title: Effects of administering sodium selenite, methylseleninic acid, and seleno-L-methionine on glucose tolerance in a streptozotocin/nicotinamide-induced diabetic mouse model.
abstract: The effects of administering the selenocompounds, sodium selenite, methylseleninic acid (MSA), and seleno-L-methionine (SeMet) on glucose tolerance were compared in the nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally treated twice with STZ (100 mg/kg) 15 min after an injection of NA (120 mg/kg) at a 1-d interval. Non-fasting blood glucose levels were then monitored weekly while orally administering the selenocompounds at 158 µg Se/kg body weight with free access to a selenium-deficient diet for 5 weeks. The mean body weights of NA/STZ-induced diabetic mice were partly restored by the administration of selenocompounds, while SeMet led to a higher selenium content and glutathione peroxidase 1 activity in the pancreas. Non-fasting and oral glucose tolerance-tested blood glucose levels, which were elevated by NA/STZ, were significantly suppressed by the administration of SeMet. These results suggest that SeMet may improve glucose tolerance in a NA/STZ-induced mild diabetic mouse model by increasing bioavailability in the pancreas.
authors.affiliation: Faculty of Pharmaceutical Sciences, Setsunan University.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ueno
authors.forename: Ryo
authors.initials: R
authors.lastname: Shimizu
authors.forename: Tomofumi
authors.initials: T
authors.lastname: Okuno
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Ogino
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Arakawa
authors.forename: Fumitoshi
authors.initials: F
authors.lastname: Sakazaki
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Nakamuro
mesh_terms: D000818:Animals; D001682:Biological Availability; D001786:Blood Glucose / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D005951:Glucose Tolerance Test; D005979:Glutathione Peroxidase / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use; D008099:Liver / Q000378:metabolism; D008297:Male; D008813:Mice, Inbred ICR; D009536:Niacinamide; D016566:Organoselenium Compounds / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use; D010179:Pancreas / Q000378:metabolism; D012645:Selenomethionine / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use; D018038:Sodium Selenite / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use; D013311:Streptozocin; D000094765:Glutathione Peroxidase GPX1
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D016566:Organoselenium Compounds; D009536:Niacinamide; D013311:Streptozocin; D012645:Selenomethionine; C008493:methylselenic acid; D005979:Glutathione Peroxidase; D018038:Sodium Selenite; D000094765:Glutathione Peroxidase GPX1; C000722068:Gpx1 protein, mouse