title: Effect of intraperitoneal needling on pancreatic beta-cell cytotoxicity mediated via alloxan in mice with an FVB/N genetic background.
abstract: The present study investigated whether pre-stimulation with intraperitoneal (i.p.) needling protects against development of diabetes in alloxan-treated transgenic (Tg) mice overexpressing the human Cu/Zn superoxide dismutase gene or non-Tg littermates of the FVB/N strain. Twenty minutes before the alloxan treatment (60 mg/kg) the mice were injected intraperitoneally with 0.05 ml saline while control mice received only the alloxan treatment. Hyperglycemic responses of the saline-injected mice to alloxan were significantly suppressed in the Tg mice (P<0.05). A similar reduction of response was also observed in non-Tg littermates, but the effect was less than that in the Tg mice. This protective effect on the diabetogenic action of alloxan was also demonstrated by an analysis of the number of days positive for urinary glucose, and by immunohistochemical analysis of pancreatic insulin-positive cells. A similar suppressive effect on the hyperglycemic response of alloxan was observed in the mice stimulated by i.p. needling alone. However, suppression of the hyperglycemic response was not observed in ICR mice receiving an i.p. injection. These results suggest that the diabetogenic action of alloxan can be suppressed by i.p. needling-mediated stimulation in mice that have a genetic background of the FVB/N strain. Since a slight protective effects of alloxan-induced diabetes was also observed in the Tg mice compared to FVB/N mice treated with only alloxan, this phenomenon could be more clearly seen in the Tg mice than in non-Tg littermates with an FVB/N background.
authors.affiliation: Laboratory of Experimental Animal Science, Nippon Veterinary and Life Science University, Nippon Veterinary and Life Science University, Musashino-shi, Tokyo, Japan.
authors.forename: Hiromi
authors.initials: H
authors.lastname: Amao
authors.forename: Rena
authors.initials: R
authors.lastname: Iwamoto
authors.forename: Yumi
authors.initials: Y
authors.lastname: Komukai
authors.forename: Yuu
authors.initials: Y
authors.lastname: Dobashi
authors.forename: Kimimasa
authors.initials: K
authors.lastname: Takahashi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tohei
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Nakama
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Toyama-Honda
mesh_terms: D015670:Acupuncture Therapy; D000496:Alloxan / Q000633:toxicity; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D003345:Corticosterone / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D015870:Gene Expression / Q000187:drug effects; D006029:Glycosuria / Q000139:chemically induced; D006579:Heterozygote; D007274:Injections, Intraperitoneal; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D000496:Alloxan; D013482:Superoxide Dismutase; D003345:Corticosterone