serum levels, whereas a significantly positive correlation was found between the two examined angiogenic factors both in the diabetic (r = 0.3464, p = 0.025) and the control group (r = 0.4619, p = 0.0013). In conclusion, serum levels of bFGF and VEGF were not found to vary significantly in diabetic youngsters in relation to controls and had no correlation with the duration and metabolic control of the disease. Nevertheless, a positive correlation was found between these two angiogenic factors both in the type 1 diabetes mellitus and the control group.

Adolescent↗
PubMed1996

The size of subcortical ischemic infarction in patients with and without diabetes mellitus.

Diabetes mellitus is associated with a higher frequency and poorer outcome of ischemic stroke. Determinants of the poorer prognosis of stroke in patients with diabetes are not well defined. We investigated whether size of cerebral infarction differs in patients with and without diabetes mellitus. We compared ischemic lesions in 41 consecutive stroke patients with subcortical infarction-22 with and 19 without diabetes mellitus. The location and size of the ischemic infarct were derived from magnetic resonance images obtained on day 3 or 4 post stroke onset. Cross-sectional infarct area was determined by direct measurement from film. The age of patients was similar in both groups. Patients with diabetes had higher prevalence of arterial hypertension, and previous stroke, and higher admission triglyceride and glucose levels compared to patients without diabetes. We found no significant difference in the size of ischemic lesions in patients with and without diabetes mellitus (1.87 vs. 1.72 cm2, respectively). We conclude that among patients with subcortical ischemic stroke the size of infarction is not different between patients with and without diabetes mellitus.

Aged↗
PubMed1998

Constrictor responses of the rat basilar artery during diabetes mellitus.

Diabetes mellitus produces abnormalities of the endothelium and impairs endothelium-dependent dilatation of large and small cerebral blood vessels. However, the effect of diabetes mellitus on cerebral vasoconstriction and the modulatory influence of nitric oxide on cerebral vasoconstriction is unclear. Thus, the first goal of this study was to examine the effect of diabetes mellitus on constrictor responses of the basilar artery in vivo. Our second goal was to examine a potential role for nitric oxide in modulating constrictor responses of the basilar artery. A craniotomy was performed over the ventral medulla to expose the basilar artery. The diameter of the basilar artery was measured using intravital microscopy in nondiabetic and diabetic (3-4 months after injection of streptozotocin; 50-60 mg/kg i.p.) rats in response to angiotensin II, arginine vasopressin, endothelin-1, and the thromboxane analogue, U-46619. Topical application of angiotensin II (10 and 100 nM) produced only minimal changes in diameter of the basilar artery which were similar in nondiabetic and diabetic rats (p>0.05). Arginine vasopressin (0.1 and 1.0 nM), endothelin-1 (10 and 50 nM), and U-46619 (10 and 100 nM) produced marked dose-related constriction of the basilar artery which also was similar in nondiabetic and diabetic rats (p>0.05). Next, we examine whether the synthesis/release of nitric oxide played a role in constriction of the basilar artery in response to the agonists. We found that L-NMMA (1.0 microM) did not alter constrictor responses of the basilar artery in nondiabetic and diabetic rats. Thus, responses of the basilar artery to important vasoactive agonists are not altered by diabetes mellitus. In addition, it does not appear that the synthesis/release of nitric oxide modulates constrictor responses of the basilar artery to angiotensin II, arginine vasopressin, endothelin-1 and U-46619. We suggest that preservation of vasoconstrictor responses, coupled with impaired vasodilator responses, may contribute to the pathogenesis of cerebrovascular abnormalities associated with diabetes mellitus.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Beneficial and detrimental effects of intensive glycaemic control, with emphasis on type 2 diabetes mellitus.

