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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding

G S Hotamisligil1, R S Johnson, R J Distel

  • 1Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. CA 92093, USA.

Science (New York, N.Y.)
|November 22, 1996
PubMed

Insights

Mice lacking the adipocyte fatty acid binding protein (aP2) remained healthy despite obesity, suggesting aP2 is key in linking obesity to insulin resistance and diabetes.

Area of Science:

  • Biochemistry
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Fatty acid binding proteins (FABPs) are small cytoplasmic proteins binding fatty acids.
  • FABPs exhibit tissue-specific expression patterns.
  • Adipocyte FABP (aP2) plays a role in fatty acid metabolism.

Purpose of the Study:

  • To investigate the role of aP2 in the development of obesity-related insulin resistance.
  • To determine if aP2 deficiency impacts metabolic responses to a high-fat diet.
  • To explore the link between aP2, fatty acid metabolism, and inflammatory markers in obesity.

Main Methods:

  • Generation and characterization of mice with a null mutation in the aP2 gene (aP2-/-).
  • Feeding wild-type and aP2-/- mice a high-fat diet to induce obesity.
  • Assessment of metabolic parameters including insulin sensitivity and glucose tolerance.
  • Measurement of adipose tissue gene expression, including tumor necrosis factor-alpha (TNF-alpha).

Main Results:

  • aP2-deficient mice were developmentally and metabolically normal.
  • Obese aP2-/- mice did not develop insulin resistance or diabetes, unlike obese wild-type controls.
  • Obese aP2-/- mice failed to express TNF-alpha in adipose tissue, a molecule linked to insulin resistance.

Conclusions:

  • aP2 is a critical mediator in the pathway connecting obesity to insulin resistance.
  • aP2 may link fatty acid metabolism to the expression of TNF-alpha in adipose tissue.
  • Targeting aP2 could offer a novel therapeutic strategy for preventing obesity-related metabolic dysfunction.

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