Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here findings in a 51-year-old Japanese man with non-insulin-dependent diabetes mellitus who complained of exercise-induced cramps. Muscle biopsy showed scattered regenerating fibers, small angular fibers and increased PAS positive particles. Electron microscopic examination revealed an abnormal accumulation of glycogen particles in subsarcolenmmal areas and between myofibrils while chemical studies showed an increased glycogen concentration and decreased phosphoglycerate mutase (PGAM), 46.9% of the normal mean value. Thus, partial PGAM deficiency, insulin resistance and mild diabetic sensory-motor polyneuropathy can induce severe cramps.
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PMID:Partial deficiency of phosphoglycerate mutase with diabetic polyneuropathy: the first Japanese patient. 893 90

An implantable venous access system provides a reliable and painless entry site for intravenous treatment. This study reports the authors' experience with such a system in adult patients with cystic fibrosis. Sixty five (87%) of 75 PAS Ports were placed successfully in 57 patients with cystic fibrosis. Because of early difficulties in advancing the catheter in patients whose veins had been traumatized by repeated courses of intravenous antibiotics, a technique was developed whereby venous entry was gained by direct subclavian puncture. This catheter insertion method was used in 53 (82%) attempts and the catheter was then passed by subcutaneous tunnelling to the port site on the ventral aspect of the upper arm. Fifty seven (88%) insertions were successful under local anaesthetic. The major early and late complications were iatrogenic pneumothorax (six cases) and infection (five cases), respectively. Late complications were more common when there was coexisting disease, e.g. diabetes mellitus, or an acute severe respiratory exacerbation, or when the Port was used for parenteral feeding. In conclusion, the PAS Port can be inserted safely by direct subclavian puncture. It was well tolerated and universally liked by the patients.
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PMID:Five years' experience of PAS Port intravenous access system in adult cystic fibrosis. 970 40

We studied the clinical characteristics, treatment and prognosis of multidrug-resistant pulmonary tuberculosis patients retrospectively. In this study, multidrug-resistant is defined as both resistant to 0.1 microgram/ml of INH and 50 micrograms/ml of RFP at least. From 1990 to 1997, out of 1841 culture positive pulmonary tuberculosis patients, 76 patients (4%) proved to be multidrug-resistant (53 males, 23 females, age 18-84, 40 originally treated cases and 36 relapse cases). Most of cases revealed resistance to other drugs in addition to INH and RFP. The combination of anti-tuberculous drugs were complicated and changed repeatedly. The incidences of administration of drugs were as follows; TH 62%, EB 58%, PZA 58%, KM 33%, PAS 33%, SM 29%, CS 20%, EVM 14%, CPM 3%. New quinolones, for example OFLX/LVFX, CPFX and SPFX, were also used frequently (62%). Eight percent of patients were operated. Bacteriologically effective drugs that meant culture negative were TH (14%), PZA (12%), KM (12%), EB (12%), SM (5%), new quinolones (16%). 67% of originally treated cases and 43% of relapse cases became culture negative. Many cases were treated for a long period. 19% of originally treated cases and 33% of relapse cases were treated more than three years. 11% of patients were died of tuberculosis. Major prognostic factors were diabetes mellitus (17%), malignancies (10%), non-adherence (9%) and other complications. Because of no absolutely effective treatment, we have to choose a treatment according to each patient. Development of new treatment is crucial.
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PMID:[Multidrug-resistant tuberculosis. 4. Treatment and prognosis of multidrug-resistant tuberculosis]. 986 30

The substitution of guanine for adenine at position 3243 of the leucine tRNA gene of mitochondrial DNA was originally described in association with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes). Diabetes mellitus associated with the mutation (mitochondrial diabetes) is a different phenotype from MELAS. We identified 11 patients with the mutation among 385 Japanese diabetic patients: two had MELAS and nine had mitochondrial diabetes. We present data on a male patient with mitochondrial diabetes who developed the nephrotic syndrome at the age of 23. Light microscopy revealed mesangial expansion, PAS-positive deposits and segmental sclerosis in the glomeruli. Scattered mesangial electron-dense deposits and thickening of the basement membrane were found on electron microscopy, suggesting that diabetic glomerulosclerosis accompanied by focal glomerulosclerosis (FGS). Mitochondrial diabetes may pre-dispose patients to renal complications, including forms of glomerulonephritis, such as FGS.
Diabetes Res Clin Pract 1999 Jun
PMID:Renal complications in patients with diabetes mellitus associated with an A to G mutation of mitochondrial DNA at the 3243 position of leucine tRNA. 1046 41

