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 order to determine the involvement of denervation in endothelium-independent, nitric oxide (NO)-dependent smooth muscle vasodilation, we have measured vascular endothelial and smooth muscle function in three groups of age- and sex-matched patients: 8 patients with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) with neuropathy; 7 NIDDM patients without neuropathy; and 10 non-diabetic control subjects. Laser Doppler probes were used to measure blood flow in the dorsum of the left foot. Vascular endothelial response was assessed by measuring vasodilatory responses to iontophoretic application of acetylcholine to the dorsum of the foot. Vascular smooth muscle activity was assessed by the response to iontophoresis of sodium nitroprusside (SNP)-a NO donor and direct vasodilator. The vasodilator response to acetylcholine, expressed as the ratio of peak to basal blood flow, was significantly reduced in both diabetic groups when compared to non-diabetic controls (geometric mean x/divided by anti-logged SD 9.81 x/divided by 1.65 versus patients with neuropathy 3.50 x/divided by 2.03, p < 0.005 and diabetic non-neuropathic subjects 3.49 x/divided by 1.67, p < 0.005). The difference between the two groups of diabetic patients was not significant. In contrast, the vasodilatation to nitroprusside was significantly reduced only in the diabetic neuropathic patients, significantly lower than in either the non-neuropathic diabetic controls or the non-diabetic controls (2.1 x/divided by 2.0 versus 6.42 x/divided by 1.56 and 7.02 x/divided by 2.05, p < 0.005). This indicates that neuropathy is important in abnormalities of endothelium-independent vasodilatation.
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PMID:NO-dependent smooth muscle vasodilatation is reduced in NIDDM patients with peripheral sensory neuropathy. 911 81

The cytokine tumor necrosis factor alpha (TNF alpha) was proposed to mediate obesity related insulin resistance upon production in fat cells and to participate in tissue remodelling leading to vascular complications upon being released by macrophages. To assess its putative role in diabetes we determined plasma levels of TNF alpha in 105 adult humans. Male nondiabetic subjects had significantly lower TNF alpha levels than female controls (4.4 +/- 0.3, n = 17 vs. 6.6 +/- 1.0 pg/ml, n = 13; p = 0.049). Men with NIDDM had elevated TNF alpha (6.7 +/- 0.6 pg/ml, n = 34) compared to nondiabetic subjects (4.4 +/- 0.3 pg/ml, n = 17; p = 0.012). Such a difference was not apparent in women. Levels of TNF alpha were correlated with serum triglyceride levels in male controls (r2 = 0.64; p = 0.007) but not in NIDDM. Neither body mass index nor glycosylated hemoglobin correlated with TNF alpha in any of the groups. The presence of retinopathy (p = 0.046) but not of neuropathy or nephropathy or macroangiopathy was associated with significantly elevated plasma TNF alpha. We conclude that plasma levels of TNF alpha are sex-dependent and that increased TNF alpha occurs in male but not female NIDDM and may participate in the development of diabetic complications.
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PMID:Circulating tumor necrosis factor alpha is elevated in male but not in female patients with type II diabetes mellitus. 913 80

The role cardiac autonomic neuropathy (CAN) plays in diabetes is not well known. The aim of this study was to identify the factors involved in CAN in diabetic patients. One hundred patients, 44 insulin-dependent (IDDM) and 56 non-insulin-dependent (NIDDM), were investigated, using five standard tests. Three of these tests were for parasympathetic control (cardiac response to the lying-to-standing, deep breathing, and Valsalva tests), and the other two measured sympathetic control (testing for orthostatic hypotension and evaluating heart and blood pressure response to the handgrip test). Results were compared to those found in a series of 40 healthy volunteers. An age-adjusted comparison with the controls, showed that 34 patients had one abnormal parasympathetic test, 23 had two, and 6 patients had three. Cardiac parasympathetic neuropathy was thus present in 63% of the patients. The handgrip test was completed by 84 diabetic patients. There was evidence of orthostatic hypotension and/or an abnormal cardiac response to the handgrip in 15 of these patients, who all had a parasympathetic abnormality as well. There was no significant association between the type of diabetes and the presence of CAN. The duration of diabetes was significantly longer in patients with CAN (9.3 +/- 0.9 years) (p < 0.01) than in those with all three parasympathetic tests normal (5.8 +/- 0.9 years) (p < 0.01). The HbA1c level was also higher in patients with CAN than in those with three normal parasympathetic tests (9.95 +/- 0.35% versus 8.17 +/- 0.42%, p < 0.005). There was a significant association between the presence of retinopathy, observed by angiofluorography, and the presence of peripheral neuropathy confirmed by the electrophysiological investigation and the presence of CAN (p < 0.001). However, more than half the patients without retinopathy or nephropathy had CAN, and 11 of the 31 patients with a normal electrophysiological investigation also had CAN. Eighteen patients (6 IDDM) without retinopathy and nephropathy, who had been diabetic for less than 2 years, also had CAN. This study shows that CAN occurs early and is frequently found in a population of unselected diabetic patients. Metabolic factors may play an important role in its occurrence. CAN is significantly associated with the presence of retinopathy, which suggests that an impairment of autonomic peripheral blood flow control might be a contributing factor in the formation of microvascular lesions.
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PMID:Factors involved in cardiac autonomic neuropathy in diabetic patients. 917

