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

Untrained grown-up and old rats with a mild Streptozotocin-diabetes show in i.v. glucose tolerance test a pathological glucose assimilation and diminished insulin secretion in comparison to control rats of the same age after a maximal run-stress. Trained rats show a different behaviour in glucose tolerance test depending on their age and seriousness of diabetes: Glucose tolerance is improved in grown-up rats with a mild diabetes and unchanged in old rats. Six-week run-training causes a significant deterioration of glucose tolerance in rats with a medium seriously Streptozotocin-diabetes and even leads to death of old rats because of decompensated metabolism. Grown-up rats with a mild diabetes stand run-stress after run-training better than the old ones. No animal with a medium seriously diabetes survives maximal run-stress, old rats don't even survive the slowly increasing run-training. - These results confirm the dualistic effect of muscular work. Metabolism of mild diabetes becomes better through muscular exertion the one of medium diabetes gets worse. Therefore a good effect of run-training is measurable only in grown-up rats not in old ones.
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PMID:[Investigations about the effect of run-training and run-stress on glucose tolerance and insulin secretion with ageing streptozotocin-diabetic rats (author's transl)]. 1 41

Streptozotocin-induced diabetes in the rat can be reversed by the transplantation of isogenic islets of Langerhans from neonatal donors. We studied the morphology of intraportally transplanted islets with the aid of the immunoperoxidase staining technique to identify insulin-, glucagon-, somatostatin-, and pancreatic polypeptide-containing cells at 24 hours, 48 hours, 1 week, 2 weeks, 4 weeks, 39 weeks, and 65 weeks after transplant. Embolized pancreatic tissue, composed of approximately 80% acini and 20% islets, is initially distributed throughout the liver mainly to terminal branches of the portal system. Endothelialization and organization occur rapidly with the smaller fragments and within the first 4 weeks for larger thrombi. Exocrine pancreatic elements largely disappear as islet cells move into the hepatic lobules from the portal spaces. At 65 weeks after transplant, all islet cell types can be identified within large complex islet structures. The results of this study establish the survival and continued function of all known rat pancreatic islet cell types long after transplantation and support the theory that islet transplantation may represent the most physiologic replacement of hormonal deficiencies in the diabetic recipient.
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PMID:The fate of intraportally transplanted islets in diabetic rats. A morphologic and immunohistochemical study. 9 48

Vitreous fluorophotometry has proved to be a useful method to evaluate the integrity of the blood-ocular barrier to fluorescein in clinical and experimental diabetes mellitus. Diabetic patients with or without background retinopathy had increased vitreous accumulation of fluorescein after intravenous injection when compared with age-matched controls. Streptozotocin-induced diabetes in rats increase vitreous fluorescein levels. In the rat, this abnormality was reversed with insulin therapy and with pancreatic islet transplantation. The breakdown of the blood-ocular barrier to fluorescein appears to be the earliest detectable ocular abnormality of diabetes.
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PMID:Vitreous fluorophotometry in diabetes mellitus. 11 99

Streptozotocin (STZ)-diabetic rats regularly retained sodium (Na+), and tended to retain potassium (K+) as well, in response to insulin. Diabetic patients have also been reported to exhibit antinatriuresis and antikaliuresis early in the course of insulin therapy. Insulin-related Na+ retention can occur without a marked reduction in blood glucose level and does not appear to be attributable to preexisting Na+ depletion, mineralocorticoid effect, or suppression of glucosuria. The decrease in urinary Na+ excretion (UNaV) in the rats incident to insulin administration was appreciably greater than the decrease in chloride (Cl-) or water excretion. The significance of this observation is uncertain. It may be, in part, a consequence of the nephrotoxicity of STZ. Insulin-related Na+ retention may be closely related pathogenetically to the Na+ retention of refeeding and may reflect a direct renal action of insulin or, less likely, an alteration of renal tubular metabolism in response to insulin-mediated changes in sytemic metabolism.
Diabetes 1975 Jul
PMID:Observations on sodium retention related to insulin treatment of experimental diabetes. 12 67

Streptozotocin-induced diabetes in rats was completely reversed by transplantation of syngeneic fetal pancreases placed beneath the kidney capsule. To accomplish complete reversal of diabetes, four or more pancreases were necessary; three resulted in partial reversal, and two produced a slight but significant effect in some recipients. Removal of the transplants resulted in the prompt return of diabetes. The islets of Langerhans in the transplants functioned homeostatically; this was indicated by regular normal blood glucose values, in addition to normal findings in blood IRI response and glucose disappearance rate after glucose injection. Disappearance of exocrine elements, with only ducts and fibrous tissue remaining, resulted in a pure endocrine organ. The advantages of this technie, such as ease of accessibility for placement, observation, and removal, are of great importance for possible application to humans.
Diabetes 1976 Jan
PMID:Fetal pancreas transplantation for reversal of streptozotocin-induced diabetes in rats. 12 81

