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Thus, we generated adipose tissue\u2013specific glucocorticoid receptor\u2013knockout (Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice to explore potential mechanisms. Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice had a lower concentration of fasting plasma nonesterified fatty acids and less hepatic steatosis. This was associated with increased protein kinase B phosphorylation and increased hepatic glycogen synthesis after an oral glucose challenge. High\u2010fat diet (HFD)\u2010fed Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were protected against the development of hepatic steatosis and diacylglycerol\u2010PKCe\u2010induced impairments in hepatic insulin signaling. Under hyperinsulinemic\u2010euglycemic conditions, hepatic insulin response was \u223c 10\u2010fold higher in HFD\u2010fed Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Insulin\u2010mediated suppression of adipose lipolysis was improved by 40% in Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Adipose triglyceride lipase expression was decreased and insulin\u2010mediated perilipin dephosphorylation was increased in Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. In metabolic cages, food intake decreased by 3 kcal\/kg per hour in Ad\u2010GcR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Therefore, physiologic adipose glucocorticoid action appears to drive hepatic lipid accumulation during stressors such as fasting. The resultant hepatic insulin resistance prevents hepatic glycogen synthesis, preserving glucose for glucose\u2010dependent organs. Absence of adipose glucocorticoid action attenuates HFD\u2010induced hepatic insulin resistance; potential explanations for reduction in hepatic steatosis include reductions in adipose lipolysis and food intake.\u2014Abulizi, A., Camporez, J.\u2010P., Jurczak, M. J., Hoyer, K. F., Zhang, D., Cline, G. W., Samuel, V. T., Shulman, G. I., Vatner, D. F. Adipose glucocorticoid action influences whole\u2010body metabolism\n                    <jats:italic>via<\/jats:italic>\n                    modulation of hepatic insulin action. FASEB J. 33, 8174\u20138185 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201802706r","type":"journal-article","created":{"date-parts":[[2019,3,28]],"date-time":"2019-03-28T21:55:06Z","timestamp":1553810106000},"page":"8174-8185","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Adipose glucocorticoid action influences whole\u2010body metabolism\n                    <i>via<\/i>\n                    modulation of hepatic insulin action"],"prefix":"10.1096","volume":"33","author":[{"given":"Abudukadier","family":"Abulizi","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo\u00e3o-Paulo","family":"Camporez","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Jurczak","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kasper F.","family":"H\u00f8yer","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"},{"name":"Department of Clinical Medicine Magnetic Resonance Research Centre Aarhus University  Aarhus Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongyan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary W.","family":"Cline","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Varman T.","family":"Samuel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"},{"name":"Veterans Affairs Medical Center  West Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald I.","family":"Shulman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"},{"name":"Howard Hughes Medical Institute Yale University School of Medicine  New Haven Connecticut USA"},{"name":"Department of Cellular and Molecular Physiology Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel F.","family":"Vatner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Yale University School of Medicine  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,4,28]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"crossref","first-page":"1457","DOI":"10.1093\/jn\/108.9.1457","article-title":"Enzyme overshoot in starved-refed rats: role of the adrenal glucocorticoid","volume":"108","author":"Wurdeman R.","year":"1978","journal-title":"J. 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