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. Author manuscript; available in PMC: 2011 Nov 3.
Published in final edited form as: Cell Metab. 2010 Nov 3;12(5):533–544. doi: 10.1016/j.cmet.2010.09.014

Figure 5. Fatbody-specific inhibition of TOR prevents obesity and heart phenotypes.

Figure 5

A) Changes in TG content of wt and fatbody-specific (lsp-Gal4) expression of TSC1-2 (n=36), S6KDN (n=36), 4EBP (n=34), FOXO (n=48), Bmm (n=36) and FAS-RNAi (n=34). wt flies show a significant increase in TGs while all of the other flies show no significant increase in TG levels after 5 days on 30% HFD. B) Bar graph of relative change in heart dysfunction for fatbody-specific (lsp-Gal4) expression of TSC1-2 (n= 24), S6KDN (n=36), 4EBP (n=24), UAS-FOXO (n=36), UAS-Bmm (n=36) and UAS-FAS-RNAi (n=24). Only FAS-RNAi had a moderate increase in the severity of all 3 cardiac dysfunction phenotypes (see C) when compared to the same genotype under HFD. C) Side Bar graph of individual aberrant heart phenotypes for wt and fatbody-specific expression of TSC1-2, S6KDN, 4EBP, FOXO; FAS-RNAi and Bmm. Only FAS-RNAi had a moderate increase in heart abnormalities under a HFDA minimum of 24 individual fly heart movies were analysed for each genotype and diet variation.