{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T00:26:38Z","timestamp":1767918398186,"version":"3.49.0"},"reference-count":61,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2016,7]]},"abstract":"\n Objective\u2014<\/jats:title>\n \n Plasma levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (ApoA-I) are reduced in individuals with defective insulin signaling. Initial studies using liver-specific insulin receptor (InsR) knockout mice identified reduced expression of type 1 deiodinase (\n Dio1<\/jats:italic>\n ) as a potentially novel link between defective hepatic insulin signaling and reduced expression of the\n ApoA-I<\/jats:italic>\n gene. Our objective was to examine the regulation of\n ApoA-I<\/jats:italic>\n expression by\n Dio1<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Approach and Results\u2014<\/jats:title>\n \n Acute inactivation of\n InsR<\/jats:italic>\n by adenoviral delivery of Cre recombinase to\n InsR<\/jats:italic>\n floxed mice reduced HDL-C and expression of both\n ApoA-I<\/jats:italic>\n and\n Dio1<\/jats:italic>\n . Overexpression of\n Dio1<\/jats:italic>\n in\n InsR<\/jats:italic>\n knockout mice restored HDL-C and ApoA-I levels and increased the expression of\n ApoA-I<\/jats:italic>\n .\n Dio1<\/jats:italic>\n knockout mice had low expression of\n ApoA-I<\/jats:italic>\n and reduced serum levels of HDL-C and ApoA-I. Treatment of C57BL\/6J mice with antisense to\n Dio1<\/jats:italic>\n reduced\n ApoA-I<\/jats:italic>\n mRNA, HDL-C, and serum ApoA-I. Hepatic 3,5,3\u2032-triiodothyronine content was normal or elevated in\n InsR<\/jats:italic>\n knockout mice or\n Dio1<\/jats:italic>\n knockout mice. Knockdown of either\n InsR<\/jats:italic>\n or\n Dio1<\/jats:italic>\n by siRNA in HepG2 cells decreased the expression of\n ApoA-I<\/jats:italic>\n and ApoA-I synthesis and secretion.\n siRNA<\/jats:italic>\n knockdown of\n InsR or Dio1<\/jats:italic>\n decreased activity of a region of the\n ApoA-I<\/jats:italic>\n promoter lacking thyroid hormone response elements (region B). Electrophoretic mobility shift assay demonstrated that reduced\n Dio1<\/jats:italic>\n expression decreased the binding of nuclear proteins to region B.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions\u2014<\/jats:title>\n \n Reductions in\n Dio1<\/jats:italic>\n expression reduce the expression of\n ApoA-I<\/jats:italic>\n in a 3,5,3\u2032-triiodothyronine-\/thyroid hormone response element\u2013independent manner.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/atvbaha.116.307330","type":"journal-article","created":{"date-parts":[[2016,5,6]],"date-time":"2016-05-06T05:50:10Z","timestamp":1462513810000},"page":"1356-1366","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Type 1\n Deiodinase<\/i>\n Regulates\n ApoA-I<\/i>\n Gene Expression and ApoA-I Synthesis Independent of Thyroid Hormone Signaling"],"prefix":"10.1161","volume":"36","author":[{"given":"Jing","family":"Liu","sequence":"first","affiliation":[{"name":"From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (J.L., A.H.-O., H.N.G.); Ionis Pharmaceuticals, Inc, Carlsbad, CA (M.J.G.); and Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, NH (V.A.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio","family":"Hernandez-Ono","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (J.L., A.H.-O., H.N.G.); Ionis Pharmaceuticals, Inc, Carlsbad, CA (M.J.G.); and Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, NH (V.A.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark J.","family":"Graham","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (J.L., A.H.-O., H.N.G.); Ionis Pharmaceuticals, Inc, Carlsbad, CA (M.J.G.); and Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, NH (V.A.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valerie Anne","family":"Galton","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (J.L., A.H.-O., H.N.G.); Ionis Pharmaceuticals, Inc, Carlsbad, CA (M.J.G.); and Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Lebanon, NH (V.A.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Henry N.","family":"Ginsberg","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (J.L., A.H.-O., H.N.G.); Ionis Pharmaceuticals, Inc, Carlsbad, CA (M.J.G.); and Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, 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