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

Nonobese diabetic (NOD) mice get spontaneous diabetes with clinical and pathological manifestations similar to those seen in human type I diabetes. NOD mice will destroy transplants of treated allogeneic islet tissue by a recurrence of the disease process that destroyed the original islet tissue. This may be prevented by treatment of the animals with combined desferrioxamine and nicotinamide. Transplanted animals become normoglycemic and remain so for the duration of the treatment. This suggests that oxygen-derived free radicals may be involved in islet damage in spontaneous diabetes.
Diabetes 1986 Nov
PMID:Combined treatment with nicotinamide and desferrioxamine prevents islet allograft destruction in NOD mice. 294 84

The study has examined the effect of streptozotocin-induced diabetes of 3 days and 10 weeks duration upon the serotonin content of the rat pancreas and small intestine. Streptozotocin administration (65 mg/kg) resulted in a significant (p less than 0.001) decrease in pancreatic serotonin after 3 days (to 18% of the non-diabetic content). Diabetes of both short- and medium-term duration had no significant effect upon the serotonin content of the small intestine suggesting that changes in mucosal serotonin levels are not responsible for the diarrhea frequently observed in streptozotocin-treated animals. The diabetogenic effect of streptozotocin and the reduction in pancreatic serotonin were abolished by prior injection of nicotinamide thus providing further evidence for co-storage of insulin and serotonin in the B cell.
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PMID:Effect of streptozotocin administration upon the serotonin content of the pancreas and small intestine of the rat. 294 36

Administration of nicotinamide (NA) is followed by a pronounced hypoglycemic effect with a simultaneous decrease of glucose content in the lens, sciatic nerve and aorta at manifest streptozotocin-induced diabetes and also by a complete normalization of parameters of the intraperitoneal glucose-tolerance test in rats with a "diabetic" type of glucose tolerance. A 14-day NA treatment of patients with diabetes mellitus results in the improvement of the glycemic profile, a decrease of glucosuria and the blood serum level of protein-bound hexoses as well as positive shifts in the condition of the cardiovascular and nervous systems.
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PMID:[Hypoglycemic effect of nicotinamide in diabetes mellitus]. 295 27

The effect of streptozotocin (SZ) on bile flow (BF) and on protein and lipid biliary outputs were studied in rats with bile fistula. SZ was given i.v. as a single dose (50 mg/kg body wt.). Nicotinamide was administrated (500 mg/kg body wt., i.p.) 10 min prior to SZ. Decreases in BF and in biliary outputs of bile acids, proteins and acid phosphatase were observed in SZ-treated rats; conversely, the biliary excretion of cholesterol and phospholipids was increased. Nicotinamide pretreatment prevented the hyperglycemia induced by SZ and also suppressed the SZ-mediated increase of cholesterol and phospholipid biliary outputs, suggesting that they could be related to the diabetic state. The results also demonstrated a direct effect of SZ on BF and on the biliary excretion of bile acids and proteins. Since SZ is used clinically, and in experimental diabetes, the effects produced by this drug on the rat liver should be considered.
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PMID:Toxic effect of streptozotocin on the biliary secretion of nicotinamide-treated rats. 295 69

Alterations in the content and structure of CoA moiety typical of hyperlipogenesis (a rise in total and free CoA levels, a drop in short-chained fatty acyl-CoA/CoA and long-chained fatty acyl-CoA/CoA ratios) were found in the liver of obese mice with non-insulin-dependent diabetes (db/db). The treatment of diabetic mice with nicotinamide, an antilipemic drug, was accompanied by a decrease in total and free CoA levels and a rise in short-chained fatty acyl-CoA content and short-chained fatty acyl-CoA/CoA and long-chained fatty acyl-CoA/CoA ratios, probably leading to the inhibition of the enzymes of primary lipogenesis steps. It is suggested that CoA moiety structure is essential as an integral index regulating the rate of fatty acid biosynthesis in diabetes mellitus.
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PMID:[Changes in the content and structure of the coenzyme A moiety in the liver of diabetic mice (db/db) administered a regimen of nicotinamide]. 295 96

This study was conducted in order to clarify whether the poly(ADP-ribose) synthetase inhibitors, nicotinamide and 3-aminobenzamide, have any influence upon the content and physicochemical properties of insulin and glucagon in streptozotocin (STZ)-treated rat pancreas. STZ-treated rats received intraperitoneal injection of 350 mg/kg nicotinamide or 50 mg/kg 3-aminobenzamide 15 min before and 180 min after the administration of STZ and once a day thereafter for 23 weeks. The blood glucose levels and body weight of nicotinamide- and 3-aminobenzamide-treated rats did not differ from those of the control rats at the end of the experiment. The insulin content in poly(ADP-ribose) synthetase inhibitor-treated rat pancreas was restored partially and reached approximately 60% of the control level, while the glucagon content did not differ from that in the normal rats. Treatment with poly(ADP-ribose) synthetase inhibitor resulted in no alteration in the physicochemical properties of extracted insulin and glucagon. Immunohistological examination of the pancreas revealed that insulin- and glucagon-containing cells in the islets in the poly(ADP-ribose) synthetase inhibitor-treated rat appeared to be normalized. These results suggest that poly(ADP-ribose) synthetase inhibitor normalizes the function but not the insulin content of B cells and that it does not act on A cells in STZ-treated rat pancreas. Restoration of the insulin content would be large enough to keep the function of B cells normal.
Diabetes Res Clin Pract
PMID:Effect of poly(ADP-ribose) synthetase inhibitor administration to streptozotocin-induced diabetic rats on insulin and glucagon contents in their pancreas. 295 3

