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Results: 5

1.
Fig. 1.

Fig. 1. From: Sirt1 protects against high-fat diet-induced metabolic damage.

Generation of a BAC-based transgenic Sirt1 mouse line. (A) Scheme of the Bacterial Artificial Chromosome (BAC) used to generate the Sirt1-tg mouse strain. (B) Levels of Sirt1 mRNA (Upper) and Sirt1 protein (Lower) in mouse embryo fibroblasts. (C) Levels of Sirt1 protein in the indicated tissues.

Paul T. Pfluger, et al. Proc Natl Acad Sci U S A. 2008 July 15;105(28):9793-9798.
2.
Fig. 2.

Fig. 2. From: Sirt1 protects against high-fat diet-induced metabolic damage.

Energy homeostasis of transgenic Sirt1 mice. (A) Body weight of wild type (WT) or transgenic (tg) Sirt1 mice during exposure to a standard chow diet (SD) or a high-fat diet (HFD). (B) Food intake. (C) Fat mass in WT and tg mice after 19 weeks of exposure to SD or HFD. (D) Lean mass. (E and F) Energy expenditure per kg of body weight after 8 weeks of SD or HFD: 5-day measurements in SD mice (E Left) or HFD mice (E Right), and total mean values (F). n = 7–8 per group; means ± SEM; *, P < 0.05.

Paul T. Pfluger, et al. Proc Natl Acad Sci U S A. 2008 July 15;105(28):9793-9798.
3.
Fig. 4.

Fig. 4. From: Sirt1 protects against high-fat diet-induced metabolic damage.

Transgenic Sirt1 mice are protected from HFD-induced hepatic glucose intolerance. (A) Glucose tolerance test (GTT) after 7 weeks of diet exposure by using an i.p. dose of 2 g of glucose per kg of body weight. (B) Pyruvate tolerance test (PTT) after 16 weeks of diet exposure by using 2 g of pyruvate per kg of body weight. (C) Insulin tolerance test (ITT) after 13 weeks of diet exposure by using 0.75 IU/kg insulin. Curves of glucose levels (Left) and values of the area under the curve (Right). n = 7–8 per group; means ± SEM; *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Paul T. Pfluger, et al. Proc Natl Acad Sci U S A. 2008 July 15;105(28):9793-9798.
4.
Fig. 3.

Fig. 3. From: Sirt1 protects against high-fat diet-induced metabolic damage.

Transgenic Sirt1 mice are protected from HFD-induced hepatosteatosis. (A) Oil red staining lipid droplets in frozen liver sections (3 per group) from both wild-type (WT) or transgenic (tg) mice on a standard diet (SD) or after high-fat diet (HFD) exposure for 19 weeks. (Scale bars, 50 μm.) (B) Gene expression analysis (real-time PCR) of hepatic Sirt1 and the transcription factor SREBP1c. n = 7–8 per group; means ± SEM; *, P < 0.05; ***, P < 0.001.

Paul T. Pfluger, et al. Proc Natl Acad Sci U S A. 2008 July 15;105(28):9793-9798.
5.
Fig. 5.

Fig. 5. From: Sirt1 protects against high-fat diet-induced metabolic damage.

Transgenic Sirt1 mice are protected from hepatic inflammation. (A) Gene expression analyses (real-time PCR) of the proinflammatory cytokines IL-6 and TNFα in livers of WT and tg mice on SD or HFD (19 weeks) (n = 7–8 per group; means ± SEM; *, P < 0.05). (B) Kaplan–Meier plot of survival curves of WT and tg mice on SD after injection of lipopolysaccharide (LPS) (n = 5 per group). (C) Luciferase reporter gene assay of WT and tg mouse embryonic fibroblasts after transfection with a pNFκB-Luc reporter vector and stimulation with 10 ng/ml of TNFα. Luminescence was measured 6 h after TNFα incubation. (n = 6–8 per group; means ± SEM; *, P < 0.05). (D) Gene expression analyses (real-time PCR) of the antioxidant proteins MnSOD and Nrf1 in livers of WT and tg mice on SD or HFD (19 weeks) (n = 7–8 per group; means ± SEM; *, P < 0.05; **, P < 0.01). (E) Model of Sirt1 effects on known molecular pathways linking dietary lipids, hepatosteatosis, and hepatic glucose intolerance.

Paul T. Pfluger, et al. Proc Natl Acad Sci U S A. 2008 July 15;105(28):9793-9798.

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