title: Treatment for hyperglycemia promotes pancreatic regeneration in rats without CCK-1 receptor gene expression.
abstract: OBJECTIVE
  Recent studies have suggested that CCK is not essential for normal pancreatic growth in mice. We examined whether the treatment of hyperglycemia participates in a non-CCK-1-receptor-mediated mechanism of pancreatic regeneration after partial (30%) pancreatectomy (Px) with use of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model for type 2 diabetes mellitus without CCK-1 receptor gene expression.
  
  
  METHODS
  Male OLETF rats were divided into five groups at 24 weeks of age. The first group was killed to examine the pancreas at 24 weeks of age (PrePx). The second group underwent a midline laparotomy and received a standard rat chow (ShamPx). The remaining three groups of rats received one of the following three treatments after Px: a standard rat chow (PxC), a diet containing acarbose (PxA), or a standard rat chow and once-daily subcutaneous injection of insulin (PxI) for 8 weeks.
  
  
  RESULTS
  PxC rats had significantly higher serum glucose levels than did PxA and PxI rats. Pancreatic weight and pancreatic contents of protein in PxA and PxI rats were significantly higher than in PxC rats. The pancreas in PxC rats was atrophic, and marked inflammatory cell infiltration was observed in the pancreas. In addition, tumor necrosis factor-alpha (TNFalpha) was expressed in the inflammatory cells, acinar cells, and islets in PxC rats. However, histologic alterations, including expression of TNFalpha, remained at a minimum in PxA and PxI rats.
  
  
  CONCLUSIONS
  We conclude that the control of serum glucose levels plays an important role in preventing pancreatic atrophy and participates in the non-CCK-1-receptor-mediated mechanisms of pancreatic growth in rats.
authors.affiliation: Third Department of Internal Medicine, University of Occupational and Environmental Health-Japan School of Medicine, Kitakyushu, Japan.
authors.forename: Mitsuyoshi
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Dong-Mei
authors.initials: DM
authors.lastname: Jia
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Fukumitsu
authors.forename: Makoto
authors.initials: M
authors.lastname: Otsuki
mesh_terms: D020909:Acarbose / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015870:Gene Expression; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007150:Immunohistochemistry; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010179:Pancreas / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery; D010180:Pancreatectomy / Q000379:methods; D051381:Rats; D020334:Rats, Inbred OLETF; D043886:Receptor, Cholecystokinin A / Q000172:deficiency* / Q000235:genetics; D012038:Regeneration / Q000187:drug effects*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D043886:Receptor, Cholecystokinin A; D014409:Tumor Necrosis Factor-alpha; D020909:Acarbose