French national health insurance has carried out two nationwide surveys as part of its programme intended to improve the care given to patients with hypertension, focusing on affiliates diagnosed with severe hypertension entitled to exemption from co-payments (patients are reimbursed 100 per cent for all care related to the corresponding disorder). The objective was to measure the difference between observed care and the quality of care delineated in the guidelines (1997) elaborated by the National Agency for Healthcare Accreditation and Evaluation (ANAES). The before and after comparison was designed to determine whether actual care is in accordance with the guideline's standards. The initial survey took place from 31 May to 12 November 1999 over the entire French territory (metropolitan and overseas departments) and concerned a representative sample of patients whose ages ranged from 20 to 80 years at the time they qualified for exemption from co-payments for severe hypertension. The method used for comparison involved the calculation of a number of different evaluation parameters, the principal one being blood pressure control, using the systolic (PAS) and diastolic (PAD) pressures reported by attending physicians. Other evaluation parameters included the quality of the therapeutic strategy utilized. A total of 10,665 patients were enrolled in the survey by using information gathered from 8377 practicing physicians. Extrapolated to the entire population in 1999, the results can be applied to 50,383 patients. The average age was 63 years and the patients had been treated for hypertension for an average of 9 years. In addition to severe hypertension, 64 per cent of the patients had other significant high-risk factors for cardiovascular disease: 44 per cent had dyslipidemia, 28 per cent had diabetes mellitus, 15 per cent were smokers. In 41 per cent of cases, the patients' blood pressures were well controlled (systolic and diastolic pressures below 140/90 mmHg or, for patients older than 60 years with only isolated systolic hypertension, systolic pressure equal to or lower than 160 mmHg); in 12 per cent of cases the patients' blood pressures were equal to the limit values; in 47 per cent of cases blood pressure was poorly controlled. Diabetics had poorly controlled blood pressure in 85 per cent of cases (systolic or diastolic pressures greater than 130/85 mmHg) and, similarly, 94 per cent of the patients who were in renal failure were poorly controlled (systolic or diastolic pressures greater than 125/75 mmHg). Preferential prescription with a particular therapeutic class, because of an existing comorbidity, was found in 68 per cent of patients whereas potentially contraindicated therapeutic classes were prescribed in 27 per cent. The daily cost of anti-hypertensive drug therapy was estimated at 8.05 francs per day per patient. Extrapolated to the study population in 1999, this represents 148.1 million francs. Less than 1 per cent of this observed cost (1.1 million francs) was economized by prescribing less expensive, alternative drug specialties in spite of the fact that an estimated 9.6 million francs could have been saved if these equivalent, alternative drugs had been prescribed. The potential saving corresponds to 6.5 per cent of the total observed cost. The care given to severely hypertensive patients is sub-optimum when compared with the ANAES guidelines (1997). In public health terms, the most preoccupying feature is poor blood pressure control because it occurs in a patient population with a high cardiovascular risk. These findings fully justify the continuation and amplification of the actions undertaken in this nationwide public health programme concerning the medical care given to hypertensive patients.
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PMID:[Treatment of severe arterial hypertension: cost of drug prescriptions in accordance with ANAES guidelines]. 1147 61

A case of Pulmonary Alveolar Proteinosis (PAP), in association with tuberculosis, is described in a 35-year-old diabetic patient. Lung biopsy showed an intra-alveolar accumulation of PAS-positive material, and multifocal granulomas compatible with tuberculosis. The bronchoalveolar culture was positive for Mycobacterium tuberculosis. PAP results from an imbalance of the mechanisms that regulate the homeostasis of the surfactant, where specific proteins are involved, especially SP-A and SP-D, the cytokines, IL-10 and GM-CSF, in addition to alveolar macrophages and type-II pneumocytes. Chemotaxis and phagocytic capacity are reduced. PAP and diabetes share several immunological disfunctions that may increase the risk for tuberculosis. Although there are no controlled studies, the diagnosis of PAP in diabetic patients with tuberculosis must be considered.
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PMID:Pulmonary alveolar proteinosis and tuberculosis in a diabetic patient: a rare or a seldom diagnosed association? 1220 86

This study was conducted to investigate the effect of Omega-3 PUFA on streptozotocin (STZ)-induced diabetic cardiomyopathy in wistar rats. After 4 weeks of STZ (60 mg/kg, i.v.) administration, the diabetic animals were randomly divided into two groups: Diabetic control and Omega-3 PUFA treated diabetic rats. Omega-3 PUFA (0.5 ml/kg) was administered to the latter group for 10 weeks. Age matched normal rats served as Normal controls. During the study, plasma glucose, glycosylated hemoglobin, plasma cholesterol, LDL and HDL cholesterol, triglyerides were evaluated in all the groups. Omega-3 PUFA treatment did not normalise but instead blunted the effect of diabetes with regards to the above parameters significantly (P<0.01). At the end of the experiment, morphometric and histochemical studies were performed on heart and myocardial enzyme markers were studied. In the diabetic control group, diabetic cardiomyopathy was characerised by elevated CPK (DC 110+/-8.85 vs. NC 39+/-5.83) and morphological changes in heart. Gravimetric ratios showed increased heart-to-body weight ratio in diabetic control over normal control group. (DC 3.38+/-0.05 vs. NC 2.48+/-0.03). Histochemical evidence showed increased accumulation of PAS-positive material in myocardial interstitium (++++). The Omega-3 PUFA treatment blunted all these adverse effects of diabetes on heart significantly (P<0.001). However, further studies are warranted to elucidate the mechanism by which Omega-3 PUFA decreases the accumulation of PAS-positive material in diabetic myocardium.
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PMID:Omega-3 polyunsaturated fatty acids inhibit the accumulation of PAS-positive material in the myocardium of STZ-diabetic wistar rats. 1271 97

