Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The WHO and the National Diabetes Data Group have produced definitions to classify subjects with blood glucose levels following oral ingestion that are higher than normal, but are less than for patients with diabetes. The term impaired glucose tolerance (IGT) has been used to describe this group who have an increased risk of developing non-insulin dependent diabetes mellitus and cardiovascular disease, compared with subjects with normal glucose tolerance. Wide intra-subject variability has been observed when glucose tolerance tests are carried out on separate occasions. This has led some researchers to suggest that IGT merely constitutes a blurred boundary between normality and diabetes but accumulating evidence now supports the hypothesis that IGT is a useful risk factor category.
 ...
PMID:Impaired glucose tolerance--fact or fiction. 868 61

Patients with diabetes mellitus were surveyed to determine magnesium utilization and supplementation patterns and the extent to which these patterns correlate with American Diabetes Association (ADA) consensus panel recommendations. Participating ADA member physicians were asked to enroll five or more patients with insulin-dependent diabetes mellitus (IDDM, or type I diabetes) or non-insulin-dependent diabetes mellitus (NIDDM, or type II diabetes) who were not currently receiving magnesium supplementation and who they believed required or could benefit from oral magnesium chloride administration. Data were then collected regarding specific patient characteristics (ie, current diabetes therapy and glucose control); concomitant diseases and cardiovascular medications; baseline serum magnesium level, if measured before initiating magnesium chloride supplementation; and magnesium chloride dosage and duration. A total of 199 patients with diabetes began treatment with magnesium chloride supplementation after enrollment by a specialist. The mean baseline serum magnesium level for patients with IDDM was 1.48 mg/dL and for patients with NIDDM was 1.44 mg/dL (normal range, 1.80 to 2.40 mg/dL). No differences in mean serum magnesium levels were observed between men and women and between those with IDDM and those with NIDDM. Glucose control, as measured by glycosylated hemoglobin Alc, did not correlate with magnesium serum levels. A concomitant cardiovascular disease was present in 70% of patients. In 78.3% of patients, supplementation was initiated because of low serum magnesium levels; in 21.7%, magnesium chloride therapy was initiated empirically. No correlation was found between serum magnesium levels and the prescribed dosage or the recommended duration of magnesium therapy. Patterns of magnesium utilization among survey respondents generally followed ADA consensus panel recommendations. A majority of diabetic patients who were given magnesium chloride supplementation had concomitant cardiovascular disease. Primary care physicians and cardiologists who treat large numbers of patients with diabetes and cardiovascular disease should be knowledgeable of the ADA consensus report because of the high prevalence of hypomagnesemia and because of the consequences of magnesium deficiency in these high-risk groups. To achieve successful long-term maintenance in these patients, additional physician education appears to be necessary regarding initial dosing strategies and recommended duration of supplementation.
 ...
PMID:Magnesium utilization survey in selected patients with diabetes. 873 89

Non-insulin-dependent diabetic (NIDDM) patients show a high incidence of cardiovascular disease, with greater risk of recurrent myocardial infarction and a less favourable clinical outcome than non-diabetic patients. The majority of NIDDM patients are treated with sulphonylurea (SU) derivatives. In the 1970's the University Group Diabetes Program concluded that tolbutamide treatment caused increased cardiovascular mortality; the study, which led to curtailment of oral antidiabetic treatment in the USA, was received with scepticism in Europe. Later criticism of its methodology reduced the impact of the study; however, the question of the safety of SU in NIDDM patients with cardiovascular disease has been re-opened in the face of new experimental data. The heart and vascular tissues do have prerequisites for SU action, i.e. SU receptors and ATP-dependent K+ (K+ATP) channels. These channels play an important role in the protection of the myocardium against ischaemia-reperfusion damage, and their closure by SU could lead to amplified ischaemic damage. Here we review evidence from animal and human studies for deleterious SU effects on ischaemia-induced myocardial damage, either by direct action or through diminished cardioprotective preconditioning. Closure of K+ATP channels by SU can lead to reduction of post-infarct arrhythmias; the drug has also been claimed to improve various atherosclerosis risk factors. The evidence for these beneficial effects of SU is also reviewed. We look at the major difficulties that hamper transfer of information from experimental studies to clinical decision-making: a) The affinity of SU for heart K+ATP channels is orders of magnitude lower than for beta-cell channels; is it reasonable to expect in vivo cardiac effects with therapeutic 'pancreatic' SU doses? b) Most studies utilized high doses of acutely administered SU; are effects similar in the chronic steady-state of the SU-treated diabetic patient? c) Convincing SU effects have been demonstrated in acutely induced ischaemia by acutely administering the drug; do such effects persist in the clinical situation of gradually progressive ischaemia? d) Ischaemia and modification of K+ATP channel activity induce complex events, some with opposing effects; what is the net result of SU action, and do different SU derivatives lead to different outcomes? e) In the chronic (and hence clinically relevant) situation, how can direct (deleterious or beneficial) SU effects be separated from beneficial effects mediated by the metabolic action of the drug? Only large prospective clinical studies, making use of advanced technology for assessment of cardiovascular function, can answer these questions. Millions of NIDDM patients are treated with SU derivatives; many are in the age group where cardiovascular risks are extremely high. The question of whether SU derivatives are beneficial or deleterious for these patients must finally be settle unequivocally.
 ...
PMID:Sulphonylurea treatment of NIDDM patients with cardiovascular disease: a mixed blessing? 873 9

