title: Reduction of incretin-like salivatin in saliva from patients with type 2 diabetes and in parotid glands of streptozotocin-diabetic BALB/c mice.
abstract: OBJECTIVE
  Diabetic xerostomia is a typical syndrome in diabetic complication. We have reported that salivatin (salivary peptide P-C) derived from human saliva potentiates glucose-stimulated insulin release and inhibits arginine-stimulated glucagon release. The present study is aimed to gain further evidence on the physiological role by investigating the diabetic state-induced change in the amount of salivatin.
  
  
  METHODS
  The amount of salivatin was measured in saliva taken from patients with type 2 diabetes with ELISA and with rabbit antiserum against human salivatin immunocytochemically in sections of parotid glands from streptozotocin-diabetic BALB/c mice.
  
  
  RESULTS
  The amount of salivatin after a meal was reduced by diabetes in both human saliva and in the serous secretory granule of mouse parotid gland acinar cells.
  
  
  CONCLUSIONS
  The above results suggest that salivatin lowers hyperglycaemia after meal and sustains the normal blood glucose levels by incretin-like mechanisms. The function may be damaged by diabetes, and this in turn might make the diabetes worse.
authors.affiliation: Department of Clinical Pharmacology, Graduate School of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan. ikukokim@ms.toyama-mpu.ac.jp
authors.forename: I
authors.initials: I
authors.lastname: Kimura
authors.forename: H
authors.initials: H
authors.lastname: Sasamoto
authors.forename: T
authors.initials: T
authors.lastname: Sasamura
authors.forename: Y
authors.initials: Y
authors.lastname: Sugihara
authors.forename: S
authors.initials: S
authors.lastname: Ohgaku
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism*; D004435:Eating; D004797:Enzyme-Linked Immunosorbent Assay; D005934:Glucagon; D052216:Glucagon-Like Peptide 1; D004763:Glucagon-Like Peptides; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016253:Microscopy, Immunoelectron; D010306:Parotid Gland / Q000473:pathology / Q000648:ultrastructure; D010446:Peptide Fragments / Q000378:metabolism; D010455:Peptides / Q000032:analysis / Q000378:metabolism*; D019518:Postprandial Period; D055232:Proline-Rich Protein Domains; D012463:Saliva / Q000737:chemistry*; D055273:Salivary Proline-Rich Proteins
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D010446:Peptide Fragments; D010455:Peptides; D055273:Salivary Proline-Rich Proteins; C524743:salivary peptide P-C; C055453:glucagon-like peptide 1 (7-36)amide; D004763:Glucagon-Like Peptides; D052216:Glucagon-Like Peptide 1; D005934:Glucagon