Diabetes mellitus is a major health problem in the world. Several clinical trials have shown that some of the major complications of diabetes mellitus can be partially prevented or delayed by intensive glycaemic control. However, there are benefits and risks in aiming for near normal blood glucose levels. Intensive glycaemic control delays the onset and progression of retinopathy, nephropathy and neuropathy. Epidemiological and observational studies have shown that cardiovascular events may be correlated with the severity and duration of diabetes mellitus, but major randomised trials have only shown weak and nonsignificant benefits of intensive glycaemic management in decreasing event rates. A modest improvement in lipid profile results from blood glucose control although, in the majority of cases, not enough to reach current targets. Detrimental effects of intensive glycaemic control include bodyweight gain and hypoglycaemia. Controversial issues in the management of patients with diabetes mellitus include the unproven increase in cardiovascular morbidity from sulphonylureas and hyperinsulinaemia, and the still unknown long term effects of newer oral antihyperglycaemic agents alone or in combination with traditional therapies (such as sulphonylureas and metformin). It is important to individualise management in setting glycaemic goals. Control of cardiovascular risk factors through blood pressure and lipid control and treatment with aspirin (acetylsalicylic acid) and ACE inhibitors have consistently shown benefits in the prevention of both macro- and microvascular complications in patients with diabetes mellitus; these measures deserve priority.

Blindness↗
PubMedDate not supplied

Primary prevention of diabetes mellitus.

Diabetes mellitus is one of the chronic noncommunicable diseases that have increased markedly in this century. The discovery of insulin and other drugs for lowering hyperglycemia have certainly reduced mortality from acute complications of diabetes and improved the quality of life of many diabetic patients. Recent advances in research into the etiology and natural history of diabetes have increased our knowledge about different types of diabetes to such an extent that primary prevention of diabetes mellitus is becoming a reality. Until now, few studies have attempted to test measures for primary prevention of diabetes. Therefore, the data supporting the possibility for primary prevention are largely indirect and need to be tested in preventive trials or in community-based prevention programs. We believe, however, that the time is right to start action in populations in which the prevalence of diabetes is known to have clearly increased recently. We summarize the evidence that can be used as the scientific basis of primary prevention of diabetes mellitus.

Diabetes Mellitus↗
PubMed2001

Diagnosis, classification, and pathogenesis of diabetes mellitus.

Diabetes mellitus is a metabolic disorder that is characterized by inappropriate hyperglycemia and is associated with both acute and chronic complications. Currently, diabetes mellitus is diagnosed by blood or plasma glucose levels. A random plasma glucose level > or = 200 mg/dL in an individual with classic symptoms is sufficient to make the diagnosis. Otherwise, a fasting plasma glucose level > or = 126 mg/dL or a 2-hour plasma glucose level > or = 200 mg/dL after an oral glucose challenge of 75 g on 2 occasions is sufficient evidence upon which to diagnose diabetes mellitus. The major types of diabetes mellitus are type 1 diabetes (insulin deficient) and type 2 diabetes (combination of insulin resistance and insulin deficiency). In both types, there is a genetic predisposition as well as environmental factors that contribute to the expression of the genetic predisposition. In type 1 diabetes, the primary abnormality is extensive deficiency of beta cell function. In type 2 diabetes, insulin resistance occurs, and the marked compensatory increases in insulin secretion necessary to maintain normal glucose tolerance cannot be achieved or maintained. As beta cell function continues to decrease, the individual progresses from normal glucose tolerance to impaired glucose tolerance to diabetes with primarily postprandial hyperglycemia to diabetes with fasting hyperglycemia. Drugs can cause diabetes by interfering with beta cell insulin secretion, by increasing insulin resistance, or by a combination of both. Atypical antipsychotic drugs have been reported to cause diabetic ketoacidosis, obesity and insulin resistance, type 2 diabetes, and hypertriglyceridemia. A monitoring system should be in place in patients started on treatment with these agents to detect metabolic abnormalities as they are evolving so that adequate and timely treatment can be initiated.

Antipsychotic Agents↗
PubMed1988

[Pathogenesis and therapy of type I and type II diabetes mellitus].