This study examined the association between limited joint mobility (LJM) and diabetic control, atherosclerotic vascular disease and other diabetic complications in non-insulin-dependent diabetic (NIDDM) patients. LJM was studied in 139 [age (mean +/- SD) 61.3 +/- 12.3 years] NIDDM patients. Limitation of several joints was examined with a goniometer and LJM was classified by the Rosenbloom method. The NIDDM patients were examined for the following diseases: history of myocardial infarction, coronary heart, cerebrovascular and peripheral vascular diseases. The diabetic complications, background and proliferative retinopathy, nephropathy, and neuropathy, were also assessed. The metabolic control of the diabetes was evaluated by the average glycosylated hemoglobin Alc (GHbA kappa) concentration and lipid values were also measured. Mean levels of GHbAlc were 8.9 vs. 8.2% (p < 0.05) in NIDDM patients with and without LJM. NIDDM patients with LJM had a 3.1- (95% confidence interval, 1.2-7.7) and a 4.0-fold risk (95% confidence interval, 1.2-13.0) for coronary heart and cerebrovascular disease respectively, when the confounding effects of age, duration of diabetes and control of diabetes were controlled using stepwise logistic regression analysis. Patients with LJM had a 9.3- (95% confidence interval, 1.1-79.0) and a 3.3-fold risk (95% confidence interval, 1.0-10.5) of proliferative retinopathy and nephropathy respectively, when the confounding effects of age and duration of diabetes were controlled, but the correlation disappeared when control of diabetes was included in the model. In conclusion, the presence of LJM is associated with the control of diabetes and with the presence of coronary heart and cerebrovascular diseases in NIDDM patients.
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PMID:Limited joint mobility in non-insulin-dependent diabetic (NIDDM) patients: correlation to control of diabetes, atherosclerotic vascular disease, and other diabetic complications. 920 97

The presence of autoantibodies to autonomic nervous tissue structures is a feature of patients with symptomatic diabetic autonomic neuropathy. It has not been established whether these autoantibodies cause, contribute to or simply reflect nervous tissue damage. Serum samples were tested for the presence of complement-fixing autoantibodies to adrenal medulla, vagus nerve, and sympathetic ganglion cells, to demonstrate: (a) reproducibility of the technique, (b) persistence of the antibodies, and (c) whether or not they occur in patients with non-insulin-dependent (Type 2) diabetes (NIDDM) with neuropathy. Examination of 37 samples, by different observers 2 years apart, revealed a high degree of concordance of both positive and negative results, demonstrating the method of testing to be highly reproducible. Re-testing of 37 patients (by analysing a second blood sample) between 0.5 and 2.7 years (mean 1.7 years) after their first test also demonstrated that antibodies, once present, normally persist; and that most patients initially negative remained so. Of 17 neuropathic NIDDM patients, 16 were negative for all three antibodies, indicating their rarity in this group of patients.
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PMID:Reproducibility and persistence of neural and adrenal autoantibodies in diabetic autonomic neuropathy. 921 11

Diabetes mellitus associated with mitochondrial tRNA mutation at position 3243(DM-Mt3243) is a new disease. Patients have a distinctly different picture from MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). During observations at the Saiseikai Central Hospital, the following findings were noted in DM-Mt3243 patients: DM-Mt3243 patients are diagnosed earlier with diabetes, compared to NIDDM (non-insulin dependent diabetes mellitus) controls without family history. DM-Mt3243 patients often need insulin more often than NIDDM controls without family history. Post-treatment neuropathy and insulin edema are often found in DM-Mt3243, and the two phenomena possibly have a similar pathophysiology related to mitochondrial dysfunction. Ambiguous psychiatric disorders of functional psychosis are observed frequently in DM-Mt3243. Mild headache is common in DM-Mt3243 cases. Ambiguous neuromuscular abnormalities such as sleep disturbance, paresthesia of the legs, edema of the legs, and palpitation may be symptoms associated with mitochondrial dysfunction in DM-Mt3243. Coenzyme Q may be effective in the relief of these neuromuscular symptoms.
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PMID:Diabetes mellitus associated with 3243 mitochondrial tRNA(Leu(UUR)) mutation: clinical features and coenzyme Q10 treatment. 926 20

