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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Butt joint, plain and round beveled MOD cavities were prepared in extracted human molars. Composite resin inlays (SR-Isosit) were fixed adhesively and analysed by quantitative SEM-evaluation after thermocycling and mechanical load application. The marginal adaptation of the inlays differed significantly depending on the type of cavosurface preparation. Best results with a high percentage of perfect margins not only before but also after in vitro load application were obtained with cavities prepared with rounded bevels.
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PMID:[The effect of modified forms of preparation on the quality of SR Isosit composite inlay margins]. 181 43

We evaluated the role of insulin availability in the induction therapy of non-insulin dependent diabetes mellitus (NIDDM). Plasma glucose (BG) and insulin (IRI) response to glucose loading (OGTT) was investigated before and after placebo and phenobarbitone (PB) therapy in patients with glucose intolerance and NIDDM treated with diet only, sulphonylureas (SU) plus metformin (M) or insulin. The antipyrine test was used to reflect the liver mixed function oxidase system. Therapy with PB, but not placebo, reduced fasting IRI and BG in subjects with glucose intolerance and improved the glucose tolerance, insulin response to glucose and antipyrine metabolism. The effects of PB on patients with NIDDM were dependent on the insulin availability and duration of the disease. Best responses were seen in hyperinsulinemic patients at the early phase of the disease. They had lowered fasting BG and IRI values, improved glucose tolerance, insulin response to OGTT and antipyrine metabolism after PB therapy. The SU plus M treated patients responded beneficially if they had high fasting and postglucose IRI values and were non-responders if they had relative insulin deficiency. Antipyrine metabolism improved among the responders and non-responders. The hyperglycemic patients treated with insulin showed improved glucose metabolism, an improved C-peptide response and antipyrine metabolism. The subjects could be classified into responders and non-responders by calculating the ratio of areas above the fasting level curve of insulin and glucose (sigma delta I-OGTT/sigma delta G-OGTT). These values for the former were 0.2-0.4 and the latter 0.03-0.04, as compared to healthy volunteers (1.0) and subjects with glucose intolerance (1.4). A PB type inducer improves insulin sensitivity but does not alter its production or secretion. The outcome of glucose metabolism is therefore dependent on insulin availability.
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PMID:Glucose tolerance and insulin response to glucose load before and after enzyme inducing therapy in subjects with glucose intolerance and patients with NIDDM having hyperinsulinemia or relative insulin deficiency. 269 84

We measured lumbar bone mineral density (L2-4 MBMD) in the postmenopausal elderly diabetic women and made comparisons with age-matched controls in terms of the age, body mass index (BMI) and % BMD of age-matched. In addition we evaluated the correlation between BMD and menarche age, menopause age, HbA1c, serum calcium, serum phosphate, serum alkaline phosphatase (S-Alp) and the ratio of urine calcium to urine creatinine (UCa/Cr). Moreover we divided non-insulin dependent diabetic patients (NIDDM) into two groups; the high BMD group and the low BMD group. Serum Alp and the ratio of UCa/Cr were compared in these two groups. The relationships between regimen of therapy and BMD were also analyzed in female NIDDM. There were no significant differences of BMD and background factors between controls and NIDDM. The ratio of UCa/Cr in the high BMD group were significantly less than that in low BMD group (p < 0.05). BMD in NIDDM with retinopathy was lower, but not significantly, than that in NIDDM without retinopathy. The methods of therapy for NIDDM such as diet alone, an oral hypoglycemic agent and insulin did not influence BMD in elderly postmenopausal diabetics. These results indicated that BMD in elderly postmenopausal diabetics are dependent on UCa/Cr and retinopathy.
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PMID:[Bone mineral density in postmenopausal elderly women with type 2 diabetes]. 859 32

