{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:20:34Z","timestamp":1784557234751,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:p>\n                    Metabolic syndrome (MS) encompasses a clustering of risk factors for cardiovascular disease, including obesity, insulin resistance, and dyslipidemia. We characterized a new mouse model carrying a dominant mutation, C57BL\/6J-\n                    <jats:italic>Nmf15<\/jats:italic>\n                    \/+ (B6-\n                    <jats:italic>Nmf15<\/jats:italic>\n                    \/+), which develops additional complications of MS such as adipose tissue inflammation and cardiomyopathy. A backcross was used to genetically map the\n                    <jats:italic>Nmf15<\/jats:italic>\n                    locus. Mice were examined in the comprehensive laboratory animal monitoring system, and dual energy X-ray absorptiometry and blood chemistry analyses were performed. Hypothalamic LEPR, SOCS1, and STAT3 phosphorylation were examined. Cardiac function was assessed by echo- and electrocardiography. Adipose tissue inflammation was characterized by\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization and measurement of Jun kinase activity. The\n                    <jats:italic>Nmf15<\/jats:italic>\n                    locus mapped to distal mouse chromosome 5 with an LOD (logarithm of odds) score of 13.8.\n                    <jats:italic>Nmf15<\/jats:italic>\n                    mice developed obesity by 12 weeks of age. Plasma leptin levels were significantly elevated in pre-obese\n                    <jats:italic>Nmf15<\/jats:italic>\n                    mice at 8 weeks of age and an attenuated STAT3 phosphorylation in the hypothalamus suggests a primary leptin resistance. Adipose tissue from\n                    <jats:italic>Nmf15<\/jats:italic>\n                    mice showed a remarkable degree of inflammation and macrophage infiltration as indicated by expression of the F4\/80 marker and increased phosphorylation of JUN N-terminal kinase 1\/2. Lipidosis was observed in tubular epithelial cells and glomeruli of the kidney.\n                    <jats:italic>Nmf15<\/jats:italic>\n                    mice demonstrate both histological and pathophysiological evidence of cardiomyopathy. The\n                    <jats:italic>Nmf15<\/jats:italic>\n                    mouse model provides a new entry point into pathways mediating leptin resistance and obesity. It is one of few models that combine many aspects of MS and can be useful for testing new therapeutic approaches for combating obesity complications, particularly cardiomyopathy.\n                  <\/jats:p>","DOI":"10.1677\/joe-09-0079","type":"journal-article","created":{"date-parts":[[2009,4,27]],"date-time":"2009-04-27T20:59:15Z","timestamp":1240865955000},"page":"17-28","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":15,"title":["A new mouse model of metabolic syndrome and associated complications"],"prefix":"10.1530","volume":"202","author":[{"given":"Yun","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patsy M","family":"Nishina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00fcrgen K","family":"Naggert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/joe.bioscientifica.com\/view\/journals\/joe\/202\/1\/17.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/joe.bioscientifica.com\/downloadpdf\/journals\/joe\/202\/1\/17.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:54:44Z","timestamp":1784555684000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/joe\/article\/202\/1\/17-28\/21870"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2009,4,24]]},"references-count":0,"journal-issue":{"issue":"1"},"URL":"https:\/\/doi.org\/10.1677\/joe-09-0079","relation":{},"ISSN":["0022-0795","1479-6805"],"issn-type":[{"value":"0022-0795","type":"print"},{"value":"1479-6805","type":"electronic"}],"subject":[],"published":{"date-parts":[[2009,4,24]]}}}