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

In NIDDM, first-phase insulin release to glucose is (almost) absent. However, in contrast to older studies which suggested that in NIDDM the B-cell is "blind" for glucose, recent evidence indicates that the B-cell is not insensitive for glucose as far as second phase release is concerned. This suggests that the metabolism of glucose is probably not deranged in NIDDM, since glucose leads to insulin release after it has been metabolized. Hyperglycaemia itself has a deleterious effect on insulin release, so-called glucose toxicity. Various mechanisms have been proposed, whereby hyperglycaemia may diminish insulin release: inhibition of Ca2+ mobilization from the endoplasmic reticulum by glucose-6-phosphate, Ca2+ uptake in the ER by glucose and inhibitory effects of protein kinase C. Whatever may prove to be the underlying mechanism(s), glucose toxicity is unlikely to be the only cause of insulin secretory disturbances in NIDDM, since the glucose level would have to be elevated before it could be toxic. Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by both defects in insulin action and insulin secretion. With regard to the defects in insulin release, much research has originated from two (partly) opposing hypotheses, namely the presence of pancreatic B-cell glucose blindness and the hypothesis of pancreatic B-cell glucose toxicity in NIDDM.
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PMID:Defects in insulin secretion in NIDDM: B-cell glucose insensitivity or glucose toxicity? 844 21

On the whole, diabetic microangiopathy can be understood as the clinical renal-retinal syndrome. About 10% of all diabetics die of end-stage renal failure, more frequent in IDDM. With an incidence of 14% diabetic retinopathy is one of the major causes of blindness in adulthood. In the non-proliferative state, the pathological changes are limited to the retina, whereas the alterations affect both retina and vitreous in the proliferative state. Photocoagulation is the treatment of choice. If photocoagulatory treatment is not possible because of cataract, vitreous surgery (pars-plana vitrectomy) could improve visual prognosis. The clinical features hypertension, proteinuria and finally renal failure define the term "diabetic nephropathy". The increased intraglomerular pressure is the main pathological alteration of incipient nephropathy. Microalbuminuria essentially determines the prognosis: in IDDM it concerns the incidence of a manifest nephropathy, in NIDDM the excessively increased incidence of cardiovascular mortality. Sonographically, the kidneys are large with bright and wide parenchyma. Along with the development of end-stage renal disease the kidney size diminishes. According to Mogensen, nephropathy is divided into five stages: Stage 1, the early stage, is defined by hypertrophy and hyperfiltration. Stage 2 shows incipient structural changes without any clinical findings. Stage 3 is characterised by persistent microalbuminuria. Stage 4 leads to increasing renal failure and stage 5 to end-stage renal disease and the necessity of dialysis treatment. Incipient nephropathy demands a strict treatment of both hypertension and diabetes. In the meantime, ACE inhibitors are the treatment of choice. In case of dialysis treatment continuous ambulant peritoneal dialysis (CAPD) is usually preferred.
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PMID:[Diabetic microangiopathy]. 847 38

Before the 1980s, only limited community-based data were available on the prevalence of diabetes in Japan. The prevalence of diabetes in subjects older than 40 years was 2-5%. In many surveys carried out in the 1990s, all subjects were examined using the 75 g glucose tolerance test and diabetes was diagnosed according to the WHO criteria. Diabetes was found in about 10% of the population older than 40 years. A higher prevalence in Japanese immigrants in the United States suggests that change of environmental factors, such as increased intake of animal fat, might further increase the prevalence of diabetes in Japan in the future. The mean BMI of NIDDM patients at their initial visit to our hospital is 22.9 + 3.4 kg m-2, compared to patients in many other developed countries and diabetic Japanese Americans. Regarding causes of death in Japanese diabetic patients, the most frequent causes were vascular diseases including renal failure 11.2%, ischaemic heart diseases 14.6%, and cerebrovascular diseases 13.5%, thus atherosclerotic diseases were less frequent compared to the data in the United States. Each year, approximately 6000 diabetic patients start haemodialysis, and diabetic retinopathy is the main cause of acquired blindness in Japan.
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PMID:Non-insulin-dependent diabetes mellitus (NIDDM) in Japan. 889 73

