{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T04:59:58Z","timestamp":1788325198554,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,1,28]],"date-time":"2022-01-28T00:00:00Z","timestamp":1643328000000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2022,1,28]],"date-time":"2022-01-28T00:00:00Z","timestamp":1643328000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100008116","name":"Diabetes Research Center","doi-asserted-by":"publisher","award":["P30 DK017047"],"award-info":[{"award-number":["P30 DK017047"]}],"id":[{"id":"10.13039\/100008116","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100011073","name":"Nutrition Obesity Research Center, University of North Carolina","doi-asserted-by":"publisher","award":["DK035816"],"award-info":[{"award-number":["DK035816"]}],"id":[{"id":"10.13039\/100011073","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000135","name":"NIH Blueprint for Neuroscience Research","doi-asserted-by":"publisher","award":["R01AR067319"],"award-info":[{"award-number":["R01AR067319"]}],"id":[{"id":"10.13039\/100000135","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000135","name":"NIH Blueprint for Neuroscience Research","doi-asserted-by":"publisher","award":["R01AG061558"],"award-info":[{"award-number":["R01AG061558"]}],"id":[{"id":"10.13039\/100000135","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000135","name":"NIH Blueprint for Neuroscience Research","doi-asserted-by":"publisher","award":["R01CA239208"],"award-info":[{"award-number":["R01CA239208"]}],"id":[{"id":"10.13039\/100000135","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000090","name":"Congressionally Directed Medical Research Programs","doi-asserted-by":"publisher","award":["PC170059"],"award-info":[{"award-number":["PC170059"]}],"id":[{"id":"10.13039\/100000090","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["BX002807"],"award-info":[{"award-number":["BX002807"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2022,4]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n Altered adipose tissue (AT) metabolism in cancer\u2010associated weight loss via inflammation, lipolysis, and white adipose tissue (WAT) browning is primarily implicated from rodent models; their contribution to AT wasting in cancer patients is unclear.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Energy expenditure (EE), plasma, and abdominal subcutaneous WAT were obtained from men (aged 65\u00a0\u00b1\u00a08\u00a0years) with cancer, with (CWL,\n n<\/jats:italic>\n \u00a0=\u00a027) or without (CWS,\n n<\/jats:italic>\n \u00a0=\u00a047) weight loss, and weight\u2010stable non\u2010cancer patients (CON,\n n<\/jats:italic>\n \u00a0=\u00a026). Clinical images were assessed for adipose and muscle area while plasma and WAT were assessed for inflammatory, lipolytic, and browning markers.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n CWL displayed smaller subcutaneous AT (SAT;\n P<\/jats:italic>\n \u00a0=\u00a00.05) and visceral AT (VAT;\n P<\/jats:italic>\n \u00a0=\u00a00.034) than CWS, and displayed higher circulating interleukin (IL)\u20106 (\n P<\/jats:italic>\n \u00a0=\u00a00.01) and WAT transcript levels of\n IL\u20106<\/jats:italic>\n (\n P<\/jats:italic>\n \u00a0=\u00a00.029),\n IL\u20101\u03b2<\/jats:italic>\n (\n P<\/jats:italic>\n \u00a0=\u00a00.042), adipose triglyceride lipase (\n P<\/jats:italic>\n \u00a0=\u00a00.026), and browning markers (\n Dio2<\/jats:italic>\n ,\n P<\/jats:italic>\n \u00a0=\u00a00.03;\n PGC\u20101a<\/jats:italic>\n ,\n P<\/jats:italic>\n \u00a0=\u00a00.016) than CWS and CON. There was no difference across groups in absolute REE (\n P<\/jats:italic>\n \u00a0=\u00a00.061), %predicted REE (\n P<\/jats:italic>\n \u00a0=\u00a00.18), circulating free fatty acids (FFA,\n P<\/jats:italic>\n \u00a0=\u00a00.13) or parathyroid hormone\u2010related peptide (PTHrP;\n P<\/jats:italic>\n \u00a0=\u00a00.88), or WAT protein expression of inflammation (IL\u20106,\n P<\/jats:italic>\n \u00a0=\u00a00.51; IL\u20101\u03b2,\n P<\/jats:italic>\n \u00a0=\u00a00.29; monocyte chemoattractant protein\u20101,\n P<\/jats:italic>\n \u00a0=\u00a00.23) or WAT protein or gene expression of browning (uncoupling protein\u20101, UCP\u20101;\n P<\/jats:italic>\n \u00a0=\u00a00.13,\n UCP\u20101<\/jats:italic>\n ,\n P<\/jats:italic>\n \u00a0=\u00a00.14). In patients with cancer, FFA was moderately correlated with WAT hormone\u2010sensitive lipase transcript (\n r<\/jats:italic>\n \u00a0=\u00a00.38,\n P<\/jats:italic>\n \u00a0=\u00a00.018,\n n<\/jats:italic>\n \u00a0=\u00a039); circulating cytokines were not correlated with expression of WAT inflammatory markers and circulating PTHrP was not correlated with expression of WAT browning markers. In multivariate regression using cancer patients only, body mass index (BMI) directly predicted SAT (\n N<\/jats:italic>\n \u00a0=\u00a025,\n R<\/jats:italic>\n 2<\/jats:sup>\n \u00a0=\u00a00.72,\n P<\/jats:italic>\n \u00a0<\u00a00.001), VAT (\n N<\/jats:italic>\n \u00a0=\u00a028,\n R<\/jats:italic>\n 2<\/jats:sup>\n \u00a0=\u00a00.64,\n P<\/jats:italic>\n \u00a0<\u00a00.001), and absolute REE (\n N<\/jats:italic>\n \u00a0=\u00a022,\n R<\/jats:italic>\n 2<\/jats:sup>\n \u00a0=\u00a00.43,\n P<\/jats:italic>\n \u00a0=\u00a00.001), while BMI and WAT UCP\u20101 protein were indirectly associated with %predicted REE (\n N<\/jats:italic>\n \u00a0=\u00a022,\n R<\/jats:italic>\n 2<\/jats:sup>\n \u00a0=\u00a00.45,\n P<\/jats:italic>\n \u00a0=\u00a00.02), and FFA was indirectly associated with RQ (\n N<\/jats:italic>\n \u00a0=\u00a022,\n R<\/jats:italic>\n 2<\/jats:sup>\n \u00a0=\u00a00.52,\n P<\/jats:italic>\n \u00a0<\u00a00.001).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Cancer\u2010related weight loss was associated with elevated circulating IL\u20106 and elevations in some WAT inflammatory, lipolytic and browning marker transcripts. BMI, not weight loss, was associated with increased energy expenditure. The contribution of inflammation and lipolysis, and lack thereof for WAT browning, will need to be clarified in other tumour types to increase generalizability. Future studies should consider variability in fat mass when exploring the relationship between cancer and adipose metabolism and should observe the trajectory of lipolysis and energy expenditure over time to establish the clinical significance of these associations and to inform more mechanistic interpretation of causation.<\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/jcsm.12918","type":"journal-article","created":{"date-parts":[[2022,1,28]],"date-time":"2022-01-28T05:39:50Z","timestamp":1643348390000},"page":"1124-1133","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["Whole\u2010body and adipose tissue metabolic phenotype in cancer patients"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3810-2427","authenticated-orcid":false,"given":"Lindsey J.","family":"Anderson","sequence":"first","affiliation":[{"name":"Geriatric Research, Education and Clinical Center Veterans Affairs Puget 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