title: Duodenal-jejunal bypass improves diabetes and liver steatosis via enhanced glucagon-like peptide-1 elicited by bile acids.
abstract: OBJECTIVE
  Bariatric surgery not only elicits weight loss but also rapidly resolves diabetes. However, the mechanisms remain unclear. The present study investigates how diabetes and liver steatosis are improved after duodenal-jejunal bypass (DJB) compared with a glucagon-like peptide-1 (GLP-1) analog and correlations between bile acids and GLP-1 secretion.
  
  
  METHODS
  We initially determined the effects of bile acids on GLP-1 in vitro and then assigned 12 male 16-week-old Otsuka Long-Evans Tokushima Fatty rats to groups that underwent DJB, a sham operation, or were treated with the GLP-1 receptor agonist, liraglutide (n = 4 each). Blood glucose, insulin, GLP-1, serum bile acids, liver steatosis, and the number of GLP-1 positive cells (L cells) in the small intestine and colon were investigated in the three groups at eight weeks postoperatively.
  
  
  RESULTS
  Levels of GLP-1mRNA were upregulated and GLP-1 secretion increased in cells incubated with bile acids in vitro. Weight gain was suppressed more in the DJB than in the sham group in vivo. Diabetes was more improved and GLP-1 levels were significantly higher in the DJB than in the sham group. Serum bile acids were significantly increased, the number of L cells in the ileum was upregulated compared with the sham group, and liver steatosis was significantly improved in the DJB compared with the other two groups.
  
  
  CONCLUSIONS
  Duodenal-jejunal bypass might improve diabetes and liver steatosis by enhancing GLP-1 secretion through increasing serum bile acids and the proliferation of L cells in the ileum, compared with liraglutide.
authors.affiliation: Department of Surgery, Institute of Health Biosciences, University of Tokushima, Tokushima, Japan.
authors.forename: Hideya
authors.initials: H
authors.lastname: Kashihara
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Shimada
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Kurita
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Sato
authors.forename: Kozo
authors.initials: K
authors.lastname: Yoshikawa
authors.forename: Jun
authors.initials: J
authors.lastname: Higashijima
authors.forename: Motoya
authors.initials: M
authors.lastname: Chikakiyo
authors.forename: Masaaki
authors.initials: M
authors.lastname: Nishi
authors.forename: Chie
authors.initials: C
authors.lastname: Takasu
mesh_terms: D000818:Animals; D050110:Bariatric Surgery / Q000379:methods*; D001647:Bile Acids and Salts / Q000097:blood / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000628:therapy*; D019858:Enteroendocrine Cells / Q000166:cytology; D005234:Fatty Liver / Q000378:metabolism* / Q000628:therapy*; D052216:Glucagon-Like Peptide 1 / Q000235:genetics / Q000378:metabolism*; D007082:Ileum / Q000166:cytology; D008297:Male; D051379:Mice; D012333:RNA, Messenger / Q000378:metabolism; D020318:Rats, Long-Evans; D015854:Up-Regulation
chemical_list: D001647:Bile Acids and Salts; D012333:RNA, Messenger; D052216:Glucagon-Like Peptide 1
keywords: bariatric surgery; gastrointestinal hormone; incretin; liraglutide