The present study deals with the hypnotic effect of pentobarbital (Pento) in relation to its metabolism in hepatic microsomes in streptozotocin (STZ, 170 mg/kg, i.p.) injected mice. Liver weight (mg/10 g body wt.) of STZ-treated mice was larger than that of the controls throughout the experimental period. Although the shortening of sleeping time induced by Pento (60 mg/kg, i.p.) was always observed, Pento-metabolizing enzyme activity (by the method of Kato et al., 1964) increased in mice with diabetes for 2 and 4 weeks but decreased in mice with diabetes for 8 weeks. Induction following phenobarbital (100 mg/kg, s.c.) and inhibition by SKF 525-A (10 mg/kg, i.p.) of hepatic metabolizing enzyme were found in both control and mice with diabetes for 2, 4 and 8 weeks, but these were not definitely correlated to their hepatic Pento-metabolizing enzyme activities. STZ-induced hyperglycemia and shortening of sleeping time by Pento were completely prevented by the pretreatment with nicotinamide (500 mg/kg, i.p.). NPH-insulin injection partially decreased hyperglycemia in STZ-diabetic mice, but sleeping time by Pento was not significantly affected. These results suggest that the hyposensitivity to Pento in STZ-diabetic mice is partially related to an abnormality of metabolism in liver such as the hyperglycemic state.
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PMID:[Changes in pentobarbital hypnosis and hepatic metabolism in streptozotocin-diabetic mice]. 296 May 99

Administration of poly(ADP-ribose) synthetase inhibitors such as nicotinamide to 90% depancreatized rats induces regeneration of pancreatic islets, thereby ameliorating the surgical diabetes (Yonemura, Y., Takashima, T., Miwa, K., Miyazaki, I., Yamamoto, H., and Okamoto, H. (1984) Diabetes 33, 401-404). In screening the regenerating islet-derived cDNA library, we came across a novel gene encoding a 165-amino acid protein. The gene was expressed in regenerating islets but not in normal pancreatic islets, insulinomas, or regenerating liver. In 90% depancreatized and nicotinamide-injected rats, the expression of the gene was increased 1 month after the partial pancreatectomy and reached a peak 3 months after the operation. The increase in expression of the gene was temporally correlated with the increase in size of regenerating islets and the decrease in urinary glucose level. The gene was also found to be activated in hyperplastic islets of aurothioglucose-treated mice. Thus, the expression of the gene in both regenerating and hyperplastic islets suggests possible roles for this gene in replication, growth, and maturation of islet beta-cells. We also found that a human pancreas-derived cDNA library contained a homologue to the gene.
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PMID:A novel gene activated in regenerating islets. 296

Clinical studies suggest that diabetes mellitus may predispose to the development of pancreatic cancer. The current study investigated the effect of experimental diabetes on the susceptibility of the Syrian hamster to the induction of exocrine pancreatic carcinoma by the carcinogen BOP. Diabetes was induced with the B-cell toxin streptozotocin. Three groups of animals were studied: nondiabetic control animals and animals with streptozotocin-induced diabetes, and a third group of animals in which the diabetogenic effect of streptozotocin was blocked with nicotinamide. Streptozotocin-induced diabetes significantly inhibited the induction of pancreatic carcinoma by BOP, decreasing the incidence of carcinoma to 24 percent compared with an incidence of 75 percent in nondiabetic control animals (p less than 0.002). In diabetic animals, the degree of inhibition of carcinogenesis paralleled the severity of the diabetes. Blocking the diabetogenic effect of streptozotocin with nicotinamide restored the incidence of induced invasive pancreatic carcinoma to that occurring in nondiabetic control animals. In the hamster model, diabetes appears to have a strong influence on susceptibility to the development of pancreatic carcinoma.
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PMID:Influence of diabetes on susceptibility to experimental pancreatic cancer. 296 53

Weanling CD-1 mice were fed either a control diet or a diet deficient in niacin/nicotinamide for one month and then injected i.v. with 60, 80, 100, 120, 140, or 160 mg/kg streptozotocin. Mice on the deficient diet developed a higher incidence of diabetes and more severe hyperglycemia than those on the control diet.
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PMID:Effect of niacin/nicotinamide deficiency on the diabetogenic effect of streptozotocin. 296 27


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