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. Author manuscript; available in PMC: 2017 Feb 23.
Published in final edited form as: Sci Signal. 2016 Feb 23;9(416):ra21. doi: 10.1126/scisignal.aac5472

Figure 3.

Figure 3

Orally administered trehalose rapidly accumulates in peripheral circulation and induces hepatic autophagy. A. Liquid chromatography-mass spectrometric analysis of serum isolated from mice administered 3 g/kg trehalose by gavage and analyzed after 0.5, 1, 2, or 4 hours. Serum analyzed at the “0 hour” trehalose-treatment time point was derived from mice 30 minutes after gavage with 0.9% NaCl. N = 5 mice per treatment group. B. Left, immunoblot analysis of crude liver lysates from mice administered 3 g/kg trehalose and analyzed after 0.5, 1, 2 or 4 hrs. Liver lysates analyzed at the “0 hour” trehalose-treatment time point were derived from mice 30 minutes after gavage with 0.9% NaCl. Right, Quantification of pAMPK, pULK-1 and LC3B-II, normalized to AMPKα, ULK1, and GAPDH, respectively. Data are shown as mean ± SEM for, N = 5 independent mice per treatment group. ***, P < 0.001 versus 0-hour treatment group (one-way ANOVA and Sidak’s post hoc analysis) C. Left, immunoblot analysis of LC3B-II in liver lysates from mice treated with or without 40 mg/kg leupeptin 1 hr prior to oral gavage with 3 g/kg trehalose. Right, quantification of LC3B-II:Actin band density ratio. Data are shown as mean ± SEM for, N = 3–4 independent mice per treatment group, ***, P < 0.001 and ****, P < 0.0001 versus saline-treated controls (2-tail T-Test). ***, P < 0.001 between trehalose-treated groups treated with leupeptin versus leupeptin-untreated group (denoted by brackets) by 2-tail T-Test.