Diabetes mellitus is a heterogenous syndrome. Insulin dependent type I diabetes is characterised by progressive beta-cell-loss, resulting in a deterioration of insulin secretion. Cause of the beta-cell-destruction is a chronic autoimmune process, which starts already months to years before manifestation of the disease. New advances in the diagnosis of the autoimmune mechanisms, which are responsible for type I diabetes might help to prevent type I diabetes by immunization or immunosuppressive therapy in the near future. At the moment multiple daily insulin injections are the substitution therapy of the choice in type I diabetes mellitus. This kind of therapy is designed to imitate the physiologic dynamics of insulin secretion in healthy subjects. In non insulin dependent diabetes a defect in insulin action seems to be the primary cause of the disease although there are also defects in insulin secretion in type II diabetes mellitus. Most type II diabetics are overweight at the beginning of the disease and the primary goal of therapy in these patients is normalization of bodyweight and improvement of peripheral and hepatic insulin sensitivity. Regular exercise is seen as a cornerstone in the treatment of type I and type II diabetes. Besides the acute blood glucose lowering effect of exercise, regular exercise has beneficial effects on the circulatory system and muscle system, leads to an increase in insulin sensitivity, to a decrease of the daily insulin dosage and to a stabilization of metabolic control. Furthermore beneficial effects of exercise on plasma lipids and lipoproteins are reported. In overweight diabetics regular exercise facilitates normalization of body weight.

Diabetes Mellitus, Type 1↗
PubMed1996

International collaborative research on management self-efficacy in diabetes mellitus.

Diabetes mellitus is a leading chronic illness in the United States and in the Netherlands. Assisting persons with diabetes and their families to manage the illness so that they can have satisfying lives is a challenge for all involved. Persons with diabetes mellitus and their significant others (family members, friends, or other caregivers) must learn and perform management behaviors in order to achieve this goal. Self-efficacy has been shown to be an important predictive variable in initiating and continuing management behaviors. In order to test the impact of self-efficacy on the management of diabetes mellitus and to conduct comparative studies in the Netherlands and the United States, a battery of valid and reliable measurement instruments were needed. Six different instruments in two languages were developed to test children with diabetes and their significant other, adults with insulin dependent diabetes and their significant other, and adults with non-insulin dependent diabetes and their significant other. An overview of the instrument development and testing is described. The testing of different formats due to language terminology and the testing of the instruments for the adults with non-insulin dependent diabetes mellitus will be presented.

Adult↗
PubMed1997

The economics of pharmacotherapy for diabetes mellitus.

Diabetes mellitus is a chronic disease that has a major social impact. Proper planning for the management of patients with diabetes mellitus requires consideration of the important costs that diabetes imposes on the health system. Most of the indirect costs (lost productivity as a result of disability, absenteeism, loss of potential productive years of life), are related to diabetic complications, which greatly exceed the rest of the costs, and are also very difficult to classify in a standard manner. Direct costs (pharmacy, hospitalisation, consultations) mostly derive from healthcare strategies that aim to reduce late complications of the condition and maintain day-to-day quality of life. Therefore, it does not seem difficult to estimate pharmaceutical expenditures. The consumption of oral antihyperglycaemic agents, insulin, injection equipment and self-monitoring equipment indicates prescription tendencies and shows the influence on costs, and provides indirect information about the quality of healthcare or patients with diabetes mellitus. Over the last few years, some developed countries have shown a progressive increase in pharmaceutical expenditure on diabetic care, whereas economically depressed countries have experienced a dramatic shortage of basic medicines such as insulin. Considering the increase in consumers, and the international distribution of illnesses, both a hypothetical excess cost (related to consumerism; incurred by the health system and the diabetic population) and an irregular distribution of economic resources are evident. A co-ordinated health plan for patients with diabetes mellitus, involving the collaboration of diabetologists and epidemiologists with the pharmaceutical industry, and appropriate training measures for patients and professionals, would improve pharmacoeconomic efficiency in managing this disorder.

Diabetes Mellitus↗
PubMed1994

Vasopressin V1 and V2 receptors in diabetes mellitus.

