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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: Nat Med. 2010 Aug 29;16(9):1001–1008. doi: 10.1038/nm.2207

Figure 5. Effects of inactivation of hypothalamic de novo lipogenesis.

Figure 5

(a–d) Body weight change (left panel) and daily food intake (right panel) (a), hypothalamic malonyl-CoA levels (b) and Ucp1 and Ucp3 mRNA in the BAT (c) of hyperthyroid (and euthyroid when indicated) rats treated with vehicle or TOFA. (d–f) Body weight change (left panel) daily food intake (right panel) (d), hypothalamic malonyl-CoA levels (e) and Ucp1 and Ucp3 mRNA and in the BAT (f) of hyperthyroid (and euthyroid when indicated) rats treated with vehicle or AICAR. (g–i) Malonyl-CoA levels in the ventral hypothalamus (g) body weight change (left panel), food intake (right panel) (h) and mRNA expression profiles in BAT (i) of hyperthyroid (or euthyroid when indicated) rats stereotaxically treated with a GFP-expressing adenoviruses or GFP plus AMPK constitutively active (AMPKα-CA) adenoviruses into the VMH. *P < 0.05, **P < 0.01, ***P < 0.001 vs. vehicle or GFP; ###P < 0.01 hyperthyroid vehicle vs. hyperthyroid TOFA or AICAR and hyperthyroid GFP vs. hyperthyroid AMPKα-CA; all data are expressed as mean ± SEM.