In view of their known high incidence of noninsulin dependent diabetes (NIDDM), we sought to determine whether Native American (Plains Indian) children and adolescents show evidence of risk factors for both NIDDM and cardiovascular disease. Children and adolescents between the ages of 4 and 19 y were recruited, and field days were organized for data collection, which included height, weight [to compute body mass index (BMI)], waist and hip circumference, family histories, quantum of Native American ancestry, and blood sampling for fasting lipids, apolipoproteins, insulin, and glucose. BMI increased with age in boys and girls and tended to be higher than in Caucasian children. The difference was significant in 5-9-y-old (p < 0.05) and 10-14-y-old (p < 0.05) boys and 10-14-y-old girls (p < 0.001). Ten- to 14-y-old girls in the highest quartile for BMI had higher triglyceride levels (p < 0.05) and lower HDL cholesterol (p < 0.001) when compared with those in the lower quartiles. In contrast, 15-19 y olds in the highest quartile for BMI had higher cholesterol, LDL cholesterol, and apolipoprotein B (p < 0.001). The mean fasting insulin levels were not related to BMI. The data suggest that, within this Plains Indian population, obesity associated with elevated lipid levels tends to begin at an early age in Native American children. Insulin levels do not appear to be related to BMI, a putative index of adiposity, in this population of children known to be prone to NIDDM in adult life.
 ...
PMID:Lipoprotein changes in relation to body mass index in Native American adolescents. 879 50

The ABCD (Appropriate Blood Pressure Control in Diabetes) trial is a large, prospective, randomized clinical trial designed to compare the effects of intensive with moderate blood pressure control on the prevention and progression of diabetic nephropathy, retinopathy, cardiovascular disease, and neuropathy in non-insulin-dependent diabetes (NIDDM). The secondary objective is to determine equivalency of the effects of a calcium channel blocker (nisoldipine) and of an angiotensin-converting enzyme inhibitor (enalapril) as a first-line antihypertensive agent in the prevention and/or progression of these diabetic vascular complications. The study consists of two study populations: a hypertensive one (diastolic blood pressure of > or = 90.0 mm Hg at the time of randomization) and a normotensive one (diastolic blood pressure of 80.0-89.0 mm Hg at the time of randomization). A total of 950 men and women aged 40-74 years were randomized and are being followed for 5 years at a single center. There were 470 randomized participants in the hypertensive population and 480 randomized participants in the normotensive population. This report summarizes the demographic, biochemical, and clinical characteristics of the randomized patients at the time of entry into the trial and evaluates the balance between the treatment groups within each population.
 ...
PMID:Baseline characteristics of participants in the Appropriate Blood Pressure Control in Diabetes trial. 887 60

Patients with diabetes mellitus have a higher rate of mortality than the general population. This higher mortality may be attributed mainly to cardiovascular disease. A high prevalence of dyslipidemia in diabetics can be one of the reasons for this. The most commonly recognized lipid abnormality in non-insulin-dependent diabetics (NIDDM) is hypertriglyceridemia, which is known to be an independent risk factor for coronary heart disease in diabetics. Hypertriglyceridemia can be produced by two mechanisms, increased synthesis of very-low-density lipoprotein (VLDL) triglyceride and removal defect of plasma triglyceride. It has been a matter of debate whether insulin always stimulates hepatic VLDL secretion but it is generally accepted that insulin deficiency results in an impairment of plasma triglyceride clearance. Considerable attention has recently been focused on the atherogenecity of postprandial hyperlipidemia, remnant lipoproteins, small, dense LDL, lipoprotein (a) [Lp(a)] and isolated hypo-alphalipoproteinemia in NIDDM subjects. Several reports suggested that these atherogenic lipoprotein abnormalities are present in NIDDMs even if they are apparently normolipidemic. Association of visceral fat obesity, insulin resistance and nephropathy may aggravate the atherogenic lipoprotein profile. Therefore, we propose here that plasma lipid levels of diabetic subjects must be more strictly controlled than for the non-diabetic population in order to avoid an increased risk for coronary heart disease. If they are obese or associated with insulin resistance or nephropathy, these conditions should be carefully controlled.
 ...
PMID:Dyslipidemia in diabetes mellitus. 887 70

