title: Pharmacological inhibition of galectin-1 by lactulose alleviates weight gain in diet-induced obese rats.
abstract: OBJECTIVE
  Galectin-1 (GAL1) is an important member of the lectin family with a carbohydrate recognition domain and has recently been demonstrated to be involved in adipose metabolism. In the present study, we investigated the effects of targeted inhibition of GAL1 by its binding inhibitor lactulose under high fat diet (HFD)-induced obesity.
  
  
  METHODS
  Effects of targeted inhibition of GAL1 by lactulose on lipid metabolism were investigated in vitro and in vivo. Changes in lipogenic capacity in lactulose-treated adipocytes were demonstrated by Oil Red O staining, triglyceride quantification and major adipogenic marker expression patterns. After lactulose treatment in Sprague-Dawley rats, various important body weight parameters, food efficiency, plasma metabolic parameters (glucose, ALT, free fatty acid, triglycerides, leptin, and insulin) and metabolic protein expression patterns were evaluated.
  
  
  RESULTS
  Lactulose treatment reduced adipogenesis and fat accumulation in vitro by down-regulation of major adipogenic transcription factors such as C/EBPα and PPARγ. In vivo treatment of lactulose to 5-week-old Sprague-Dawley male rats significantly alleviated HFD-induced body weight gain and food efficiency as well as improved plasma and other metabolic parameters. In addition, lactulose treatment down-regulated major adipogenic marker proteins (C/EBPα and PPARγ) in adipose tissue as well as stimulated expression of proteins involved in energy expenditure and lipolysis (ATP5B, COXIV, HSL, and CPT1).
  
  
  CONCLUSIONS
  In conclusion, reduced adipogenesis and increased energy expenditure mediated by lactulose treatment synergistically contribute to alleviation of HFD-induced body weight gain. Therefore, pharmaceutical targeting of GAL1 using lactulose would be a novel therapeutic approach for the treatment of obesity.
authors.affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk 712-714, Republic of Korea.
authors.forename: Rajib
authors.initials: R
authors.lastname: Mukherjee
authors.affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk 712-714, Republic of Korea. Electronic address: jwyun@daegu.ac.kr.
authors.forename: Jong Won
authors.initials: JW
authors.lastname: Yun
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D050156:Adipogenesis / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D019440:Anti-Obesity Agents / Q000494:pharmacology / Q000627:therapeutic use; D059305:Diet, High-Fat / Q000009:adverse effects*; D004305:Dose-Response Relationship, Drug; D037483:Galectin 1 / Q000037:antagonists & inhibitors* / Q000097:blood; D007792:Lactulose / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D051379:Mice; D009765:Obesity / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015430:Weight Gain / Q000187:drug effects* / Q000502:physiology
chemical_list: D019440:Anti-Obesity Agents; D037483:Galectin 1; D007792:Lactulose
keywords: Adipogenesis; Adipose tissue; Galectin-1; Lactulose; Obesity