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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraportal transplantation of isogeneic adult islets in diabetic rats resulted in long-lasting amelioration of the metabolic disorder. The effect upon diabetes-induced kidney changes (enlargement of mesangial space, capillary changes, cell-proliferation) was examined quantitatively by morphometric studies. The major effect was a remarkable reduction of the mesangial space and re-widening of the capillary lumina. The number of endothelial cells was lowered. Regarding epithelial and mesangila cells no difference was observed between normal, diabetic and transplanted animals of age-matched groups.
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PMID:Islet transplantation in experimental diabetes of the rat. VI. Rate of regression in diabetic kidney lesions after isogeneic islet transplantation: quantitative measurements. 10 83

In view of some data of the literature suggesting that immunological changes could play a role in the pathogensis of diabetes mellitus and of its complications, we carried out a study of the lymphocyte populations of 44 diabetic subjects by means of E, EA, EAC rosettes and membrane immunofluorescence. A quarter of the patients had decreased E rosettes: all of these had long-lasting, insulin-dependent, poorly controlled diabetes. Some of these patients had also increased membrane IgG globulins. In 5 patients with recent onset, insulin-independent diabetes, E rosettes were increased. No significant changes of EA and EAC rosettes were observed. These findings suggest that changes of lymphocyte populations do not play any role in the pathogenesis of diabetes, while these may be the consequence of the metabolic disorder and these may favour the onset of complications of the disease.
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PMID:[Immunological changes in diabetes mellitus. Study of lymphocyte populations]. 31 18

Metabolic disorders and immunological factors are discussed in connection with the pathogenesis of diabetic microangiopathy. Renal biopsies were obtained from 22 diabetics (8 women aged 18 to 53, 14 men aged 15 to 52). 7 of the 22 patients had been suffering from diabetes for 2 weeks to 3 years, 10 for 7 to 25 years, 2 showed a pathological glucose-tolerance test, i.e., they had been "latent" diabetics, and 3 patients, had been so-called "potential" subjects of diabetes due to hereditary traits or delivery of big babies. They were examined by light miroscopy as well as by immunofluorescence microscopy. A number of cases were chosen for the differentiation and counting of glomerular cells (n=8) as well as for electron microscopic (n=7) and polarizing-microscopic (n=6) examinations. Histologically, focal proliferations of mesangial cells as well as an increase in mesangial substance in the glomeruli was found in all cases, although in a varying degree of intensity. These results were confirmed by both the glomuerular cell count and electron-microscopic examination. Immunofluorescence microscopy made it possible to detect frequently both IgA (9/17) and IgG (9/17), usually in either linear or mesangial arrangements whereas it was less frequently possible to detect IgM (1/17) and albumin (1/8) and impossible to detect beta1C in the glomerulus. Labeled insulin was detected five times in the glomerulus. Polarizing-microscopic measurements made in order to discover possible submicroscopic variations in the structure of GBM showed deviations in the average values of anisotropic indices from the controls in the group of long-term diabetics only. The pathogenesis of diabetic microangiopathy may be described as an inflow of immunoglobulins and serum proteins into the mesangium because of an alteration of the capillary endothelium, the mesangial cell being thus caused to overfunction, proliferate and produce an excess of mesangial matrix. In prolonged diabetes the mesangial cell, so far as its own metabolism is concerned, will finally be affected to the point where its power of synthesis is modified in the sense of an excess and/or faulty composition of GBM (glomerular basement membrane).
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PMID:Renal biopsies performed on diabetics. 33 62

66 placentas of mothers with protodiabetes or of the White-classes A/a, respectively, are investigated morphologically. The results are correlated with the clinical findings. Complications during pregnancy as well as the perinatal mortality (5.7 per cent) are less frequent in early stages before the diabetes become manifest. Severe diabetic disturbances of placental maturation we have found in protodiabetics in 15.4 per cent, in the White-classes A/a in 18.9%. In the White-classe D the frequency is 49.5 per cent. Accordingly, the diagnostic possibilities are smaller than in cases with manifest diabetes mellitus. Diabetic disturbances of placental maturation can be demonstrated already in few cases of the material in protodiabetics and in patients with glucosuria during pregnancy and with suspicion of diabetes mellitus, but without diabetic fetopathy. Therefore in our opinion diagnosis of diabetic metabolic disorder may be possible by some morphologic criterias of the placenta in very early stages of diabetes before clinical manifestation.
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PMID:[Morphology of the placenta in premanifest maternal diabetes mellitus (author's transl)]. 34 37

Diabetic nephropathy is a dangerous and insidious complication of diabetes mellitus. The course is variable and from the statistical point of view usually unfavorable. The pathogenesis of the complaint is not fully known. Of the numerous hypotheses, the one most favored is a defective glucose metabolism with uncontrolled inundation of the kidney cells with glucose. The predominant symptom is proteinuria. Early recognition and optimal correction of the metabolic disorder may possibly delay the manifestation of diabetic nephropathy for a time. The use of Somatostatin is attracting great attention today. With such a preparation, the stabilization of diabetes could be facilitated.
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PMID:[Clinical aspects of diabetic nephroangiopathy (author's transl)]. 40 65

