{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:45:08Z","timestamp":1761561908641},"reference-count":64,"publisher":"The Endocrine Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,12,1]]},"abstract":"<jats:p>GH is important in metabolic control, and mice with disruption of the gene encoding the GH receptor (GHR) and GH binding protein (GHR\u2212\/\u2212 mice) are dwarf with low serum IGF-1 and insulin levels, high GH levels, and increased longevity, despite their obesity and altered lipid and metabolic profiles. Secondary complications of high-fat diet (HFD)-induced obesity are reported to be associated with hypothalamic inflammation and gliosis. Because GH and IGF-1 can modulate inflammatory processes, our objective was to evaluate the effect of HFD on hypothalamic inflammation\/gliosis in the absence of GH signaling and determine how this correlates with changes in systemic metabolism. On normal chow, GHR\u2212\/\u2212 mice had a higher percentage of fat mass and increased circulating nonesterified free fatty acids levels compared with wild type (WT), and this was associated with increased hypothalamic TNF-\u03b1 and phospho-JNK levels. After 7 weeks on a HFD, both WT and GHR\u2212\/\u2212 mice had increased weight gain, with GHR\u2212\/\u2212 mice having a greater rise in their percentage of body fat. In WT mice, HFD-induced weight gain was associated with increased hypothalamic levels of phospho-JNK and the microglial marker Iba-1 (ionized calcium-binding adapter molecule 1) but decreased cytokine production. Moreover, in GHR\u2212\/\u2212 mice, the HFD decreased hypothalamic inflammatory markers to WT levels with no indication of gliosis. Thus, the GH\/IGF-1 axis is important in determining not only adipose tissue accrual but also the inflammatory response to HFD. However, how hypothalamic inflammation\/gliosis is defined will determine whether it can be considered a common feature of HFD-induced obesity.<\/jats:p>","DOI":"10.1210\/en.2014-1367","type":"journal-article","created":{"date-parts":[[2014,9,19]],"date-time":"2014-09-19T16:30:23Z","timestamp":1411144223000},"page":"4856-4867","source":"Crossref","is-referenced-by-count":22,"title":["The Absence of GH Signaling Affects the Susceptibility to High-Fat Diet-Induced Hypothalamic Inflammation in Male Mice"],"prefix":"10.1210","volume":"155","author":[{"given":"Eva","family":"Baquedano","sequence":"first","affiliation":[{"name":"Department of Pediatrics (E.B., A.M.R.-L., J.A.C., L.M.F., J.A.), Universidad Aut\u00f3noma de Madrid; Department of Endocrinology, Hospital Infantil Universitario Ni\u00f1o Jes\u00fas 28009, Madrid, Spain; Instituto de Investigaci\u00f3n Sanitaria Princesa; and Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Fisiopatolog\u00eda de la Obesidad y Nutrici\u00f3n, Instituto de Salud Carlos III, 28009 Madrid, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ana M.","family":"Ruiz-Lopez","sequence":"first","affiliation":[{"name":"Department of Pediatrics (E.B., A.M.R.-L., J.A.C., L.M.F., J.A.), Universidad Aut\u00f3noma de Madrid; Department of Endocrinology, Hospital Infantil Universitario Ni\u00f1o Jes\u00fas 28009, Madrid, Spain; Instituto de Investigaci\u00f3n Sanitaria Princesa; and Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Fisiopatolog\u00eda de la Obesidad y Nutrici\u00f3n, Instituto de Salud Carlos III, 28009 Madrid, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elahu G.","family":"Sustarsic","sequence":"first","affiliation":[{"name":"The Edison Biotechnology Institute (E.G.S., J.H., E.O.L., J.J.K.) and Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James","family":"Herpy","sequence":"first","affiliation":[{"name":"The Edison Biotechnology Institute (E.G.S., J.H., E.O.L., J.J.K.) and Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward O.","family":"List","sequence":"first","affiliation":[{"name":"The Edison Biotechnology Institute (E.G.S., J.H., E.O.L., J.J.K.) and Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie A.","family":"Chowen","sequence":"first","affiliation":[{"name":"Department of Pediatrics (E.B., A.M.R.-L., J.A.C., L.M.F., J.A.), Universidad Aut\u00f3noma de Madrid; Department of Endocrinology, Hospital Infantil Universitario Ni\u00f1o Jes\u00fas 28009, Madrid, Spain; Instituto de Investigaci\u00f3n Sanitaria Princesa; and Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Fisiopatolog\u00eda de la Obesidad y Nutrici\u00f3n, Instituto de Salud Carlos III, 28009 Madrid, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laura M.","family":"Frago","sequence":"first","affiliation":[{"name":"Department of Pediatrics (E.B., A.M.R.-L., J.A.C., L.M.F., J.A.), Universidad Aut\u00f3noma de Madrid; Department of Endocrinology, Hospital Infantil Universitario Ni\u00f1o Jes\u00fas 28009, Madrid, Spain; Instituto de Investigaci\u00f3n Sanitaria Princesa; and Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Fisiopatolog\u00eda de la Obesidad y Nutrici\u00f3n, Instituto de Salud Carlos III, 28009 Madrid, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John J.","family":"Kopchick","sequence":"first","affiliation":[{"name":"The Edison Biotechnology Institute (E.G.S., J.H., E.O.L., J.J.K.) and Department of Biomedical Sciences, 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