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

The morphology of the rat bladder was studied following 8 weeks of streptozotocin-induced diabetes, at which stage distension of the bladder had occurred. Evidence is presented for hypertrophy of the smooth muscle of the bladder wall in experimental diabetes. It is suggested that the morphological changes found in the diabetic rat bladder are associated with polyuria. The results are discussed in relation to clinical studies of bladder dysfunction in diabetes mellitus.
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PMID:The smooth muscle of rat bladder in the early stages of streptozotocin-induced diabetes. 669 1

The BB rat model of spontaneous diabetes mellitus was discovered in 1974 in Ottawa in a colony of specific pathogen-free Wistar rats. Investigations to determine the cause of rapid weight loss and death in a few weanling rats from this colony revealed polydypsia, polyuria, glucosuria, ketonuria, and hyperglycemia. These signs regressed and normal weight gain occurred when daily insulin therapy was given. Histologic studies of the pancreas of affected animals showed fibrosis and absence of beta cells. The original colony was established by crossbreeding the clinically normal parents of the diabetic animals. Approximately 10% of the offspring of these matings became diabetic. This incidence was increased to approximately 25% by father-daughter mating, suggesting a genetic component in the etiology.
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PMID:The discovery and development of the BB rat colony: an animal model of spontaneous diabetes mellitus. 686 71

The effects of a high fat diet (30% (w/w) corn oil) on chronic streptozotocin-diabetic rats were investigated at the whole body level and at the enzyme level. The diet caused significant decreases in the extent of polydipsia (66% decrease), polyphagia (49%), polyuria (67%) and glycosuria (70%). The activities of selected hepatic enzymes from the glycolytic, gluconeogenic, ureogenic and lipogenic clusters were determined. The fat diet caused significant decreases (range: 47 to 54%) in the activity of the ureogenic enzymes carbamyl phosphate synthetase, ornithine transcarbamylase and arginase; had no effect on the glycolytic enzymes glucokinase, hexokinase and pyruvate kinase; partially decreased the diabetes-induced elevated activities of the gluconeogenic enzymes phosphoenolpyruvate carboxykinase (63% decrease), serine dehydratase (90%), alanine aminotransferase (31%) and aspartate aminotransferase (65%), and partially reversed the activity of one lipogenic enzyme, ATP citrate lyase.
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PMID:The effects of a high fat diet on chronic streptozotocin-diabetic rats. 692 68

The etiology of diabetes in some conditions of iron overload is not known. We studied growth, glucose tolerance, and pancreatic islet cell morphology and cytochemistry in rats administered parenteral FeNTA. These rats developed glucosuria, slowing of growth with eventual weight loss, polyuria, polydipsia, and death. They had normal fasting plasma glucose levels but decreased glucose tolerance and insulin response to glucose. Although no Prussian blue staining of iron was observed in pancreatic islets by light microscopy, at the ultrastructural level insulin-secreting beta-cells showed ferrin iron deposits localized to the plasmalemma and the cytoplasmic surface of secretory granule membranes. Prussian blue staining was also observed in parenchymal cells of the liver, heart, and kidney, in order of decreasing intensity. Animals treated with an equivalent dose of NTA, saline, or iron-dextran in saline had normal growth and response to glucose and did not exhibit pancreatic iron deposits at the light or ultrastructural level. These results support the hypothesis that iron affects pancreatic islet cell function and may be an etiologic agent of diabetes mellitus in hemochromatosis.
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PMID:Iron nitrilotriacetate--induced experimental diabetes in rats. 698 19

Rats made diabetic with streptozotocin received a single subcutaneous implant of an insulin polymer pellet that released insulin continuously at approximately 2 U/day. Continuous normoglycemia was achieved for up to 1 mo. Mean glucose level for treated animals was 113 mg/dl as compared with 398 mg/dl for untreated diabetic controls. Diurnal blood glucose values for treated animals ranged from 71 to 116 mg/dl. Polyuria and glycosuria were corrected by the presence of the insulin + polymer. Treated animals gained weight normally and reached a mean weight of 350 g, whereas untreated control animals lost weight, to a mean of 150 g. When insulin + polymer preparations were periodically implanted and removed at 7-day intervals, normoglycemia was only associated with the presence of implants.
Diabetes 1980 Jan
PMID:One month of sustained release of insulin from a polymer implant. 699 15