Diabetes mellitus causes hypertonicity, increased plasma arginine vasopressin (AVP), polydipsia, and polyuria. Downregulation of AVP V2 receptors may contribute to the polyuria through diminished V2 receptor-mediated free water retention. After 2 wk of streptozotocin-induced diabetes mellitus, the diabetic rats had raised plasma glucose, AVP, and osmolality levels (P < 0.001) compared with nondiabetic controls (Sham). Insulin treatment (4 U long-acting insulin sc, daily) partially lowered these values (P < 0.01). There was a reduction in the number of renal and hepatic V1 receptors in the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The receptor affinity remained unchanged. In parallel, there was a reduction in maximum AVP-activated total inositol phosphate production in the liver and kidney of the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The density and affinity of renal V2 receptors and AVP-stimulated adenosine 3',5'-cyclic monophosphate production in the diabetic and diabetic+insulin animals were unchanged compared with the sham. These results demonstrate differential regulation of AVP receptors and suggest that downregulation of renal V2 receptors does not contribute to the polyuria of diabetes. In contrast, downregulation of V1 receptors might contribute to diminished V1 receptor-mediated biological responses to AVP seen in diabetes mellitus.

Animals↗
PubMedDate not supplied

[Prediabetic states and the prevention of diabetes mellitus].

Diabetes mellitus predisposition is observed in the increased insulin activity of the pancreatic islet, followed by its exhaustion, and in its congenital or postnatal decreased activity. The former is seen in obese subjects, in large-born children and their mothers or in the children, whose mothers suffered from diabetes mellitus during pregnancy. The latter is discovered in hereditary diabetes mellitus, in hypertension and angiosclerosis. To avert diabetes mellitus in predisposed subjects a fixed-calory diet should be recommended for the pancreatic islet protection. Systematic blood and urine examinations are to be performed for revealing the initial pancreatic islet damage. Prophylactic treatment of these patients is realized by endocrinologists and the selection for therapy is carried out by special physicians.

Diabetes Mellitus↗
PubMed1998

Endothelial dysfunction in diabetes mellitus.

Diabetes mellitus is associated with accelerated atherosclerosis and an increased prevalence of cardiovascular disease. Although the link between diabetes and cardiovascular disease is not fully understood, loss of the modulatory role of the endothelium could be implicated in the pathogenesis of diabetic vascular complications. There is substantial evidence that vasodilatation mediated by endothelium-derived nitric oxide (NO) is impaired in animal models of diabetes and in patients with insulin-dependent and non-insulin-dependent diabetes mellitus. NO is a principal factor involved in the antiatherosclerotic properties of the endothelium. NO interferes with key events in the development of atherosclerosis, such as vascular tone, monocyte and leukocyte adhesion to the endothelium, platelet-vessel wall interaction, and smooth muscle proliferation. Therefore, the pathogenesis of diabetic vascular disease may involve a reduced bioavailability of endothelium-derived NO. Although mechanisms by which diabetes contributes to endothelial dysfunction are currently unknown, it is likely that hyperglycemia, the hallmark of diabetes mellitus, may initiate this abnormality. Hyperglycemia-induced endothelial dysfunction may result from decreased production of NO, inactivation of NO by oxygen-derived free radicals, and/or increased production of endothelium-derived contracting factors, which oppose the protective activity of NO. This review summarizes evidence for endothelial dysfunction in diabetic patients and animals and the effects of prolonged exposure to elevated glucose in normal blood vessels and cultured endothelium. A better understanding of the mechanism(s) of hyperglycemia-induced endothelial dysfunction may unmask new preventive strategies to reduce cardiovascular morbidity and mortality in this condition.

Animals↗
PubMed2005

Intradermal reactions to purified protein derivative in patients with diabetes mellitus.

