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

A case of N-3 pyridylmethyl-N' 4 nitrophenyl urea (Vacor) rodenticide poisoning in a 52-year-old man is presented. Vacor is structurally related to alloxan and streptozotocin, agents that have been used extensively to produce diabetes mellitus in laboratory animals. Seven days after ingestion of Vacor, the patient presented in diabetic ketoacidosis complicated by postural hypotension and adynamic ileus. The patient recovered from ketoacidosis but has continued to require insulin. With infusion of arginine, glucagon rose from 185 to 650 pg./ml. and C-peptide from 0.5 to 3.4 ng./ml. Six weeks after onset of diabetes, no anti-islet-cell antibodies were detected. Muscle capillary basement membrane thickness on electron microscopy was found to be 1,918 +/- 194 A. The absence of hyperglycemia after Vacor ingestion should not lead to complacency on the part of the attending physician. The patient must be observed closely for development of ketoacidosis and treated prophylactically with nicotinamide, the suggested antidote.
Diabetes Care
PMID:Diabetes mellitus and autonomic dysfunction after vacor rodenticide ingestion. 15 23

An intravenous injection of 40 or 65 mg/kg streptozotocin induced not only diabetes but also severe hypertension in rats. Whereas the hyperglycemia developed fully within a few days after the injection of streptozotocin, the hypertension progessively advanced and reached maximum level several weeks after the treatment and lasted more than 20 weeks. Twenty mg/kg streptozotocin did not induce hyperglycemia but significantly increased blood pressure several weeks after the treatment. Arrest of growth, polyuria, glycosuria, hyperlipemia and lenticular cataracts developed in the animals treated with 40 or 65 mg/kg streptozotocin, but in none of the animals treated with 20 mg/kg. In histological examinations in the 24th week after the treatment, degranulation and necrosis in the pancreatic beta-cells, and vacuolization and deposition of PAS-positive materials in the renal proximal tubules were found in the animals treated with 40 or 65 mg/kg streptozotocin.
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PMID:Chronic hypertension induced by streptozotocin in rats. 15 77

Nonketotic hyperosmolar diabetic coma is a rare manifestation of juvenile diabetes, in contrast to adult onset diabetes. To date only 20 cases have been published, the majority of them infants and toddlers. This type of diabetic coma is seen with unusual frequency in children with Down's syndrome and psychomotor retardation. The clinical picture is characterised by severe dehydration, hyperglycemia with often extremely high blood sugar levels, hyperosmolarity and glucosuria without ketonuria. Mortality in children has been high (24%). This paper reports the case of a 14-month-old girl with Down's syndrome. Clinical and therapeutic as well as pathogenetic aspects are discussed.
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PMID:[Hyperosmolar nonketotic diabetic coma in children]. 15 87

Renal clearance studies were performed on rats both during the administration of streptozotocin and sequentially during the following 8 days as hyperglycemia progressed. Although GFR was depressed 30 min after the drug administration, GFR steadily rose during the following days to become 52% greater than control levels. Renal size did not change during this short period, and it is suggested that glomerular hemodynamic changes are responsible. A maximal tubular reabsorptive capacity for glucose (TmG) could not be satisfactorily demonstrated in normal rats, although glucose reabsorption was significantly depressed at high-filtered loads. At comparable filtered loads, glucose reabsorption in diabetic rats was almost complete in contrast to normal rats, and the increases in GFR and renal tubular sodium reabsorption are presumed to be the major factors. The administration of insulin to normal and diabetic rats was followed by a significant diuresis as well as an increase of 1% to 4% in the fraction of filtered sodium excreted although GFR was unaltered. This shows that even a 35% to 60% reduction in the filtered load of glucose can significantly depress renal sodium reabsorption. It is concluded that this is a good animal model in which to study the effects of diabetes on renal function as well as the in vivo interrelationships of sodium and glucose reabsorption.
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PMID:Acute effects of streptozotocin diabetes on rat renal function. 15 16

Spontaneously hypertensive rats (SHR) were more sensitive to the diabetogenic effects of streptozotocin than normotensive Wistar-Kyoto (WKY) rats. Thus, 10 days after intravenous administration of 25 mg/kg streptozotocin in SHR, mean pancreatic insulin content was decreased by 42% (p less than 0.05), and mean plasma glucose concentration was increased from 85 to 215 mg/dl (p less than 0.001), whereas between 37.5 and 50 mg/kg of streptozotocin was required to produce similar effects in normotensive WKY rats. Also, there was a progressive decrease in blood pressure in SHR injected with 25, 35.7, or 50 mg/kg of streptozotocin, whereas blood pressure was progressively increased after streptozotocin in normotensive WKY rats. The opposite effects of streptozotocin-induced diabetes on blood pressure in SHR and WKY rats could be observed at similar degrees of hyperglycemia and are presently unexplained.
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PMID:Streptozotocin-induced diabetes in the spontaneously hypertensive rat. 15 97

