Tuberous sclerosis and insulin resistance. Unlikely bedfellows reveal a TORrid affair - PubMed (original) (raw)

Review

doi: 10.4161/cc.4.1.1343. Epub 2005 Jan 3.

Affiliations

• PMID: 15611656
• DOI: 10.4161/cc.4.1.1343

Review

Tuberous sclerosis and insulin resistance. Unlikely bedfellows reveal a TORrid affair

O Jameel Shah et al. Cell Cycle. 2005 Jan.

Abstract

The TSC1-TSC2 tumor suppressor complex serves as an interface between insulin and nutrient signaling pathways and the cell growth machinery. Recent work has indicated that the TSC1-TSC2 complex plays a role in the pathobiology of a number of tumor predisposition syndromes, including tuberous sclerosis (TSC1/2), Peutz-Jeghers syndrome (LKB1), and Cowden's syndrome (PTEN), in which the TSC/Rheb/mTOR axis is inappropriately active secondary to loss of tumor suppressor function. Recent work has demonstrated that TSC deficiency imposes a negative autoregulatory loop that suppresses insulin signaling at the post-receptor level, effectively resulting in cell autonomous insulin resistance. Exploitation of this insulin signaling deficiency may hold promise among tailored clinical therapies designed to manage tuberous sclerosis.

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