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Obes Surg. 2009 Nov;19(11):1564-73. doi: 10.1007/s11695-009-9949-9. Epub 2009 Aug 27.

Differential intra-abdominal adipose tissue profiling in obese, insulin-resistant women.

Author information

1
Division of Endocrinology, Department of Medicine, Stanford University Medical Center, 300 Pasteur Drive Rm S-025, Stanford, CA 94305, USA. aliceliu@stanford.edu

Abstract

BACKGROUND:

We recently identified differences in abdominal subcutaneous adipose tissue (SAT) from insulin-resistant (IR) as compared to obesity-matched insulin sensitive individuals, including accumulation of small adipose cells, decreased expression of cell differentiation markers, and increased inflammatory activity. This study was initiated to see if these changes in SAT of IR individuals were present in omental visceral adipose tissue (VAT); in this instance, individuals were chosen to be IR but varied in degree of adiposity. We compared cell size distribution and genetic markers in SAT and VAT of IR individuals undergoing bariatric surgery.

METHODS:

Eleven obese/morbidly obese women were IR by the insulin suppression test. Adipose tissue surgical samples were fixed in osmium tetroxide for cell size analysis via Beckman Coulter Multisizer. Quantitative real-time polymerase chain reaction for genes related to adipocyte differentiation and inflammation was performed.

RESULTS:

While proportion of small cells and expression of adipocyte differentiation genes did not differ between depots, inflammatory genes were upregulated in VAT. Diameter of SAT large cells correlated highly with increasing proportion of small cells in both SAT and VAT (r = 0.85, p = 0.001; r = 0.72, p = 0.01, respectively). No associations were observed between VAT large cells and cell size variables in either depot. The effect of body mass index (BMI) on any variables in both depots was negligible.

CONCLUSIONS:

The major differential property of VAT of IR women is increased inflammatory activity, independent of BMI. The association of SAT adipocyte hypertrophy with hyperplasia in both depots suggests a primary role SAT may have in regulating regional fat storage.

PMID:
19711137
PMCID:
PMC3181138
DOI:
10.1007/s11695-009-9949-9
[Indexed for MEDLINE]
Free PMC Article

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