A female mouse spontaneously exhibiting polyuria and glucosuria accompanied by rapid weight loss waa found in one of two sublines derived from the CTS mice. Eight mating pairs were made using its offspring and selection was performed for both spontaneous diabetes and reproductive ability. After six generations of the selective breeding the diabetic (nod) and the control (non) lines were established. A marked sex difference was observed in the incidence of diabetic symptoms in the nod mouse. The cumulative incidence of the onset up to 30 weeks of age was 80% in females and less than 20% in males. The onset of diabetes was abrupt in both sexes, and spontaneous remission was not observed. However, daily administration of insulin induced an increase of body weight and a prolongation of life span. Diabetic symptoms are biochemically characterized by polyuria, polydipsia, hyperglycemia, glucosuria and hypercholesteremia. Pathological examination revealed a high frequency of lymphocyte infiltration around and/or into the Langerhans' islet. It was observed even at the prediabetic stage over five weeks of both sexes. The number and size of the islets were markedly reduced in the overt diabetic mice. Although the mechanism of the pathogenesis is not clear yet, the nod mouse may be a useful animal model for investigating the human juvenile type diabetes.
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PMID:Breeding of a non-obese, diabetic strain of mice. 699 40

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

The development of proteinuria and its response to insulin therapy in acute experimental diabetes was examined in 11 female rats by sequentially measuring 24 h excretion of glucose and total protein before diabetes, during 5-37 days of acute streptozotocin diabetes, during and after 7-14 days of continuous subcutaneous insulin administration. Induction of diabetes promptly resulted in marked polyuria (78 +/- 9 ml/24 h), and glycosuria (6.6 +/- 0.7 g/24 h), while proteinuria quadrupled (from 4.7 +/- 0.7 to 18.8 +/- 1.8 mg/24 h, p less than 0.001). Concurrent with amelioration of polyuria and glycosuria by insulin treatment, proteinuria decreased strikingly (8.5 +/- 1.2 mg/24 h, p less than 0.001) Polyuria and glycosuria resumed after discontinuing continuous subcutaneous insulin, and proteinuria promptly returned to pretreatment levels (19.0 +/- 2.5 mg/24 h). Similarly decreased proteinuria (8.8 +/- 0.9 mg/24 h) recurred in five rats retreated with insulin after 100 days of diabetes. Elevated proteinuria was not associated with lysozymuria or consistent changes in glomerular filtration rate. The rapid fluctuations in proteinuria attending acute diabetes and its effective treatment suggest that metabolic aberrations of diabetes may directly effect renal handling of proteins.
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PMID:Proteinuria in the acutely diabetic rat and its response to insulin treatment. 702 30

The fa-gene was transferred from the Zucker rat (13 M strain) to the Wistar Kyoto (WKY) rat. The survey, performed at the 10th generation of backcrossing, showed that Wistar fatty rats (fa/fa), a congenic strain of WKY, developed obesity and obesity-related features, such as hyperinsulinemia and hyperlipemia, in the same manner as Zucker fatty rats. Males, but not females, showed hyperglycemia, glucosuria, and polyuria as early as 8 wk of age. Tolerance and insulin response to oral glucose were decreased with advancing age in males. The diabetic changes appeared to be caused by an interaction between predisposition to develop diabetes in the WKY rat and fa-induced obesity. This is because WKY rats were found to be less sensitive to insulin than Zucker rats by both the glucose tolerance test and the steady-state blood glucose method which estimates overall insulin sensitivity.
Diabetes 1981 Dec
PMID:A new genetically obese-hyperglycemic rat (Wistar fatty). 703 Aug 30

Insulin-induced hyperglycemia was diagnosed in 8 dogs with diabetes mellitus. Owners sought veterinary care because of polydipsia, polyuria, polyphagia, persistent morning glycosuria, or seizures in their dogs. These abnormalities had persisted despite increasing the dosage of insulin. Insulin-induced posthypoglycemic hyperglycemia was diagnosed by determining blood glucose concentrations every 2 hours during a 24-hour period, beginning at 8 A.M. Wide fluctuations in the blood glucose concentration were reduced by decreasing the daily insulin dose. The signs observed by the owners disappeared after the insulin dose was reduced.
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PMID:Insulin-induced hyperglycemia in diabetic dogs. 704 78


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