title: Most of the interleukin 1 receptor antagonist, cathepsin S, macrophage migration inhibitory factor, nerve growth factor, and interleukin 18 release by explants of human adipose tissue is by the non-fat cells, not by the adipocytes.
abstract: The present studies were designed to compare the relative release of interleukin 1 receptor antagonist (IL-1Ra), cathepsin S, macrophage migration inhibitory factor (MIF), nerve growth factor (NGF), and interleukin 18 (IL-18) by adipocytes as compared with the non-fat cells present in subcutaneous and omental adipose tissue from morbidly obese gastric bypass patients as compared with obese abdominoplasty patients. The release of IL-1Ra, cathepsin S, and MIF by explants of human adipose tissue incubated for 48 hours averaged 6, 9, and 19 pmol/g, respectively, and was far greater than the release of NGF (0.05 pmol/g) or IL-18 (0.006 pmol/g). The release by human adipocytes of IL-1Ra, cathepsin S, and MIF was 0.13, 0.32, and 2.6 pmol/g, respectively, over 48 hours, whereas NGF release was 0.003 and IL-18 0.001 pmol/g. Only the total release of MIF by human adipose tissue explants was enhanced, whereas that of IL-18 was significantly reduced in explants from morbidly obese women. Most of (55%-73%) the release of IL-1Ra, cathepsin S, MIF, NGF, and IL-18 was by the adipose tissue matrix, whereas release by stromal-vascular (SV) cells was 3% to 28% of total release over 48 hours by the adipose tissue matrix, SV cells and adipocytes. The release of NGF by adipocytes was 42%, that of MIF was 27%, and for the other factors 15% or less of release over 48 hours by the adipose tissue matrix, SV cells, and adipocytes. Our results suggest that the non-fat cells in human adipose tissue contribute to most of the release of NGF, IL-18, IL-1Ra, cathepsin S, and MIF seen during primary culture of adipose tissue explants from obese women.
authors.affiliation: Department of Molecular Sciences, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. jfain@utmem.edu
authors.forename: John N
authors.initials: JN
authors.lastname: Fain
authors.forename: David S
authors.initials: DS
authors.lastname: Tichansky
authors.forename: Atul K
authors.initials: AK
authors.lastname: Madan
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism; D017667:Adipocytes / Q000378:metabolism*; D000273:Adipose Tissue / Q000166:cytology / Q000378:metabolism*; D000328:Adult; D001808:Blood Vessels / Q000166:cytology / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D002403:Cathepsins / Q000378:metabolism*; D004247:DNA / Q000096:biosynthesis; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D020382:Interleukin-18 / Q000378:metabolism*; D050356:Lipid Metabolism; D008263:Macrophage Migration-Inhibitory Factors / Q000378:metabolism*; D008875:Middle Aged; D020932:Nerve Growth Factor / Q000378:metabolism*; D009924:Organ Culture Techniques; D012313:RNA / Q000096:biosynthesis; D012795:Sialoglycoproteins / Q000378:metabolism*; D017154:Stromal Cells / Q000378:metabolism
chemical_list: C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D020382:Interleukin-18; D008263:Macrophage Migration-Inhibitory Factors; D012795:Sialoglycoproteins; D012313:RNA; D004247:DNA; D020932:Nerve Growth Factor; D002403:Cathepsins; C028217:cathepsin S