<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6</volume><submitter>Jang H</submitter><pubmed_abstract>Adipose tissue hyperplasia with increased number of adipocytes is implicated in a protective rather than deleterious effect on obesity-associated metabolic disorder. It is poorly understood how the adipose tissue cellularity is regulated. Tc1 is a gene of vertebrates that regulates diverse downstream genes. Young Tc1-deleted mice fed on standard chow diet show expanded adipose tissue with smaller adipocytes in size compared to wild type controls, representing adipose tissue hyperplasia. Tc1&lt;sup>-/-&lt;/sup> mice show enhanced glucose tolerance and reduced serum lipids. Adipocyte-derived stem cells (ADSCs) from Tc1&lt;sup>-/-&lt;/sup> mice show enhanced proliferative and adipogenic capacity compared to wild type controls, suggesting that the adipose hyperplasia is regulated at the stem cell level. PPARγ and CEBPα are up-regulated robustly in Tc1&lt;sup>-/-&lt;/sup> ADSCs upon induction for adipogenesis. Wisp2 and Dlk1, inhibitors of adipogenesis, are down-regulated in Tc1&lt;sup>-/-&lt;/sup> ADSCs compared to controls. Tc1-transfected NIH3T3 cells show higher β-catenin reporter signals than vector transfected controls, suggesting a role of canonical Wnt signaling in the Tc1-dependent adipose regulation. Our data support that Tc1 is a novel regulator for adipose stem cells. Adipose tissue hyperplasia may be implicated in the metabolic regulation of Tc1&lt;sup>-/-&lt;/sup> mice.</pubmed_abstract><journal>Scientific reports</journal><pagination>35884</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5075883</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Adipose tissue hyperplasia with enhanced adipocyte-derived stem cell activity in Tc1(C8orf4)-deleted mice.</pubmed_title><pmcid>PMC5075883</pmcid><pubmed_authors>Lee S</pubmed_authors><pubmed_authors>Song K</pubmed_authors><pubmed_authors>Kim KW</pubmed_authors><pubmed_authors>Jang H</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Lee I</pubmed_authors><pubmed_authors>Woo DC</pubmed_authors><pubmed_authors>Kim M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Adipose tissue hyperplasia with enhanced adipocyte-derived stem cell activity in Tc1(C8orf4)-deleted mice.</name><description>Adipose tissue hyperplasia with increased number of adipocytes is implicated in a protective rather than deleterious effect on obesity-associated metabolic disorder. It is poorly understood how the adipose tissue cellularity is regulated. Tc1 is a gene of vertebrates that regulates diverse downstream genes. Young Tc1-deleted mice fed on standard chow diet show expanded adipose tissue with smaller adipocytes in size compared to wild type controls, representing adipose tissue hyperplasia. Tc1&lt;sup>-/-&lt;/sup> mice show enhanced glucose tolerance and reduced serum lipids. Adipocyte-derived stem cells (ADSCs) from Tc1&lt;sup>-/-&lt;/sup> mice show enhanced proliferative and adipogenic capacity compared to wild type controls, suggesting that the adipose hyperplasia is regulated at the stem cell level. PPARγ and CEBPα are up-regulated robustly in Tc1&lt;sup>-/-&lt;/sup> ADSCs upon induction for adipogenesis. Wisp2 and Dlk1, inhibitors of adipogenesis, are down-regulated in Tc1&lt;sup>-/-&lt;/sup> ADSCs compared to controls. Tc1-transfected NIH3T3 cells show higher β-catenin reporter signals than vector transfected controls, suggesting a role of canonical Wnt signaling in the Tc1-dependent adipose regulation. Our data support that Tc1 is a novel regulator for adipose stem cells. Adipose tissue hyperplasia may be implicated in the metabolic regulation of Tc1&lt;sup>-/-&lt;/sup> mice.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Oct</publication><modification>2025-04-04T09:20:46.58Z</modification><creation>2019-03-27T02:27:21Z</creation></dates><accession>S-EPMC5075883</accession><cross_references><pubmed>27775060</pubmed><doi>10.1038/srep35884</doi></cross_references></HashMap>