title: Turnover of acinar and islet cells in the pancreas of monosodium glutamate-treated obese mice.
abstract: OBJECTIVE
  Subcutaneous administrations of monosodium glutamate (MSG) to neonatal animals result in obesity and induce the toxicity on the central nervous system, and furthermore, have an effect on entero-pancreatic hormone. The effect of MSG on the cell turnover of organs, especially the pancreas, has received little attention until now. This study was designed to examine the effect of MSG on pancreatic cell turnover by immunohistochemistry and [(3)H]thymidine autoradiography.
  
  
  METHODS
  Male JcI-ICR strain mice were SC injected with MSG (2 mg/g body weight daily) for 5 days after birth, received 112 repeated injections of [(3)H]thymidine at 6-hour intervals for 28 days after birth, and then were killed immediately thereafter, or 30, 60, or 120 days after the last injection. Autoradiography was performed on sections immunostained for glucagon, insulin, and somatostatin.
  
  
  RESULTS
  After continuous labeling, most pancreatic cells were labeled, and thereafter, labeling of cells decreased in control and MSG-treated mice. The mean grain counts of acinar cells in MSG-treated mice decreased more slowly than those in control mice. On the other hand, those of islet cells, including glucagon, insulin, and somatostatin cells, decreased more rapidly in MSG-treated mice than those in control mice.
  
  
  CONCLUSIONS
  Cell turnover of acinar cells was decelerated and that of islet cells including glucagon, insulin, and somatostatin cells was accelerated in MSG-treated mice pancreas. MSG-induced hypothalamic lesions exert the contrary influences on the cell turnover of acinar and islet cells.
authors.affiliation: Fourth Department of Internal Medicine, Tokyo Medical University, Tokyo, Japan.
authors.forename: Daiju
authors.initials: D
authors.lastname: Nakayama
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Magami
authors.forename: Takeshi
authors.initials: T
authors.lastname: Azuma
authors.forename: Hideto
authors.initials: H
authors.lastname: Inokuchi
authors.forename: Masaya
authors.initials: M
authors.lastname: Furukawa
authors.forename: Junko
authors.initials: J
authors.lastname: Ohyashiki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Yoshimoto
authors.forename: Junichiro
authors.initials: J
authors.lastname: Mizuguchi
authors.forename: Fuminori
authors.initials: F
authors.lastname: Moriyasu
authors.forename: Keiichi
authors.initials: K
authors.lastname: Kawai
authors.forename: Takanori
authors.initials: T
authors.lastname: Hattori
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002455:Cell Division; D005934:Glucagon / Q000032:analysis; D007150:Immunohistochemistry; D007328:Insulin / Q000032:analysis; D007515:Islets of Langerhans / Q000473:pathology*; D007700:Kinetics; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009765:Obesity / Q000139:chemically induced* / Q000473:pathology*; D010179:Pancreas / Q000737:chemistry / Q000473:pathology*; D012970:Sodium Glutamate / Q000008:administration & dosage*; D013004:Somatostatin / Q000032:analysis; D014316:Tritium
chemical_list: D007328:Insulin; D014316:Tritium; D013004:Somatostatin; D005934:Glucagon; D012970:Sodium Glutamate