To study the progression of diabetic retinography in relation to diabetes treatment and glycaemic control in patients with non-insulin dependent (Type 2) diabetes mellitus (NIDDM), we performed a prospective study in a cohort of 1378 diabetic patients, aged > or = 40 years at diagnosis, of whom 333 were treated with insulin, and 1045 with oral antihyperglycaemic agents or diet alone. In the latter group 174 patients changed to insulin therapy during follow-up. We used the Wisconsin scale to grade retinopathy, recorded blindness (visual acuity < or = 0.1) and visual impairment (visual acuity 0.2-0.4), and measured the average HbA1c for each patient during a mean 3.1 year study period. In a multivariate analysis, patients who changed treatment from oral agents or diet alone to insulin therapy had a relative risk of 2.0 (95% confidence interval 1.7-2.3) for progression of retinopathy > or = 3 levels compared with all other patients in the study. The increase in risk remained even after controlling for mean HbA1c (relative risk 1.6; 95% confidence interval 1.3-1.9). Progression > or = 3 levels was significantly associated with a higher incidence of macular oedema and deterioration of visual acuity (p < 0.001). The relative risk for blindness/visual impairment due to retinopathy was 2.7 (95% confidence interval 1.8-4.0) in the group with changed treatment compared with all the other patients in the study. Poor glycaemic control (Hba1c%) before the start of insulin therapy and any retinopathy at baseline were significant risk factors for progression in the group with changed treatment (both p < 0.01). In the whole study group, poor glycaemic control was significantly associated with retinopathy progression > or = 3 levels; the relative risk for those having mean HbA1c above the median being 1.7 (95% confidence interval 1.4-2.1), compared to those with a HbA1c value below the median. Moderate non-proliferative diabetic retinopathy at baseline was also associated with progression (relative risk 2.5; 95% confidence interval 1.4-4.5). In contrast, insulin treatment at baseline was not associated with an increased risk of retinopathy progression. In conclusion, while hyperglycaemia was a risk factor for the progression of retinopathy in all patients, change of treatment from oral drugs to insulin was associated with a 100% increased risk of retinopathy progression and a 3-fold increased risk of blindness/visual impairment.
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PMID:The effect of glycaemic control and the introduction of insulin therapy on retinopathy in non-insulin-dependent diabetes mellitus. 927 3

Blind diabetic patients face particular difficulties in blood glucose self monitoring (BGSM). We investigated the quality of BGSM in blind and severely visually impaired diabetic patients and assessed the effects of training in BGSM using a blood glucose meter with voice edition of values and a modified test strip holder for easier placement of blood samples on the strip (One Touch II talk (OT II)). Twenty-six insulin-treated diabetic patients (23 IDDM and 3 NIDDM) participated. At baseline the quality of BGSM was checked in 14 patients who already regularly performed BGSM without external help. Thereafter all 26 patients received an extensive instruction in BGSM for blind patients. At re-examination, after a mean period of 41 days, the quality of BGSM performed by the patients without assistance was checked in three different blood samples. Blood glucose was measured in the same sample by a routine laboratory method. At baseline the mean absolute difference between BGSM and the reference method was -0.3 mmol l(-1) (range; +/- SD) (-7.7-4.8; +/- 2.6 mmol l(-1)); 74% of BGSM measurements deviated by more than 10% from the reference values and 43% by more than 20%. At follow-up all 26 patients reported daily BGSM without external help. The mean absolute difference between BGSM and the reference method was -0.1 (-2.7-2.8; +/- 0.9 mmol l(-1)); 25% of BGSM measurements deviated by more than 10 % from the laboratory reference values and 5% by more than 20%. The results of this study suggest that a substantial number of blind diabetic patients do not perform BGSM on their own at all and in those who do the reliability of the results is poor. However, after extensive instruction, the majority of blind diabetic patients should be able to perform BGSM and to obtain reliable results.
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PMID:Self monitoring of blood glucose in blind diabetic patients. 927 99

Treatment of diabetic complications consumes health care resources. Intensive therapy was shown by the Diabetes Control and Complications Trial (DCCT) to avert complications. Economic analyses and models have been used to evaluate the cost-effectiveness of intensive therapy for people with type 1 and type 2 diabetes. An economic analysis of the DCCT estimated the cost of intensive therapy to be two to three times greater than that of conventional therapy. In contrast, an economic model predicts that intensive therapy, as compared with conventional therapy, could reduce blindness from 34 to 20% or by 41%, end-stage renal disease from 24 to 7% or by 71%, and lower-extremity amputations from 7 to 4% or by 43%. Although intensive therapy is more expensive, when the costs of complications are factored in, it becomes cost-effective for treatment of type 1 diabetes. Similarly, a model to evaluate the cost-effectiveness of intensive therapy for people with type 2 diabetes found that the lifetime costs of general and diabetes-related medical care would be approximately two times greater. However, the reduction in lifetime costs of complications, which would produce substantial reductions in costs of treatment, largely offsets the difference. Intensive therapy for type 1 and type 2 diabetes may be more expensive than conventional therapy, but from an economic perspective, it is comparable in cost to pharmacological therapies for people with hypertension and hypercholesterolemia. From a health system viewpoint, intensive therapy represents a fruitful long-term financial investment.
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PMID:The effects of treatment on the direct costs of diabetes. 985 Apr 82