Diabetes mellitus is known to adversely affect the immune system. Immune dysfunction is also associated with the etiology of diabetes mellitus. Immune dysfunction is associated with diminished chemotactic, phagocytic and monocyte activity. There is also increased T-cell activity. All these are associated with acute hyperglycemia. We investigated the cellular arm of the immune system of patients with diabetes mellitus using intradermal reactions (IDR) to purified protein derivative (PPD). Both groups high blood glucose [HBG] vs. low blood glucose [LBG]) were homogeneous in terms of size and sex and average age (24. vs. 22.; 21 F vs 25 M; 56.5yrs. vs. 54.5 yrs.). The LBG had a greater average duration of diabetes (13.6 yrs vs. 9.3 yrs), which suggests an increased tendency to complications of diabetes mellitus. The results showed an average blood glucose and IDR (HBG vs. LBG) of 235.8 +/- 46.5 mg/dl vs. 144.3 +/- 26.7 mg/dl and 18.5 +/- 8.5 mm vs. 12.2 +/- 7.0 mm respectively. These results showed that IDR is significantly affected by hyperglycemia. This increased IDR may be a consequence of the synergy between interferon-gamma and tumor necrosis factor alpha which is a significant factor in diabetes. Also, there is an accentuation of this synergy following injection of PPD. It appears to be clear that IDR to PPD may be influenced by the diabetic state, especially acute hyperglycemia. However, it also appears that IDR to PPD may not be an adequate method for assessing cutaneous cell-mediated immunity.

Blood Glucose↗
PubMed2001

Renal insufficiency accelerates atherosclerosis in patients with type 2 diabetes mellitus.

Diabetes mellitus is a strong risk factor for the progression of atherosclerosis. In patients with chronic renal failure on hemodialysis, advanced atherosclerosis is reported to be present. We examined how renal insufficiency affects intima-medial thickness (IMT) of the carotid and femoral arteries in patients with type 2 diabetes mellitus. IMT was measured by B-mode ultrasonography in 115 patients with type 2 diabetes mellitus (65 men, 50 women; 58 +/- 13 years old). The IMT of the carotid and the femoral artery of patients with creatinine clearance less than 80 mL/min (n = 55) were significantly greater than those of patients with creatinine clearance 80 mL/min or greater (n = 60; P < 0.01 and P < 0.05). Linear regression analyses showed that there was a significant negative correlation between creatinine clearance and IMT of the carotid artery (r = -0.330; P < 0.001) and femoral artery (r = -0.336; P < 0.001). Multiple regression analyses revealed that age and creatinine clearance significantly and independently affected the IMT of the carotid artery (R(2) = 0.176; P < 0.0001), and age, duration of diabetes, and smoking affected the IMT of the femoral artery (R(2) = 0.287; P < 0.0001). These findings show that decreased renal function accelerates atherosclerosis in patients with type 2 diabetes mellitus and that chronic renal failure is a significant, independent risk factor for carotid atherosclerosis in these patients.

Age Factors↗
PubMed1995

Renal functional reserve in subjects with diabetes mellitus.

Diabetic nephropathy develops in approximately 35% of patients with insulin-dependent diabetes mellitus (IDDM) and in a similar proportion of patients with non-insulin-dependent diabetes mellitus (NIDDM). However, we remain at present unable to identify the susceptible subset prior to the development of microalbuminuria. Up to 25% of IDDM patients and a variable proportion of NIDDM patients manifest glomerular hyperfiltration in the first few years of diabetes. It has been debated whether this basal hyperfiltration is predictive of future renal disease and whether better prediction can be achieved by the use of the renal haemodynamic response to a protein meal, defined by some authors as renal reserve. The concept of renal functional reserve in patients with diabetes mellitus is complicated by the dependence of the GFR response on basal GFR, the influence of the prevailing metabolic conditions, and because the response differs to different stimuli. We review the factors affecting renal hemodynamics and renal hemodynamic responses in the context of supranormal, normal, and impaired renal function in diabetes. We conclude that although the measurement of renal functional reserve may help clarify important pathophysiological mechanisms, the assessment of basal GFR in clinical practice is all that is required for predictive and monitoring purposes.

Diabetes Mellitus, Type 1↗