Diabetologia

, Volume 44, Issue 10, pp 1268–1273 | Cite as

Fatty acid binding protein expression in different adipose tissue depots from lean and obese individuals

  • R. M. Fisher
  • P. Eriksson
  • J. Hoffstedt
  • G. S. Hotamisligil
  • A. Thörne
  • M. Rydén
  • A. Hamsten
  • P. Arner
Article

Abstract.

Aims/hypothesis:

This study investigated the expression of adipose tissue fatty acid binding proteins (FABPs) in subcutaneous and visceral human adipose tissue depots from lean and obese individuals.

Methods:

Adipocyte lipid binding protein (ALBP) and keratinocyte lipid binding protein (KLBP) expression was quantified by western blot in subcutaneous and omental adipose tissue from 20 obese and 9 lean individuals. RNA expression was quantified by Northern blot in the obese subjects.

Results:

In the obese subjects, ALBP protein and RNA expression was higher in subcutaneous compared with omental adipose tissue (increases of 31 ± 14 % and 40 ± 13 % respectively, both p < 0.05), whereas in the lean group, KLBP protein levels were 32 ± 9 % lower in subcutaneous fat (p < 0.03). However, the ALBP/KLBP ratio was greater in subcutaneous compared to omental adipose tissue from both lean and obese subjects: increases of 187 ± 71 % (p = 0.01) and 52 ± 23 % (p = 0.17) respectively for the protein ratio, and 21 ± 6 % for RNA (p = 0.01, obese individuals). In lean subjects, insulin concentrations correlated positively with the ALBP/KLBP protein ratio in both depots (both p≤ 0.03).

Conclusion/interpretation:

There are regional differences in adipose tissue FABP expression, which could be influenced by obesity. However, the ALBP/KLBP ratio is greater in subcutaneous than visceral adipose tissue in lean as well as in obese subjects. Investigation of adipose tissue FABPs could further our understanding of the role of fatty acids in the insulin resistance syndrome. [Diabetologia (2001) 44: 1268–1273]

Keywords Adipocyte lipid binding protein keratinocyte lipid binding protein adipocyte fatty acid obesity. 

Copyright information

© Springer-Verlag Berlin Heidelberg 2001

Authors and Affiliations

  • R. M. Fisher
    • 1
  • P. Eriksson
    • 1
  • J. Hoffstedt
    • 2
  • G. S. Hotamisligil
    • 4
  • A. Thörne
    • 3
  • M. Rydén
    • 2
  • A. Hamsten
    • 1
  • P. Arner
    • 2
  1. 1.Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institute, Stockholm, SwedenSE
  2. 2.Department of Medicine, Huddinge University Hospital, Karolinska Institute, Stockholm, SwedenSE
  3. 3.Department of Surgery, Huddinge University Hospital, Karolinska Institute, Stockholm, SwedenSE
  4. 4.Department of Nutrition, Harvard School of Public Health, Boston, USAUS

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