Diabetes, known since antiquity, has been defined by glycosuria. In 1886, when Minkowski demonstrated that pancreatectomized dogs developed diabetes, the islets of Langerhans became a focus of the search for an active principle culminating in the discovery and the isolation of insulin in 1921 by Banting, Best and Collip. In 1959, the radioimmunoassay of Yalow and Berson solidified the concept of insulin resistance in non-insulin dependent diabetes (NIDDM). In 1971, the insulin receptor was defined as a cell surface protein that initiated the insulin signal transduction cascade. Today, we know that NIDDM accounts for at least 90% of all diabetes worldwide and involves approximately 100 million people. The microvascular complications of NIDDM are the same as for insulin dependent diabetes (IDDM) and are related to the intensity and duration of hyperglycaemia. Further, it is clear from the Diabetes Control and Complications Trial (DCCT) that all microvascular complications can be reduced with intensive control of the blood glucose. Macrovascular disease is also accelerated in NIDDM, including both hypertension and dyslipidemia. The major risk factor for NIDDM are age, obesity, physical inactivity, and genetic background. The earliest features seen in individuals destined to develop NIDDM is insulin resistance, but for hyperglycaemia to ensure there must be a defect in insulin secretion. Thus, insulin resistance defines the prehyperglycaemic phase of NIDDM, but varying degrees of insulin secretory deficiency define the hyperglycaemic phase. Macrovascular risk occurs throughout the lifetime of the individual, whereas microvascular risk ensues with the inception of hyperglycaemia. Tomorrow, we will understand more clearly whether lifestyle changes, such as diet and exercise, or new classes of drugs, can delay or prevent NIDDM. Clinical trials are now beginning to test whether impaired glucose tolerance (IGT) can be delayed or prevented from moving to overt NIDDM. The genetics of NIDDM are under intense study. Mutations in the insulin receptor lead to NIDDM in a small number of patients, and mutations in the glucokinase gene lead to maturity onset diabetes of the young (MODY). Work is now underway to study other candidate genes as well as work on positional cloning techniques to identify diabetes genetic loci. The hormone Leptin has just been discovered and is a major regulator of body weight. In summary, the most important new emphasis on the treatment of NIDDM is the recognition of the importance of hyperglycaemia and our ability to both treat and possibly prevent this metabolic perturbation. This joins the longer-term emphasis on cardiovascular risk reduction from both treatment and prevention of hypertension and dyslipidemia.
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PMID:Non-insulin dependent diabetes--the past, present and future. 928 27

The United Kingdom Prospective Diabetes Study (UKPDS) is the largest study ever performed in the field of diabetes. It has been carried on in more than 5000 patients with newly diagnosed type 2 diabetes and followed during almost 15 years. The main goals of the study were to investigate the effects of improving blood glucose and/or blood pressure control on diabetic complications, and to compare the advantages and inconvenients of the most important pharmacological approaches. The results of the UKPDS have been presented at the last Congress of the European Association for the Study of Diabetes (EASD) in Barcelona, September 10-11, 1998. They essentially showed that improving blood glucose or arterial blood pressure control allows to significantly reduce the incidence of complications associated to diabetes. Best results were observed in individuals in whom treatments of both hyperglycemia and hypertension were intensified. For each risk factor, no threshold has been found so that every reduction in blood glucose or arterial pressure is accompanied by a nearly linear diminution in the incidence of diabetic complications. The type of pharmacological treatment appears to have a less prominent influence, even if metformin appears to exert the most favourable effects in the group of obese patients with type 2 diabetes.
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PMID:[Lessons from the "United Kingdom Prospective Diabetes Study"]. 983 82

Current agents for the treatment of Type 2 diabetes mellitus improve the metabolic profile but do not reinstate normality. They also reduce chronic diabetic complications, but they do not eliminate them. Thus, new agents with novel actions are required to complement and extend the capabilities of existing treatments. Insulin resistance and beta-cell failure, which are crucial components in the pathogenesis of Type 2 diabetes, remain the underlying targets for new drugs. Recently introduced agents include a short-acting non-sulphonylurea insulin-releaser, repaglinide, which synchronizes insulin secretion with meal digestion in order to reduce post-prandial hyperglycaemia. The thiazolidinedione drugs, troglitazone, rosiglitazone and pioglitazone represent a new class of agonists for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma). PPARgamma increases the transcription of certain insulin-sensitive genes, thereby improving insulin sensitivity. The intestinal lipase inhibitor orlistat and the satiety-inducer sibutramine are new weight-reducing agents that may benefit glycaemic control in obese Type 2 diabetes patients. Several further new insulin-releasing agents, and agents to retard carbohydrate digestion and modify lipid metabolism stand poised to enter the market. The extent to which they will benefit glycaemic control remains to be seen. However, the prospect of permanently arresting or reversing the progressive deterioration of Type 2 diabetes continues to evade therapeutic capture.
Baillieres Best Pract Res Clin Endocrinol Metab 1999 Jul
PMID:New agents for Type 2 diabetes. 1076 69