Hyperglycaemia reduces proliferation of bovine aortic endothelial cells in vitro. A similar effect in vivo may contribute to long-term complications of diabetes such as impaired wound-healing and retinopathy. We report the effect of increased glucose concentrations, glycated basic fibroblast growth factor (FGF-2) and bovine serum albumin-derived advanced glycation endproducts (BSA-AGE) on the proliferation of bovine aortic endothelial cells. Glucose (30 and 50 mmol/l) had an antiproliferative effect on endothelial cells. This effect may be mediated through reduced mitogenic activity of FGF-2. The glycation of FGF-2 with 250 mmol/l glucose-6-phosphate led to reduced mitogenic activity compared to native FGF-2. BSA-AGE at concentrations of 10, 50 and 250 microg/ml had an antiproliferative effect on cultured endothelial cells. Aminosalicylic acid at a concentration of 200 micromol/l proved to be more effective than equimolar concentrations of aminoguanidine in protecting endothelial cells against the antiproliferative effects of both high (30 mmol/l) glucose and 50 microg/ml BSA-AGE. FGF-2 glycated in the presence of 4 mmol/l aminosalicylic acid or aminoguanidine retained mitogenic activity compared to that glycated in their absence. Compounds like aminoguanidine and, in particular, aminosalicylic acid protect endothelial cells against glucose-mediated toxicity and may therefore have therapeutic potential.
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PMID:Aminosalicylic acid reduces the antiproliferative effect of hyperglycaemia, advanced glycation endproducts and glycated basic fibroblast growth factor in cultured bovine aortic endothelial cells: comparison with aminoguanidine. 1284 56

In 3T3-L1 adipocytes, insulin-stimulated GLUT4 translocation requires phosphorylation of the protein designated Akt substrate of 160 kDa (AS160). Both insulin and contractions activate Akt in skeletal muscle. Therefore, we assessed the effects in skeletal muscle of each stimulus on phosphorylation of proteins, including AS160, on the Akt phosphomotif. Isolated rat epitrochlearis muscles were incubated with insulin (for time course and dose response), stimulated to contract, or incubated with 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) and used to assess the following: serine-phosphorylation of Akt (P-Akt), immunoreactivity with an antibody recognizing the Akt phosphomotif (alpha-phospho-[Ser/Thr] Akt substrate [PAS]), and PAS immunoreactivity of samples immunoprecipitated with anti-AS160. P-Akt peaked at 5 min of insulin, and PAS immunoreactivity subsequently peaked for proteins of 250 kDa (10 min) and 160 kDa (15 min). P-Akt, PAS-160, and PAS-250 increased significantly with 0.6 nmol/l insulin. Contractile activity led to increased P-Akt and PAS immunoreactivity of proteins of 160 and 250 kDa. The 160-kDa protein was confirmed to be AS160 based on elevated PAS immunoreactivity in AS160 immunoprecipitates. Wortmannin inhibited insulin (120 nmol/l) and contraction effects on AS160 phosphorylation. Incubation with AICAR caused increased phosphorylation of AMP-activated protein kinase and AS160 but not Akt. Our working hypothesis is that phosphorylation of these putative Akt substrates is important for some of the insulin and contraction bioeffects.
Diabetes 2005 Jan
PMID:Increased phosphorylation of Akt substrate of 160 kDa (AS160) in rat skeletal muscle in response to insulin or contractile activity. 1561 9

The impairment of insulin secretion, a major feature of type 2 diabetes, is caused by beta-cell mass reduction and functional failure. Pancreatic beta-cell mass reduction is variable in humans, not exceeding 50%, and has been associated with amyloid deposits. In the present study, we have chronologically compared the endocrine pancreas morphology of Wistar control rats (W) and Goto-Kakizaki (GK) rats, an animal model of non obese type 2 diabetes. We have also characterised and compared their body weight, glycaemia (fasting and after oral glucose load) as well as other biochemical parameters. GK rats were always glucose intolerant and fasting hyperglycaemia arised at four week of age. Wistar rats had mild glucose intolerance in their first two weeks of life. GK rats had a total beta-cell mass always decreased when compared to controls, but above 40%. In adult GK rats (12 weeks old) alterations in the architecture of a sub-population of islets occurred which displayed signs of prominent fibrosis, with cluster of beta-cells widely separated by strands of connective tissue and deposits of PAS positive material. Our findings demonstrate that, using GK rats from the Coimbra colony, beta-cell mass reduction is one of the primary features in the pathological sequence leading to diabetes. Structural lesions of the islets, that will further increase beta-cell mass reduction and compromise beta-cell function, will appear latter mainly due to hyperglycaemia.
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PMID:[Morphological changes of islet of Langerhans in an animal model of type 2 diabetes]. 1563 48


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