title: Inhibition of adipose tissue PPARγ prevents increased adipocyte expansion after lipectomy and exacerbates a glucose-intolerant phenotype.
abstract: OBJECTIVE
  Adipose tissue plays a fundamental role in glucose homeostasis. For example, fat removal (lipectomy, LipX) in lean mice, resulting in a compensatory 50% increase in total fat mass, is associated with significant improvement in glucose tolerance. This study was designed to further examine the link between fat removal, adipose tissue compensation and glucose homeostasis using a peroxisome proliferator-activated receptor γ (PPAR γ; activator of adipogenesis) knockout mouse.
  
  
  METHODS
  The study involved PPARγ knockout (FKOγ) or control mice (CON), subdivided into groups that received LipX or Sham surgery. We reasoned that as the ability of adipose tissue to expand in response to LipX would be compromised in FKOγ mice, so would improvements in glucose homeostasis.
  
  
  RESULTS
  In CON mice, LipX increased total adipose depot mass (~60%), adipocyte number (~45%) and changed adipocyte distribution to smaller cells. Glucose tolerance was improved (~30%) in LipX CON mice compared to Shams. In FKOγ mice, LipX did not result in any significant changes in adipose depot mass, adipocyte number or distribution. LipX FKOγ mice were also characterized by reduction of glucose tolerance (~30%) compared to shams.
  
  
  CONCLUSIONS
  Inhibition of adipose tissue PPARγ prevented LipX-induced increases in adipocyte expansion and produced a glucose-intolerant phenotype. These data support the notion that adipose tissue expansion is critical to maintain and/or improvement in glucose homeostasis.
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: A D
authors.initials: AD
authors.lastname: Booth
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: A M
authors.initials: AM
authors.lastname: Magnuson
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Cox-York
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Wei
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: D
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Pagliassotti
authors.affiliation: Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, Colorado, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Foster
mesh_terms: D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism; D050156:Adipogenesis / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D005260:Female; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D018149:Glucose Intolerance; D015187:Lipectomy / Q000379:methods; D050356:Lipid Metabolism / Q000502:physiology; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009765:Obesity / Q000378:metabolism*; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*
chemical_list: D047495:PPAR gamma; D005947:Glucose
keywords: PPAR gamma; adipocytes; adipokines; compensation; lipids; proliferation; visceral obesity