title: Ghrelin upregulates PepT1 activity in the small intestine epithelium of rats with sepsis.
abstract: BACKGROUND
  Sepsis causes nutritional substrate malabsorption; hence, preventing gut barrier problems and improving the nutritional status in sepsis is a compelling issue.
  
  
  OBJECTIVE
  We tested whether ghrelin administration affects peptide transporter 1 (PepT1) activity in the intestinal epithelium of rats with sepsis.
  
  
  METHODS
  Sixty male Sprague-Dawley rats were randomly divided into sham-operated, sepsis, and ghrelin-treated groups. The cecum of sham-operated rats was separated after laparotomy without ligation and perforation. Sepsis group rats underwent cecal ligation and puncture (CLP). Mucosal specimens were used for immunohistochemstry, real-time PCR, and western blotting to detect PepT1 distribution, and mRNA and protein expression levels, respectively. TNF-α, IL-1β, and ghrelin levels were estimated in serum and intestinal mucosal tissue by ELISA. High-performance liquid chromatography was used to measure PepT1 uptake by the epithelial cells. Moreover, survival, body weight, and food intake of the rats were recorded during the 7-day treatment period.
  
  
  RESULTS
  All rats in the sham-operated group survived, and 80% of rats in the sepsis group died within 7d of CLP. Treatment with ghrelin attenuated the CLP-induced body weight loss, intestine mucosa damage, and the survival rate was better. In addition, ghrelin attenuated increases in TNF-α and IL-1β production. The expressions of PepT1 mRNA and protein were higher in ghrelin-treated group rats than in sepsis rats. Moreover, the uptake function of PepT1 was better in ghrelin-treated group rats.
  
  
  CONCLUSIONS
  Ghrelin treatment can reduce the inflammatory response and greatly upregulate the physiological function of PepT1 in intestinal epithelial cells of rats with sepsis.
authors.affiliation: Intensive Care Unit, Zhejiang Provincial People's Hospital, NO. 158, Shangtang Road, Hangzhou 310014, China. Electronic address: liujqaticu@163.com.
authors.forename: Jingquan
authors.initials: J
authors.lastname: Liu
authors.affiliation: Intensive Care Unit, Yanpu Hospital, Tongji University, NO. 450, Tengyue Road, Shanghai 200090, China. Electronic address: joysb1969@sina.com.
authors.forename: Bin
authors.initials: B
authors.lastname: Shi
authors.affiliation: Department of Respiratory Medicine, The Affiliated Hospital of Hangzhou Normal University, The 2nd People's Hospital of Hangzhou, Hangzhou 310014, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Shi
authors.affiliation: Department of General Intensive Care Unit, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Guoguang
authors.initials: G
authors.lastname: Ma
authors.affiliation: Department of General Intensive Care Unit, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Hongze
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Central Laboratory, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Lou
authors.affiliation: Department of General Intensive Care Unit, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Hongxiang
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of General Intensive Care Unit, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Shengxia
authors.initials: S
authors.lastname: Wan
authors.affiliation: Department of Central Laboratory, Songjiang Hospital Affiliated First People's Hospital, Shanghai Jiao Tong University, NO. 746, Zhongshan Road, Shanghai 201600, China.
authors.forename: Dongyu
authors.initials: D
authors.lastname: Liang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D054439:Ghrelin / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000378:metabolism*; D008026:Ligation / Q000379:methods; D008297:Male; D000074011:Peptide Transporter 1; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000378:metabolism*; D027981:Symporters / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D054439:Ghrelin; D053583:Interleukin-1beta; D000074011:Peptide Transporter 1; D012333:RNA, Messenger; C489940:Slc15a1 protein, rat; D027981:Symporters; D014409:Tumor Necrosis Factor-alpha
keywords: Cecal ligation and puncture; Ghrelin; Inflammatory response; PepT1; Sepsis