Quantitative morphological data are presented from a series of studies assessing both nerve fiber and capillary pathology in 30 diabetic patients with varying stages and symptoms of neuropathy. There is a significant relationship between clinical measures of neuropathic severity and myelinated fiber loss. However, unmyelinated fibers continue to regenerate even in patients with established neuropathy. Microvascular abnormalities, particularly basement membrane thickening and endothelial cell hyperplasia, are an early feature of diabetic microangiopathy and relate to neuropathic severity. There are no neurophysiological or morphological differences between patients with type 1 and type 2 diabetes nor between diabetic patients with and without painful neuropathy.
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PMID:The pathology of human diabetic neuropathy. 928 99

We investigated the results of urine culture between the mid-urine and the bladder puncture urine in 30 cases of diabetes millitus. The results showed that female elderly NIDDM and the patients with diabetic retionopathy, nephropathy and neuropathy had higher incidence of urinary infections. When the leukocyte count in routine urine examination was more than 10 increases/HP, the incidence of urinary infection was higher. The urine culture with bladder puncture was more reliable than midurine. In addition, the nuring care for prevention of the urinary infection in diabetes was dicussed.
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PMID:[Urinary tract infections in patients with diabetes mellitus and related factors]. 930 32

Although the detailed pathogenesis of diabetic polyneuropathy is not known, several mechanisms appear to be involved and may occur sequentially. Hence, the early and much researched activation of the polyol-pathway appears to secondarily affect nonenzymatic glycation, perturbation of vasoactive substances, the immune system and neurotrophism. These metabolic abnormalities may be differentially expressed in the neuropathy occurring in insulin dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM) diabetes. This notion is supported by differences in the structural abnormalities of the neuropathies in the two types of diabetes. Distinct and characteristic nodal changes occur in IDDM but not in NIDDM neuropathy, which also shows a milder axonal atrophy. On the other hand, nerve fiber loss which characterizes diabetic neuropathy tends to be focal in the older NIDDM patients, suggesting a more prominent vascular genesis. A further characteristic feature of diabetic neuropathy is blunted fiber regeneration, which probably is consequent to impairments of the necessary immune response and local synthesis of neurotrophic factors. Nerve biopsies from diabetic patients, although not necessary for diagnosis, provide valuable tissue for biochemical and molecular analysis of underlying mechanisms, the detailed elucidation of which will facilitate the design of targeted therapies.
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PMID:Neuropathology of diabetic neuropathy and its correlations with neurophysiology. 935 80

Since 1990 in most Eastern European countries health care systems have been decentralized or are undergoing the processes of decentralization. Increasingly, diabetic patients are no longer treated by diabetologists but by non-specialized physicians. During the same period structured treatment and teaching programmes have been introduced and health care is increasingly influenced by the St. Vincent declaration. To show the effect of these changes on the quality of diabetes care 90% (n = 244) of all insulin-treated diabetic patients aged 16 to 60 years and living in the city of Jena (100247 inhabitants) were studied in 1994/1995. The results were compared with the baseline examination of 1989/1990 (n = 190). HbA1c (HbA1c/mean normal) in IDDM patients under specialized care was similar in 1994/1995 (1.54 +/- 0.27, n = 47) to 1989/1990 (1.52 +/- 0.31, n = 131, p = 0.0018), but higher under non-specialized care (1.71 +/- 0.38, n = 80, p = 0.0087). In the total group of NIDDM patients there was no significant change in HbA1c (1994/1995: 1.75 +/- 0.4, n = 117, vs 1989/1990: 1.78 +/- 0.4, n = 59, p = 0.67), but with a tendency to higher HbA1c under non-specialized (1.81 +/- 0.4, n = 79) compared to specialized care (1.66 +/- 0.39, n = 38, p = 0.06). Incidence of severe hypoglycaemia (IDDM 0.13; NIDDM 0.04), ketoacidosis (0.02; 0.01) and the prevalence of nephropathy (21%; 35%) and neuropathy (24%; 38%) remained unchanged in comparison to 1989/1990, whereas there was an increase in the prevalence of diabetic retinopathy. Specialized care is mandatory for patients with IDDM.
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PMID:The JEVIN trial: a population-based survey on the quality of diabetes care in Germany: 1994/1995 compared to 1989/1990. 938 29


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