{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T01:52:29Z","timestamp":1769737949745,"version":"3.49.0"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2013,8,22]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Metabolic disorders with visceral obesity have become a major medical problem associated with the development of hypertension, type 2 diabetes, and dyslipidemia and, ultimately, life\u2010threatening cardiovascular and renal diseases. Adipose tissue dysfunction has been proposed as the cause of visceral obesity\u2010related metabolic disorders, moving the tissue toward a proinflammatory phenotype.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Here we first report that adipose tissues from patients and mice with metabolic disorders exhibit decreased expression of\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              \/\n              <jats:italic>Agtrap<\/jats:italic>\n              , which is a specific binding modulator of the angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              type 1 receptor, despite its abundant expression in adipose tissues from normal human and control mice. Subsequently, to examine a functional role of\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              in the pathophysiology of metabolic disorders, we produced homozygous\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              deficient (\n              <jats:italic>Agtrap<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) mice, which exhibited largely normal physiological phenotype at baseline. Under dietary high fat loading,\n              <jats:italic>Agtrap<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice displayed systemic metabolic dysfunction, characterized by an increased accumulation of pad fat, hypertension, dyslipidemia, and insulin resistance, along with adipose tissue inflammation. Conversely, subcutaneous transplantation of donor fat pads overexpressing\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              derived from\n              <jats:italic>Agtrap<\/jats:italic>\n              transgenic mice to\n              <jats:italic>Agtrap<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              recipient mice improved the systemic metabolic dysfunction.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              These results demonstrate that\n              <jats:italic>Agtrap<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice are an effective model of metabolic disorders with visceral obesity and constitute evidence that\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              plays a protective role against insulin resistance, suggesting a new therapeutic target in metabolic disorders. Identification of\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              as a novel receptor binding modulator of adipose tissue inflammation not only has cardiovascular significance but may have generalized implication in the regulation of tissue function.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.113.000312","type":"journal-article","created":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T04:41:56Z","timestamp":1375332116000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["Angiotensin Receptor\u2013Binding Protein ATRAP\/\n            <i>Agtrap<\/i>\n            Inhibits Metabolic Dysfunction With Visceral Obesity"],"prefix":"10.1161","volume":"2","author":[{"given":"Akinobu","family":"Maeda","sequence":"first","affiliation":[{"name":"Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kouichi","family":"Tamura","sequence":"additional","affiliation":[{"name":"Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromichi","family":"Wakui","sequence":"additional","affiliation":[{"name":"Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toru","family":"Dejima","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masato","family":"Ohsawa","sequence":"additional","affiliation":[{"name":"Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, 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