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. 2017 Mar;27(3):427–439. doi: 10.1101/gr.212175.116

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Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 3. — The transcriptional response to fasting in liver is comprised of two TF modules. (A) Nascent RNA levels of fasting-induced genes in primary hepatocytes following a 3-h treatment with different combinations of glucagon (gluc), corticosterone (cort), and WY-14643 (wy). (B) Time course of fasting-induced genes shows an early induction of gluconeogenic genes and a later induction of FAO/ketogenic genes in liver. (C) Glucose production in primary hepatocytes following treatment with different combinations of glucagon, corticosterone, and WY-14643. (D) Nascent RNA levels of Ppara following corticosterone treatment (3 h) in primary hepatocytes. (E) Nascent RNA levels of Pdk4 in primary hepatocytes following 1, 3, and 8 h of treatment with different combinations of WY-14643 and corticosterone: (*) statistical significance (P ≤ 0.05) compared to a nontreated sample (NT) in each time point. (F) Time course of serum corticosterone and β-hydroxybutyrate levels during fasting: (*) statistical significance (P ≤ 0.05) compared to control values (fed). (n.s.) Not significant.