title: Propionic acid affects immune status and metabolism in adipose tissue from overweight subjects.
abstract: BACKGROUND
  Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short-chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation.
  
  
  METHODS
  Human omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex-ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR.
  
  
  RESULTS
  Treatment of adipose tissue explants with propionic acid results in a significant down-regulation of several inflammatory cytokines and chemokines such as TNF-α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed.
  
  
  CONCLUSIONS
  We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.
authors.affiliation: Top Institute Food and Nutrition, Wageningen, The Netherlands.
authors.forename: Sa'ad
authors.initials: S
authors.lastname: Al-Lahham
authors.forename: Han
authors.initials: H
authors.lastname: Roelofsen
authors.forename: Farhad
authors.initials: F
authors.lastname: Rezaee
authors.forename: Desiree
authors.initials: D
authors.lastname: Weening
authors.forename: Annemieke
authors.initials: A
authors.lastname: Hoek
authors.forename: Roel
authors.initials: R
authors.lastname: Vonk
authors.forename: Koen
authors.initials: K
authors.lastname: Venema
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D009852:Omentum / Q000378:metabolism; D050177:Overweight / Q000276:immunology*; D011422:Propionates / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D016207:Cytokines; D051275:Glucose Transporter Type 4; D011422:Propionates; D012333:RNA, Messenger; C495692:SLC2A4 protein, human; D008071:Lipoprotein Lipase; C029658:propionic acid