{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T01:30:26Z","timestamp":1778117426233,"version":"3.51.4"},"reference-count":77,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2022,5,17]],"date-time":"2022-05-17T00:00:00Z","timestamp":1652745600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK084171"],"award-info":[{"award-number":["DK084171"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2022,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    C1q\/TNF\u2010related proteins (CTRP1\u201015) constitute a conserved group of secreted proteins of the C1q family with diverse functions. In vitro studies have shown that CTRP11\/C1QL4 can inhibit adipogenesis, antagonize myoblast fusion, and promote testosterone synthesis and secretion. Whether CTRP11 is required for these processes in vivo remains unknown. Here, we show that knockout (KO) mice lacking CTRP11\u00a0have normal skeletal muscle mass and function, and testosterone level, suggesting that CTRP11 is dispensable for skeletal muscle development and testosterone production. We focused our analysis on whether this nutrient\u2010responsive secreted protein plays a role in controlling sugar and fat metabolism. At baseline when mice are fed a standard chow, CTRP11 deficiency affects metabolic parameters in a sexually dimorphic manner. Only\n                    <jats:italic>Ctrp11<\/jats:italic>\n                    \u2010KO female mice have significantly higher fasting serum ketones and reduced physical activity. In the refeeding phase following food withdrawal,\n                    <jats:italic>Ctrp11<\/jats:italic>\n                    \u2010KO female mice have reduced food intake and increased metabolic rate and energy expenditure, highlighting CTRP11\u2019s role in fasting\u2013refeeding response. When challenged with a high\u2010fat diet to induce obesity and metabolic dysfunction, CTRP11 deficiency modestly exacerbates obesity\u2010induced glucose intolerance, with more pronounced effects seen in\n                    <jats:italic>Ctrp11<\/jats:italic>\n                    \u2010KO male mice. Switching to a low\u2010fat diet after obesity induction results in greater fat loss in wild type relative to KO male mice, suggesting impaired response to obesity reversal and reduced metabolic flexibility in the absence of CTRP11. Collectively, our data provide genetic evidence for novel sex\u2010dependent metabolic regulation by CTRP11, but note the overall modest contribution of CTRP11 to systemic energy homeostasis.\n                  <\/jats:p>","DOI":"10.1096\/fj.202200189rr","type":"journal-article","created":{"date-parts":[[2022,5,17]],"date-time":"2022-05-17T12:13:12Z","timestamp":1652789592000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["CTRP11 contributes modestly to systemic metabolism and energy balance"],"prefix":"10.1096","volume":"36","author":[{"given":"Dylan C.","family":"Sarver","sequence":"first","affiliation":[{"name":"Department of Physiology Johns Hopkins University School of Medicine  Baltimore Maryland USA"},{"name":"Center for Metabolism and Obesity Research Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cheng","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Physiology Johns Hopkins University School of Medicine  Baltimore Maryland USA"},{"name":"Center for Metabolism and Obesity Research Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dana","family":"Carreno","sequence":"additional","affiliation":[{"name":"Department of Physiology Johns Hopkins University School of Medicine  Baltimore Maryland USA"},{"name":"Center for Metabolism and Obesity Research Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander","family":"Arking","sequence":"additional","affiliation":[{"name":"Department of Physiology Johns Hopkins University School of Medicine  Baltimore Maryland USA"},{"name":"Center for Metabolism and Obesity Research Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chantelle E.","family":"Terrillion","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Behavioral Sciences Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan","family":"Aja","sequence":"additional","affiliation":[{"name":"Center for Metabolism and Obesity Research Johns Hopkins University School of Medicine  Baltimore Maryland USA"},{"name":"Department of Neuroscience Johns Hopkins University School of Medicine  Baltimore Maryland USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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