Skip to main content
. Author manuscript; available in PMC: 2014 Jan 22.
Published in final edited form as: Cell Metab. 2009 Oct;10(4):249–259. doi: 10.1016/j.cmet.2009.08.013

Figure 1. Acute Application of Palmitate induces Leptin Resistance in the CNS.

Figure 1

A Food intake of 10-week-old, overnight fasted male C57/BL6 mice, which were intracerebroventricularly (ICV) injected with either vehicle (BSA) or palmitate at different concentrations (10pmol, 20pmol, 50pmol, and 66pmol), followed by refeeding for 4 hours ad libitum on normal diet.

B Food intake of 10-week-old, overnight fasted male C57/BL6 mice, which were ICV injected with either vehicle (BSA) or palmitate (66pmol) 30 min prior to ICV injection of leptin (500ng) or the respective vehicle (0.9% saline), followed by refeeding for 4 hours ad libitum on normal diet.

C Left panel: Representative western blot analysis of phosphorylated STAT3 and STAT3 (n=3) in dissected arcuate nuclei of 10-week-old, overnight fasted male C57/BL6 mice, which were ICV injected with either vehicle (BSA) or palmitate (66pmol) 30 min prior to ICV injection of leptin (500ng) or the respective vehicle (0.9% saline). Right panel: Densitometrical analysis of phosphorylated STAT3 of Palmitate + Leptin injected mice (n=7) as compared to mice injected with BSA + Leptin (n=6).

Displayed values are means ± S.E.M.; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001.