<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE128631" accession="SRP188988">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP188988</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA528309</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE128631</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Rdh1 supresses adiposity by promoting brown adipose adaptation to fasting and re-feeding</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Rdh1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Here we show that Rdh1-null mice fed low-fat diet gain more weight as adiposity thann wild-type mice by 20 weeks old, despite neither consuming more calories nor decreasing activity. RNAseq revealed dysregulation of 424 BAT genes in null mice, with segregated predominantly into differences after fasting vs after re-feeding. Rdh1-generated atRA in BAT regulates multiple genes that promote BAT adaptation to whole-body energy status, such as fasting and re-feeding. Overall design: Transcriptome analysis of brown adipose tissue from Rdh1KO and WT mice after 16h fasting and 16h fasting followed by 6h re-feeding.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE128631</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>30788515</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