The search for the genetic basis of NIDDM has magnified the need for an efficient representation of the pre-NIDDM phenotype. The overall goal is to relate specific mutations on the genome to specific changes in physiologic function which lead to NIDDM. Unfortunately, there is still not a clear understanding of the molecular cause of NIDDM in most individuals. Therefore, one must take an alternative approach: to express in quantitative terms the various tissue processes which determine the ability to regulate the blood glucose in fasting and after carbohydrate administration. A minimal list of such processes includes the provision of glucose by the liver, insulin sensitivity, insulin secretion, and glucose effectiveness. The latter function is the ability of glucose per se to enhance glucose disappearance from blood, independent of a dynamic insulin response. Approaches to measuring the list of functions which determine the glucose tolerance are reviewed: they include the minimal model method, which quantitates insulin sensitivity (Sl) and glucose effectiveness (SG), and a combined model approach, which measures insulin secretion. These methods are being developed for large populations. Such a development is important for elucidating the causes of reduced glucose tolerance in populations, and examining the relation between such causes and outcomes including diabetes and cardiovascular disease. Of particular importance for diabetes development is the characteristic hyperbolic relationship between insulin secretion and insulin action. This relationship, the "hyperbolic law of glucose tolerance' indicates that insulin secretion can only be assessed in terms of the ambient degree of insulin sensitivity. By applying this principle, it is clear that latent pancreatic islet-cell dysfunction has been underestimated, and may be significant even in subjects with impaired glucose tolerance. Finally, new explorations of insulin control of liver glucose output indicate that this process may be under the control of free fatty acids. The latter realization indicates that the insulin effect on lipolysis is what is critical for determination of glucose output in the fasting state, and that insulin resistance at the level of the adipocyte may determine the extent of fasting hyperglycaemia, and may be an important factor in the overall phenotype in prediabetic and NIDDM individuals.
 ...
PMID:Toward an integrated phenotype in pre-NIDDM. 889 86

Although most cohort studies have shown that diabetes is a risk factor for cardiovascular disease, the mechanisms remain unclear. Hyperglycaemia defines this disorder but does not provide the criteria for causality. However, there are new indications for the possible role of a potentially atherogenic and diabetogenic syndrome rooted in insulin resistance, which was first described by Reaven as "syndrome X". In its complete form, this syndrome includes hyperinsulinaemia, glucose intolerance, dyslipidaemia, elevated blood pressure and fibrinolytic impairment. The complex pathophysiological processes leading to the clustering of these abnormalities are still unclear but probably relate to excessive intra-abdominal fat deposits (clinically expressed by upper body fet distribution) and combined insulin resistance and hyper-insulinaemia. The presence of insulin resistance and hyperinsulinaemia in pre-diabetic individuals, and their predictive role in non-insulin dependent diabetes mellitus, has been documented in various ethnic groups, suggesting a two-step process in the natural history of the disease, i.e. "compensated" insulin resistance followed by failure of insulin secretory response leading to a hyperglycaemic (diabetic) phase. In Caucasians at least, in whom the insulin-resistance syndrome includes clear abnormalities in its most potentially atherogenic elements, this natural history suggests that the cardiovascular complications associated with non-insulin dependent diabetes mellitus originate from the initial "pre-diabetic" phase of the disease. Early prevention would theoretically require intervention before hyperglycaemia occurs (or even if it will never occur) for all upper body obese subjects who present with insulin-resistance syndrome.
 ...
PMID:Insulin-resistance syndrome and cardiovascular complications of non-insulin-dependent diabetes mellitus. 889 91

Non-insulin dependent diabetes mellitus carries a markedly elevated risk of cardiovascular disease. For that reason the efficacy of any treatment modality for this disease should be assessed in terms of the known cardiovascular risk factors, as for example serum lipids. Sulfonylurea do not affect serum lipid levels to any significant extent. These drugs promote beta-cell secretion by dosing potassium ion channels. These channels are also present in vascular smooth muscle cells. Some, though not all, sulfonylureas are able to inhibit the vascular dilatory response to potassium ion openers, thereby adversely affecting the cardioprotective vascular response to ischaemia. Sulfonylureas, in contrast to insulin, seem able to inhibit the fibrinolytic system, possibly via the stimulating effect of proinsulin on the endothelial PAI-1 expression. These observations need further confirmation. Of clinical importance is the frequent occurrence of hypoglycaemia for which several risk factors are recognized.
 ...
PMID:Role of sulfonylureas in non-insulin-dependent diabetes mellitus: Part II--"The cons". 891 91

To elucidate the prevalence and relevant factors of glucose intolerance and its effect on the development of cardiovascular disease in the current general Japanese population, we conducted a cross-sectional survey of glucose intolerance by a 75-g oral glucose tolerance test in 2,490 subjects aged 40-79 years old selected from a Japanese community, Hisayama, in 1988, and followed them for 5 years. The prevalence of diabetes (NIDDM) was 13% for men and 9% for women, and that of impaired glucose tolerance (IGT) was 20% and 19%, respectively. Both IGT and NIDDM were significantly associated with factors related to insulin resistance including the sum of insulin concentrations. In addition, subjects with IGT and NIDDM had a significantly higher risk of occurrence of cardiovascular disease (stroke and coronary heart disease) than did those with normal glucose tolerance.
 ...
PMID:[Prospective population survey of IGT in a Japanese community, Hisayama]. 891 40


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>