Women suffering from type-2 diabetes mellitus (NIDDM) show a more android fat pattern than healthy females, but to date no exact determination of their fat distribution differences exists. Measurements at 15 specified body sites with an optical device, the LIPOMETER, provide a subcutaneous adipose tissue topography (SAT-Top) of the individual. SAT-Top of 20 female NIDDM patients and 122 healthy controls was measured. ROC curve analysis was applied to evaluate the discriminative power of each body site and to provide cutoff values. Then a classification tree by the CART algorithm was established, showing SAT-Top differences between the two groups. Best discriminating results were achieved by the neck site (ROC area index = 0.76, sensitivity = 61.3%, specificity = 77.8%), the four sites of the thigh (area indices from 0.71 to 0.76), and a linear combination of all body sites stemming from a previous factor analysis, which provides condensed information of the extremities SAT-Top (area index = 0.80, sensitivity = 80.4%, specificity = 64.6%). The results could be improved by a summary measure of "android fat pattern" (area index = 0.89, sensitivity = 73.6%, specificity =88.3%) and a proportional measure of SAT-distribution, the relative neck (area index = 0.84, sensitivity = 83.0%, specificity = 70.5%). Overall, 136 (95.8%) of the 142 subjects were correctly classified by the classification tree (sensitivity = 75%, specificity = 99.2%). Both methods show the expected increased upper trunk obesity and decreased lower body obesity of NIDDM women compared with healthy females. Am. J. Hum. Biol. 12:388-394, 2000. Copyright 2000 Wiley-Liss, Inc.
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PMID:ROC and CART analysis of subcutaneous adipose tissue topography (SAT-Top) in type-2 diabetic women and healthy females. 1153 29

Type 2 diabetes mellitus is not a single disease but a genetically heterogeneous group of metabolic disorders sharing glucose intolerance. The precise underlying biochemical defects are unknown and almost certainly include impairments of both insulin secretion and action. The rapidly increasing prevalence of T2D world wide makes it a major cause of morbidity and mortality. Understanding the genetic aetiology of T2D will facilitate its diagnosis, treatment and prevention. The results of linkage and association studies to date demonstrate that, as with other common diseases, multiple genes are involved in the susceptibility to T2D, each making a modest contribution to the overall risk. The completion of the draft human genome sequence and a brace of novel tools for genomic analysis promise to accelerate progress towards a more complete molecular description of T2D.
Best Pract Res Clin Endocrinol Metab 2001 Sep
PMID:The genetics of type 2 diabetes. 1155 72

Maturity-onset diabetes of the young is a heterogeneous group of autosomal dominantly inherited, young-onset beta-cell disorders. At least two consecutive generations are affected with a family member diagnosed before 25 years of age. Diabetes is caused either by mutations in the glucokinase gene (glucokinase MODY) or by mutations in transcription factors (transcription factor MODY). Glucokinase maturity-onset diabetes of the young is a mild, non-progressive hyperglycaemia caused by a resetting of the pancreatic glucose sensor. It is treated with diet, and complications are rare. Pregnancies affected by glucokinase mutations have specific management strategies and prognosis. Transcription factor maturity-onset diabetes of the young, caused by mutations in the hepatocyte nuclear factor genes HNF-1alpha, HNF-4alpha and HNF-1beta, and in insulin promoter factor-1 results in a progressive beta-cell defect with increasing treatment requirements and diabetic complications. Cystic renal disease is a prominent feature of HNF-1beta mutations. Further maturity-onset diabetes of the young genes remain to be identified. MODY is part of the differential diagnosis of diabetes presenting in the first to third decades of life. Diagnostic molecular genetic testing is available for the more common genes involved.
Best Pract Res Clin Endocrinol Metab 2001 Sep
PMID:Maturity-onset diabetes of the young: from clinical description to molecular genetic characterization. 1155 73

Diabetic nephropathy can develop in up to one-third of patients with type 1 diabetes and approximately 25% of patients with type 2 diabetes. This complication is important as it not only leads to renal failure but is associated with a high risk of coronary artery disease and other vascular complications. Although hyperglycaemia is necessary for the development of diabetic nephropathy, it is not sufficient, genetic factors also being important. This is evidenced by studies showing that only a subgroup of patients are at risk of nephropathy and that nephropathy clusters in families. The genes involved in susceptibility to diabetic nephropathy have yet to be identified. Most studies to date have been case-control in design, and there have been conflicting results. Genes suggested as having a role include those encoding angiotensin-1 converting enzyme, apolipoprotein E, heparan sulphate and aldose reductase. In order to clarify the role of these and other candidate genes in nephropathy, association studies in families are necessary. Because of the large number required, this will require international collaboration. A genetic marker for nephropathy would enable the earlier detection of this complication, thus facilitating screening and targeted intervention. An understanding of the role of susceptibility genes will ultimately allow the development of novel therapeutic strategies.
Best Pract Res Clin Endocrinol Metab 2001 Sep
PMID:Genetics of diabetic nephropathy. 1155 75


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