title: Transplantation of non-visceral fat to the visceral cavity improves glucose tolerance in mice: investigation of hepatic lipids and insulin sensitivity.
abstract: OBJECTIVE
  Intra-abdominal transplantation of non-visceral adipose tissue in rodents, simulating increased abdominal fat in obesity, paradoxically improves glucose tolerance and insulin sensitivity. We hypothesised that this improvement is due to transplant-induced enhanced uptake of fatty acids by adipose tissue, thus reducing fatty acid flux into, and triacylglycerol storage in, the liver.
  
  
  METHODS
  In Experiment 1, mice were sham-operated or received heterologous epididymal white adipose tissue (WAT; EWAT) or visceral WAT (VWAT) transplantation to the portal and splanchnic circulation regions in the visceral cavity. In Experiment 2, inguinal WAT (IWAT) or EWAT was removed and subsequently transplanted to the visceral cavity of the same mouse (autotransplant). IWAT and EWAT autotransplants were repeated in Experiment 3 and compared with heterotransplants.
  
  
  RESULTS
  Heterotransplantation of VWAT did not alter glucose tolerance, whereas auto- or hetero-transplantation of EWAT or IWAT significantly improved glucose tolerance. Transplantation-induced improvements in glucose tolerance 4 weeks after surgery coincided with decreased liver triacylglycerol, decreased portal plasma lipids and increased hepatic insulin sensitivity. By 8 weeks, these changes were apparent only in mice with autotransplantation. Heterologous EWAT transplantation-induced glucose improvement persisted without altered liver metabolism.
  
  
  CONCLUSIONS
  Increases in visceral fat, via transplantation of visceral or non-visceral adipose tissue, is not a major risk factor for glucose intolerance. In fact, there are dynamic metabolic improvements following transplantation that include decreased portal lipids and improved liver metabolism, but these improvements are transient under certain circumstances.
authors.affiliation: Obesity Research Center, Department of Psychiatry, University of Cincinnati, 2170 E. Galbraith Road, Cincinnati, OH 45237, USA. Michelle.Foster@uc.edu
authors.forename: M T
authors.initials: MT
authors.lastname: Foster
authors.forename: H
authors.initials: H
authors.lastname: Shi
authors.forename: S
authors.initials: S
authors.lastname: Softic
authors.forename: R
authors.initials: R
authors.lastname: Kohli
authors.forename: R J
authors.initials: RJ
authors.lastname: Seeley
authors.forename: S C
authors.initials: SC
authors.lastname: Woods
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism / Q000473:pathology / Q000637:transplantation; D000818:Animals; D004195:Disease Models, Animal; D004822:Epididymis; D018149:Glucose Intolerance / Q000209:etiology* / Q000517:prevention & control; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology / Q000637:transplantation; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D056128:Obesity, Abdominal / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010537:Peritoneum / Q000601:surgery; D011994:Recombinant Proteins / Q000378:metabolism; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous
chemical_list: D008055:Lipids; D011994:Recombinant Proteins; C485184:enhanced green fluorescent protein; D049452:Green Fluorescent Proteins