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Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling

Author

Listed:
  • Jeremie Boucher

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • Marcelo A. Mori

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School
    Present addresses: Department of Biophysics. Federal University of São Paulo. São Paulo, Brazil (M.A.M.).)

  • Kevin Y. Lee

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • Graham Smyth

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • Chong Wee Liew

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • Yazmin Macotela

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School
    Present addresses: Instituto de Neurobiología, Universidad Nacional Autonoma de Mexico, Queretaro 76230, Mexico (Y.M.).)

  • Michael Rourk

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • Matthias Bluher

    (University of Leipzig)

  • Steven J. Russell

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

  • C. Ronald Kahn

    (Section on Integrative Physiology and Metabolism, Brigham and Women's Hospital and Harvard Medical School)

Abstract

Insulin and insulin-like growth factor 1 (IGF-1) have important roles in adipocyte differentiation, glucose tolerance and insulin sensitivity. Here to assess how these pathways can compensate for each other, we created mice with a double tissue-specific knockout of insulin and IGF-1 receptors to eliminate all insulin/IGF-1 signalling in fat. These FIGIRKO mice had markedly decreased white and brown fat mass and were completely resistant to high fat diet-induced obesity and age- and high fat diet-induced glucose intolerance. Energy expenditure was increased in FIGIRKO mice despite a >85% reduction in brown fat mass. However, FIGIRKO mice were unable to maintain body temperature when placed at 4 °C. Brown fat activity was markedly decreased in FIGIRKO mice but was responsive to β3-receptor stimulation. Thus, insulin/IGF-1 signalling has a crucial role in the control of brown and white fat development, and, when disrupted, leads to defective thermogenesis and a paradoxical increase in basal metabolic rate.

Suggested Citation

  • Jeremie Boucher & Marcelo A. Mori & Kevin Y. Lee & Graham Smyth & Chong Wee Liew & Yazmin Macotela & Michael Rourk & Matthias Bluher & Steven J. Russell & C. Ronald Kahn, 2012. "Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling," Nature Communications, Nature, vol. 3(1), pages 1-11, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1905
    DOI: 10.1038/ncomms1905
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    Cited by:

    1. Masaji Sakaguchi & Shota Okagawa & Yuma Okubo & Yuri Otsuka & Kazuki Fukuda & Motoyuki Igata & Tatsuya Kondo & Yoshifumi Sato & Tatsuya Yoshizawa & Takaichi Fukuda & Kazuya Yamagata & Weikang Cai & Yu, 2022. "Phosphatase protector alpha4 (α4) is involved in adipocyte maintenance and mitochondrial homeostasis through regulation of insulin signaling," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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