Diabetic retinopathy is still the most common cause of blindness among people under 65 years of age in the Western world. Early detection of sight-threatening retinopathy is vital, as in many cases it can be treated successfully with photocoagulation. Accordingly, screening programmes using fundus photography have been introduced in many countries, and in Sweden repeat examination at two-year intervals has been recommended. Since up to 30 per cent of patients with type 2 diabetes (according to the previous criteria) have been shown to manifest diabetic retinopathy at diabetes diagnosis, an initial ophthalmological examination at diagnosis is recommended. The new diagnostic criteria for diabetes, according to which patients with fasting blood glucose levels of 6.1 (6.6 mmol/L are also classed as diabetic, will increase the number of diabetic patients. Until such information becomes available as to the prevalence of sight-threatening retinopathy at diabetes diagnosis in that subgroup, it is suggested that type 2 diabetes patients should continue to undergo retinal examination at diabetes diagnosis.
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PMID:[Eye complications in diabetes. According to new criteria patients with diabetes should have ophthalmological examination at the time of diagnosis]. 986 4

Diabetic retinopathy remains the leading cause of visual disability and blindness among professionally active adults in economically developed societies, which is of particular concern because the prevalence and incidence of Type 2 diabetes mellitus is expected to increase sharply during the next decade. Retinopathy is fundamentally similar in Type 1 and Type 2 diabetes mellitus, and it is widely accepted that if detected and treated early, loss of vision and blindness from diabetic retinopathy may be prevented. Studies such as the Diabetes Control and Complications Trial (DCCT), the United Kingdom Prospective Diabetes Study Group (UKPDS), the Diabetic Retinopathy Study (DRS) and the Early Treatment Diabetic Retinopathy Study (ETDRS) have established accepted guidelines for the management of diabetic retinopathy. Good metabolic control is particularly important in the early phases of the disease, and will delay the onset of retinopathy and decrease the rate of progression. When advanced stages of retinopathy are reached, laser photocoagulation is effective in decreasing the development to blindness by over 50%. However, preventable blindness still occurs despite the tight control of blood glucose levels and the use of retinal photocoagulation. To reduce the risk of visual impairment and blindness caused by diabetes, diabetic patients must be taught how to control their blood glucose levels, regular eye examinations must be carried out and the conditions for timely laser photocoagulation must be created. The implementation of screening and treatment programmes for visual impairment in diabetes has proved to be worthwhile in terms of costs and health benefits.
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PMID:Lowering the risk of visual impairment and blindness. 986 92

The objective of this study was to assess the role of free fatty acids (FFAs) as insulin secretagogues in patients with type 2 diabetes. To this end, basal insulin secretion rates (ISR) in response to acute increases in plasma FFAs were evaluated in patients with type 2 diabetes and in age- and weight-matched nondiabetic control subjects during 1) intravenous infusion of lipid plus heparin (L/H), which stimulated intravascular lipolysis, and 2) the FFA rebound, which followed lowering of plasma FFAs with nicotinic acid (NA) and was a consequence of increased lipolysis from the subject's own adipose tissue. At comparable euglycemia, diabetic patients had similar ISR but higher plasma beta-hydroxybutyrate (beta-OHB) levels during L/H infusion and higher plasma FFA and beta-OHB levels during the FFA rebound than nondiabetic control subjects. Correlating ISR with plasma FFA plus beta-OHB levels showed that in response to the same changes in FFA plus beta-OHB levels, diabetic patients secreted approximately 30% less insulin than nondiabetic control subjects. In addition, twice as much insulin was secreted during L/H infusion as during the FFA rebound in response to the same FFA/beta-OHB stimulation by both diabetic patients and control subjects. Glycerol, which was present in the infused lipid (272 mmol/l) did not affect ISR. We concluded that 1) assessment of FFA effects on ISR requires consideration of effects on ISR by ketone bodies; 2) ISR responses to FFA/beta-OHB were defective in patients with type 2 diabetes (partial beta-cell lipid blindness), but this defect was compensated by elevated plasma levels of FFAs and ketone bodies; and 3) approximately two times more insulin was released per unit change in plasma FFA plus beta-OHB during L/H infusion than during the FFA rebound after NA. The reason for this remains to be explored.
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PMID:Effects of fatty acids and ketone bodies on basal insulin secretion in type 2 diabetes. 1007 59

Diabetes mellitus is one of the most common chronic diseases in the developed countries and is a major cause of blindness, renal failure or amputations, all of which require expensive health-care resources. Diabetes is also associated with the increased risk of cardiovascular and cerebrovascular diseases and a substantial reduction in life expectancy. Therefore, prevention of diabetes is desirable. Recently, epidemiological studies have provided a basis of understanding the environmental determinants of diabetes and several prospective studies have shown that in the aggregate, intensive therapy improves health-care status by improving not only microvascular disease but also macrovascular disease in both type 1 and type 2 diabetes.
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PMID:[Prevention of diabetes mellitus]. 1019 48


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