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:
- Shota Okagawa & Masaji Sakaguchi & Yuma Okubo & Yuri Takekuma & Motoyuki Igata & Tatsuya Kondo & Naoki Takeda & Kimi Araki & Bruna Brasil Brandao & Wei-Jun Qian & Yu-Hua Tseng & Rohit N. Kulkarni & Na, 2024.
"Hepatic SerpinA1 improves energy and glucose metabolism through regulation of preadipocyte proliferation and UCP1 expression,"
Nature Communications, Nature, vol. 15(1), pages 1-19, December.
- 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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