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Articles, Behavioral/Systems/Cognitive

The Role of Hypothalamic Mammalian Target of Rapamycin Complex 1 Signaling in Diet-Induced Obesity

Daniela Cota, Emily K. Matter, Stephen C. Woods and Randy J. Seeley
Journal of Neuroscience 9 July 2008, 28 (28) 7202-7208; DOI: https://doi.org/10.1523/JNEUROSCI.1389-08.2008
Daniela Cota
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Emily K. Matter
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Stephen C. Woods
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Randy J. Seeley
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    Figure 1.

    During exposure to an HF diet, leptin is unable to modulate either food intake or hypothalamic mTORC1 signaling. A, B, Effect of intracerebroventricular leptin (10 μg in 2 μl saline) on 24 h food intake (A) and body weight (B) of rats maintained on an HF or LF diet for 3 weeks (mean ± SEM of 4–7 rats used for each treatment group). *p < 0.05 versus saline-treated rats; #p < 0.05 versus HF/leptin-treated rats. C, Intracerebroventricular leptin increases hypothalamic mTORC1 signaling on an LF diet. Representative Western blots from the hypothalami of saline-treated (5) or leptin-treated (5) rats are shown. β-Actin was used as a loading control. D, Quantification by image analysis of hypothalamic STAT3, S6K1, and S6 phosphorylation. Error bars indicate SEM. *p < 0.05, **p < 0.005 versus saline condition. E, Intracerebroventricular leptin does not affect hypothalamic mTORC1 signaling on an HF diet. Representative Western blots from hypothalami of saline-treated (5) or leptin-treated (7) rats are shown. β-Actin was used as a loading control. F, Quantification by image analysis of hypothalamic STAT3, S6K1, and S6 phosphorylation. Error bars indicate SEM. *p < 0.05 versus saline condition.

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    Figure 2.

    S6K1−/− mice do not respond to the anorectic action of leptin. A, S6K1−/− mice, although smaller, have a body composition comparable with WT mice when expressed as a percentage of body weight. Eight S6K1−/− mice and 11 WT were used. B, C, Leptin (5 mg/kg, i.p.) does not affect either food intake (B) or body weight change (C) in S6K1−/− mice. Four to six mice (mean ± SEM) were used for each treatment group. *p < 0.05, ***p < 0.001 versus WT/PBS condition.

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    Figure 3.

    During exposure to an HF diet, CNTFAx15 induces anorexia and increases hypothalamic mTORC1 signaling. A, B, Effect of intracerebroventricular CNTFAx15 (1.5 μg in 2 μl of PBS) on food intake (A) and body weight (B) of rats maintained on an HF or LF diet for 3 weeks. Six to seven rats (mean ± SEM) were used for each treatment group. C, E, Intracerebroventricular CNTFAx15 increases hypothalamic mTORC1 signaling on the LF and HF diets. Representative Western blots from PBS- or CNTFAx15-treated rats are shown. Seven brains were examined in each condition. β-Actin was used as a loading control. D, F, Quantification by image analysis of hypothalamic STAT3, S6K1, and S6 phosphorylation. Error bars indicate SEM. *p < 0.05, **p < 0.005, ***p < 0.001 versus PBS condition.

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    Figure 4.

    The ability of CNTFAx15 to reduce food intake depends on functional S6K1. A, B, CNTFAx15 (0.6 mg/kg, i.p.) does not affect either food intake (A) or body weight change (B) in S6K1−/− mice. Five to seven mice (mean ± SEM) were used for each treatment group. **p < 0.005 versus WT/PBS condition.

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    Figure 5.

    Exposure to an HF diet for either 4 weeks or 1 d dampens hypothalamic S6K1 phosphorylation. A, C, Representative Western blots from animals fed the HF or LF diet. B, D, Quantification by image analysis of hypothalamic S6K1 phosphorylation. Five to seven brains were examined in each condition. β-Actin was used as a loading control. Error bars indicate SEM. *p < 0.05 versus LF.

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The Journal of Neuroscience: 28 (28)
Journal of Neuroscience
Vol. 28, Issue 28
9 Jul 2008
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The Role of Hypothalamic Mammalian Target of Rapamycin Complex 1 Signaling in Diet-Induced Obesity
Daniela Cota, Emily K. Matter, Stephen C. Woods, Randy J. Seeley
Journal of Neuroscience 9 July 2008, 28 (28) 7202-7208; DOI: 10.1523/JNEUROSCI.1389-08.2008

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The Role of Hypothalamic Mammalian Target of Rapamycin Complex 1 Signaling in Diet-Induced Obesity
Daniela Cota, Emily K. Matter, Stephen C. Woods, Randy J. Seeley
Journal of Neuroscience 9 July 2008, 28 (28) 7202-7208; DOI: 10.1523/JNEUROSCI.1389-08.2008
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