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Comment
. 2019 Mar 26;116(13):5852-5854.
doi: 10.1073/pnas.1901970116. Epub 2019 Mar 11.

Unexpected systemic phenotypes result from focal combined deficiencies of forebrain insulin receptor/IGF-1 receptor signaling

Sam Gandy  1   2   3 , Derek M Huffman  4   5
Affiliations
Comment

Unexpected systemic phenotypes result from focal combined deficiencies of forebrain insulin receptor/IGF-1 receptor signaling

Sam Gandy et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Focal forebrain IR/IGF1R DKO eliminates signaling by receptor homodimers and hybrids in hippocampus or central amygdala. (A) Focal forebrain IR/IGF1R DKO eliminates homodimers and IR/IGF1R heterodimers and precludes distinct and collateral insulin, IGF-1, and IGF-2 signaling via these receptors. HR, IR/IGF1R hybrid receptors; IRS, insulin receptor substrate. (B) Targeted DKO in forebrain causes dramatic region-specific phenotypes. Hippo-DKO mice show anxiety, learning behavior deficits, and glucose intolerance, while CeA-DKO mice show defective thermogenesis via a previously unknown pathway linking this brain region to interscapular brown adipose tissue function. (C) Axial human brain magnetic resonance image showing bilateral hippocampi (red) and amygdalae (yellow).
See this image and copyright information in PMC

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