These investigations delineate the recently described suppression of a form of cellular hypersensitivity in mice with streptozotocin-induced diabetes mellitus using a variety of cell-mediated immunologic responses in animals with several different forms of diabetes. Streptozotocin- and alloxan-induced diabetic mice and db/db genetically determined diabetic mice showed reductions in the areas of inflammation around Schistosoma mansoni eggs injected into the pulmonary vasculature of 68, 70, 77%, respectively. In contrast, streptozotocin-induced diabetes had no effect on the nonimmunologic foreign body granuloma around divinyl benzene copolymer beads injected into the pulmonary arterioles. Animals protected from diabetes by treatment with nicotinamide before streptozotocin administration did not develop hyperglycemia and had normal areas of immunologic granuloma formation around schistosome eggs. Treatment with insulin reversed the suppression of schistosome egg granuloma formation in both streptozotocin- and alloxan-diabetic animals. Two additional in vivo parameters of cellular immunologic reactivity were examined in streptozotocin-induced diabetes: delayed footpad swelling was essentially eliminated; skin graft survival across the H-2 area was significantly prolonged from 10.2 days in the controls to 14.4 days in moderately diabetic A/J mice. These observations suggest that diabetes mellitus is associated with suppression of cell-mediated reactions in vivo and that the defect is reversible with insulin treatment.
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PMID:Induced and spontaneous diabetes mellitus and suppression of cell-mediated immunologic responses. Granuloma formation, delayed dermal reactivity and allograft rejection. 13 Mar 84

Male Wistar rats were treated with an i.v. dose of 100 mg/kg of Streptozotocin (STZ). Either 5 days or 1, 2 or 3 months after induction of diabetes, the adrenal function of these animals was studied. Short course diabetes (5 days) was accompanied by adrenal hypertrophy and high plasma corticosterone levels; during later periods the diabetic rats consistenly showed signs of adrenal hyperactivity, yet both adrenal weight and plasma corticosterone tended to be lower than in the 5 day-treated animals. Adrenal incubations with 14C-progesterone showed that 5 days and one month diabetic animals synthesized more deoxycorticosterone than controls; production of corticosterone and 18-hydroxydeoxycorticosterone was normal at all time periods studied. Synthesis of 18-hydroxycorticosterone, a compound which affects sodium metabolism, was increased in 5 day-treated rats; thereafter, the function of the zona glomerulosa seemed to be impaired in diabetic rats. These results suggest that early after induction of diabetes there is adrenal hyperfunction of the mixed type (i.e. gluco and mineralcorticoid), and that in the later periods (2-3 months), the deranged metabolism of the diabetic rat acts as a chronic stress.
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PMID:The influence of streptozotocin diabetes on adrenal function in male rats. 13 18

Streptozotocin diabetic rats have larger kidneys than non-diabetic rats. In the present study the rate of kidney growth during the first seven days of diabetes was correlated with the blood glucose concentration. Over a wide range of blood glucose concentrations (116-340 mg/100 ml) the kidney weight, protein content and protein/DNA ratio were closely correlated with the glucose values.
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PMID:Renal hypertrophy in experimental diabetes: relation to severity of diabetes. 14 90

The rates of DNA synthesis in islet and acinar cells were compared at different intervals following streptozotocin-induced diabetes. Streptozotocin, injected I.V. at a dosage of 65 mg/kg, consistently produced a diabetic-like state in young rats, ages 33 to 42 days. At two, four, and seven days after streptozotocin administration, no significant difference in DNA synthesis per mm2 of islet and acinar tissue was evident. However, four days after streptozotocin injection, a significant increase over control values was observed in the number of cells per islet incorporating tritiated thymidine. Following streptozotocin administration, beta cells generally appeared degranulated but not necrotic. Transformation of acinar cells or ductal elements to beta cells was not observed, suggesting that proliferating beta cells are the progeny of pre-existing beta cells. This study suggests that a brief, temporary period of compensatory proliferation of beta cells follows the initial insult of the diabetogenic agent streptozotocin in young rats.
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PMID:DNA synthesis in pancreatic islet and acinar cells in rats with streptozotocin-induced diabetes. 14 Aug 41

Hyperglycemia induced in animals by beta cell toxins or by pancreatectomy can be reversed by pancreatic islet transplantation. Abnormal carbohydrate metabolism in juvenile onset human diabetics has also been corrected, albeit temporarily because of graft rejection, by pancreatic transplantation. It does not necessarily follow that naturally occurring diabetes in animals or adult onset diabetes in man would respond to similar treatment. Islet transplantation was studied in mice with chemically induced or genetically determined diabetes. Streptozotocin-induced diabetic mice were permanently cured by syngeneic islets and, when immunosuppressed, were rendered normoglycemic for six weeks after receiving xenogeneic rat islets. In contrast, histocompatible islets from normoglycemic coisogenic donors were ineffective in hyperglycemic db/db recipients as were xenogeneic rat islets in immunosuppressed db/db hosts. However, when islets were isolated from db/db donors and transplated to genetically normal coisogenic mice, which had been rendered hyperglycemic with streptozotocin, they became normoglycemic. Apparently the metabolic defect in the db/db mice, which is similar in some ways to human maturity onset diabetes, does not reside in their islets as these cells can function normally if transplanted to genetically nondiabetic hosts. In two other types of genetic diabetes (ob/ob and NZO) islet transplantation was more effective. Pancreatic transplantation is unlikely to be the proper treatment for all types of diabetes even if technical and immunological problems are overcome.
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PMID:Islet transplantation in genetically determined diabetes. 14 16


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