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

Jeremie Boucher, Marcelo A. Mori, Kevin Y. Lee, Graham Smyth, Chong Wee Liew, Yazmin Macotela, Michael Rourk, Matthias Bluher, Steven J. Russell and C. Ronald Kahn ()
Additional contact information
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
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
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

Nature Communications, 2012, vol. 3, issue 1, 1-11

Abstract: 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.

Date: 2012
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms1905 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1905

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms1905

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().