Total Parenteral Nutrition Modulates Hormone Release by Stimulating Expression and Activity of Inducible Nitric Oxide Synthase in Rat Pancreatic Islets

Endocrine ◽  
2001 ◽  
Vol 16 (2) ◽  
pp. 097-104 ◽  
Author(s):  
Albert Salehi ◽  
Mats Ekelund ◽  
Ragnar Henningsson ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Pancreatic Islets ◽  
Inducible Nitric Oxide Synthase ◽  
Hormone Release ◽  
Oxide Synthase ◽  
Expression And Activity ◽  
Inducible Nitric Oxide

Effects of Cisplatin Administration on the Inducible Nitric Oxide Synthase and Somatostatin in the Pancreatic Islets

1997 ◽  
Vol 3 (S2) ◽  
pp. 163-164
Author(s):  
Ying Wang ◽  
Surinder K. Aggarwal
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pancreatic Islets ◽  
Inducible Nitric Oxide Synthase ◽  
Clinical Situation ◽  
Severe Nausea ◽  
Before And After ◽  
Cancer Agent ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Cisplatin, a potent broad spectrum anti-cancer agent, has been proven effective in the treatments of bladder, lung, ovarian, head and neck, and testicular cancers. Drawbacks of this chemotherapeutic drug are its toxic side-effects, which include severe nausea, vomiting, stomach distention, peptic ulcer and hyperglycemia. Cisplatin treatment induces the hyperglycemia both in clinical situation and the rodents. Because of the role of the inducible nitric oxide synthase (i-NOS) and somatostatin on the dysfunction of the β-cell of the pancreatic islets and the suppression of the insulin secretion, these were studied using immunocytochemical methods before and after cisplatin treatments using rats.Wistar rats (100-150 g) were divided into two groups of 6 animals each. One group received injections of cisplatin (9 mg/kg) in 0.85% saline in 5 divided dosages over a 5 days period. The other group received the vehicle of injection only. Rats were killed one day after the last injection.

scholarly journals Efficacy of 1400 W, a novel inhibitor of inducible nitric oxide synthase, in preventing interleukin-1beta-induced suppression of pancreatic islet function in vitro and multiple low-dose streptozotocin-induced diabetes in vivo

2002 ◽  
pp. 543-551 ◽  
Author(s):  
T Rydgren ◽  
S Sandler
Keyword(s):  
Nitric Oxide ◽  
Body Weight ◽  
Nitric Oxide Synthase ◽  
Pancreatic Islets ◽  
Inducible Nitric Oxide Synthase ◽  
Low Dose ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

OBJECTIVE: Nitric oxide (NO), generated by inducible nitric oxide synthase (iNOS), has been implicated in beta-cell destruction in type 1 diabetes. In the present study, we tested a highly selective iNOS inhibitor, 1400 W, against interleukin-1beta (IL-1beta) induced suppression of rat pancreatic islets, and investigated whether 1400 W could prevent multiple low-dose streptozotocin (MLDS) induced diabetes in mice. Furthermore, we studied if 1400 W affected lipopolysaccharide (LPS) induced increase in plasma nitrite+nitrate (NO(x)) in mice. DESIGN AND METHODS: Precultured rat pancreatic islets were exposed for 48 h to 0, 1, 10 or 50 micromol/l 1400 W in the presence or absence of 25 U/ml IL-1beta, whereupon islet functions were analyzed. MLDS-treated mice were given 5.9 mg/kg body weight of 1400 W intraperitoneally daily or 14 mg/kg body weight twice a day. Blood glucose was monitored and degree of pancreatic mononuclear infiltration was determined. Mice previously injected intraperitoneally with LPS (500 microg) were given 1400 W (14 mg/kg body weight) intraperitoneally and plasma NO(x) was determined after 3, 6 and 10 h. RESULTS: The inhibitor alone did not affect islet functions. 1400 W (50 micromol/l) fully counteracted both the suppression of glucose oxidation rate, (pro)insulin biosynthesis and nitrite accumulation caused by IL-1beta. Cytokine-induced decrease in medium insulin accumulation and glucose-stimulated insulin release was partly counteracted by 1400 W, suggesting that inhibition of insulin release was partially NO independent. LPS-induced increase in plasma NO(x) was markedly inhibited for up to 10 h after 1400 W administration. Irrespective of 1400 W treatment, animals treated with MLDS developed hyperglycemia and pancreatic insulitis. CONCLUSIONS: 1400 W counteracted IL-1beta-induced suppression of rat islets in vitro and LPS induction of NO(x) in vivo, however, it failed to protect against MLDS diabetes in vivo. The latter might be due to a failure by 1400 W in vivo to inhibit NO formation at the level of the pancreatic islet.

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