The prevalence of diabetes was investigated in 473 patients who had been fitted with pacemakers because of severe bradycardiac arrhythmia. Irrespective of the type of arrhythmia, 36.1% of the male and 45.5% of the female patients exhibited overt diabetes. The metabolic disorder was known in about half (55%) of the cases; average duration of known diabetes in these patients was 7.1 years (0.5-23 years). The more frequent occurence of diabetes in women was attributed to the frequency of overweight (twice as high) in this group. Only one fifth of the male and one tenth of the female patients had myocardial infarction as a sign of manifest coronary arteriosclerosis. The 6 to 10 times higher diabetes prevalence of pacemaker patients compared to the general population of corresponding age may indicate ischemic damage to the conduction system caused by diabetes-specific vascular changes.
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PMID:Diabetes prevalence in patients with bradycardiac arrhythmias. 61 87

We studied the prevalence and the risk factor among the patients of gout in Mexico. Research was conducted in the National Institute of Cardiology and in our private practice. Prevalence of hiperuricemia and gout in the Institute of Cardiology was of 1% (970 out of nearly 100,000 patients). We divided those cases of two subgroups: Reumatology patients (333) and Cardiovascular patients (529). In the first group primary gout was (96.3), and (50.32% in the second. Risk factor was quite different too: nephropathy 9.9%, lithiasis 9.3%, pyelonephritis 2.7%, cardioangiosclerosis 12.9%, aortosclerosis 6.6%, coronary insufficiency 6.3%, myocardial infarction 0.9%, arterial hypertension 24.6% obesity 56.1% and diabetes 9.9% in the Reumatology group; in the Cardiovascular one, nephropathy 14.3%, lithiasis 12.2%, pyelonephritis 7.1%, cardioangiosclerosis 62.7%, aortosclerosis 31.7%, coronary insufficiency 24.9%, myocardial infarction 29%, arterial hypertension 51%, obesity 54.8% and diabetes 20.4%. Among the private practice patients prevalence was of 10.1% (961). In an early age (39 years) in men and a later one for women (53 years). Other characteristics of epidemiology and risk factor are: primary gout 89%, atherosclerosis 5%, coronary disease 4.6%, lithiasis 4.7%, nephropathy 2%, pyelonephritis 1%, obesity 43%, and diabetes 4.6%. In an small group of patients of our private practice we made an exhaustive study of risk factor and the metabolic disorder of lipids. We found the following frequency: 9.3 of nephropathy, 31.2% of lithiasis, 18.7% of pyelonephritis, 68.9% of cardioangiosclerosis, 46.8% de coronary insufficiency, 9.3% of myocardial infarction, 68.7% of arterial hypertension, 68.7% of obesity and 18.7% of diabetes. In the lipid profile we found an increase in triglicerids and prebeta lipoprotein. We have amply discussed the relation between hiperuricemia and pathology considered as a risk factor from the genetic point of view as well as the metabolic and circumstancial aspect. From all that we concluded that risk is multifactorial.
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PMID:[Various epidemiological aspects of hyperuricemia and gout in Mexico: incidence and the cardiovascular risk factor]. 72 44

By investigation of the carbohydrate metabolism in 357 patients with polyneuropathy observed in hospital in recent years, and by statistical comparison with a control group in the literature, an attempt was made to find out whether subclinical diabetes can cause diabetic polyneuropathy to a greater extent. In spite of the more frequent occurrence in the total number of patients, a more significant etiological role for this type of metabolic disorder in polyneuropathy cannot be concluded from the results. Whether a more unspecific, general polyneuropathy-promoting influence is to be ascribed to it must remain open.
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PMID:[Subclinical diabetes and polyneuropathy (author's transl)]. 82 15

Spontaneous hyperglycemia, hyperinsulinemia and obesity are common features for at least one period of the lifetime in some strains of mice. Both genetic and environmental factors are involved in the pathogenesis of the diabetes-like syndrome, making these strains excellent models for studies in both obesity and diabetes-like states. The metabolic peculiarities can be due to a dominant gene, as for the yellow obese, or a single recessive gene, as in the obese and the diabetes mouse; or they can be of polygenic origin, as for the KK and the NZO mouse. However, the severity of the metabolic disorder is due to the interaction of the mutant genes iwth modifiers in the bat genes themselves. Studies on the pathophysiology and biochemistry of these animals have revealed interstrain differences, different patterns of development of the metabolic disorder, and different degrees of severity of the diabetes-like syndrome. Although the primary causes of the syndrome remain unclear in some strains, an involvement of hypothalamic feeding centers has been implicated.
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PMID:Laboratory animals exhibiting obesity and diabetes syndromes. 83 44

Dogs were made alloxan-diabetic and randomly distributed into either of two prospective treatment groups. In one group it was intended that the metabolic signs of diabetes be controlled poorly, and commercial insulin was administered in doses inadequate to prevent chronic, severe hyperglycemia and glucosuria. In the other group it was intended that the metabolic disorder be well controlled, and the animals received food and commercial insulin twice daily such that the hyperglycemia and glucosuria became mild or infrequent. Experimental improvement of the carbohydrate disorder was accompanied by amelioration of hyperlipemia and other clinical signs of deficient insulin activity. By 60 months of diabetes, retinal capillary aneurysms, pericyte ghosts, obliterated vessels, and other microvascular abnormalities typical of diabetes were apparent in each animal of the poor-control group. Better control was found to reduce significantly the incidence and severity of microvascular lesions. The data suggest that the mechanism responsible for diabetic retinopathy is initiated as a result of deficient insulin activity and that the development of the microvascular complications of diabetes are preventable and may be inhibited by careful control of the metabolic disorder.
Diabetes 1977 Aug
PMID:Relationship of microvascular disease in diabetes to metabolic control. 88 98


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