Nineteen inbred strains of male mice were infected with encephalomyocarditis virus. Five strains became hyperglycemic and had abnormal values in glucose tolerance tests; three strains remained normoglycemic but had abnormal values in glucose tolerance tests; and the remaining strains showed no abnormalities in blood glucose levels or glucose tolerance tests. Female mice from three of five strains tested also developed hyperglycemia, but in one strain (DBA/2) the hyperglycemia was less severe in females than in males. Castrated DBA/2 males developed less severe hyperglycemia than uncastrated males, even though the degree of damage to beta cells appeared to be similar in the two groups. Host factors apparently influence both the development and expression of virus-induced diabetes mellitus.
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PMID:Virus-induced diabetes mellitus. III. Influence of the sex and strain of the host. 16 72

Spontaneous diabetes mellitus was reported in a Mandrillus leucophaeus (drill baboon) and a Mpacaca cyclopis (Formosan rock macaque). Each had hyperglycemia, impaired clearance of glucose during tolerance test, and reduced concentrations of immunoreactive insulin; the M cyclopis also had increased triglyceride and prebetalipoprotein concentrations. Both monkeys had extensive amyloid infiltration into the islets of Langerhans and loss of beta cells. Beta cell obliteration can account for the appearance of the diabetic syndrome in these and other nonhuman primate species.
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PMID:Spontaneous diabetes mellitus in Macaca cyclopis and Mandrillus leucophaeus: case reports. 16 51

We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas. Twelve young, healthy men were given 1 g of tolbutamide by mouth before and after 12 days of double-blind treatment with 1 g per day of halofenate, or placebo. There was a significant increase in serum tolbutamide at eight, 10 and 12 hours (P less than 0.01) and a significant (P less than 0.01) decrease in serum glucose at one, four and six hours after halofenate treatment, but not after placebo. In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both. No appreciable decrease in serum glucose levels was noted in diabetic patients receiving sulfonylurea and clofibrate. This interaction between halofenate and sulfonylureas is clinically important, especially in view of the association of hyperlipemia and diabetes.
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PMID:Potentiation of hypoglycemic effect of sulfonylureas by halofenate. 17 74

Tests were set up on 59 albino male-rats with reproduced functional overstress and depletion of the insular system of the pancreas thorough a long-term (for 50, 100 days) peroral introduction of glucose (2 g/100 g body weight, every other day) and with and alloxan-induced diabetes (achieved by poisoning the animals with a 2.5% alloxan solution, 15 mg/100 g administered in a single dose intraperitoneally). A comparison of the data obtained ascertained the presence of a number of similar pathobiochemical changes in the metabolism, viz. hyperglycemia, an increase of the free cholesterol fraction, a diminution of the bound cholesterol fraction and a fall of the insulin-like activity (ILA) in the blood serum, a rise in glycogen and beta-lipoproteids in the liver; morphologically--a reduced count of Langerhan's islands beta-cells, less intensive colouration of the specific granulation in their cytoplasma manifestations of vacuolar and granular dystrophy of the liver. Further tests were staged on 23 rabbits involving a long-term introduction of glucose (in amounts of 25 g/kg every other day) and a cholesterol-induced atherosclerosis (by administering 0.2 g/kg of cholesterol in oil, daily), which also showed similar changes in the figures of the carbohydrate and fat-lipoids metabolism, such as hyperglycemia, an increased level of total lipids, cholesterol and its fractions, beta-lipoproteids, a fall of ILA in the blood serum, as well as variations in the morphological picture of the aortic wall. The above findings suggest that a protracted administration of glucose can produce both diabetogenic and atherogenic effects.
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PMID:[Diabetogenic and atherogenic effects of glucose]. 17 88

A patient with pre-existing diabetes mellitus who was receiving corticosteroids in an effort to prevent transplant rejection was presented. The patient's hyperglycemia was exacerbated by the corticosteroids, and the discussion centered around this aspect of the case. The clinical effects of glucocorticoids on carbohydrate metabolism were reviewed, and four general points were made: (1) the chronic effects of corticoids on glucose tolerance are much less pronounced than the acute effects; (2) the degree of impariment is proportional to the pre-existing status of glucose tolerance; (3) development of frank diabetes mellitus in a previously normal patient is unusual; and (4) the abnormalities of carbohydrate metabolism induced by glucocorticoids fit the pattern of an insulin resistant state. The subject was reviewed and relevant in vivo and in vitro observations were presented in support of the above concepts, and to help identify the pathophysiologic mechanisms involved. It was postulated that glucocorticoids affect glucose metabolism by decreasing glucose utilization and by increasing hepatic glucose production. The possible mechanisms underlying these effects were discussed.
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PMID:Effects of glucocorticoids on carbohydrate metabolism. 17 80


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