{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T19:41:50Z","timestamp":1789587710519,"version":"build-2803163510"},"reference-count":115,"publisher":"Wiley","issue":"15","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100005202","name":"Muscular Dystrophy Association","doi-asserted-by":"publisher","award":["962344)"],"award-info":[{"award-number":["962344)"]}],"id":[{"id":"10.13039\/100005202","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Duchenne muscular dystrophy (DMD) is a fatal neuromuscular disease caused by dystrophin deficiency and characterized by progressive muscle wasting. DMD is frequently accompanied by obesity and insulin resistance (IR); however, their influence on disease progression remains unknown. Moreover, the extent to which these comorbidities may interact with glucocorticoids, a commonly used intervention, is also unknown. We hypothesized that a high\u2010fat, high\u2010sucrose diet (HFHSD) would cause IR and accelerate disease progression, and treatment with prednisolone (Pred) would mitigate these effects. To test this hypothesis, 6\u2010week\u2010old C57 and mdx mice were fed a control diet (CD) or a HFHSD for 19\u00a0weeks, with or without Pred. In C57 and mdx mice, the HFHSD increased body fat percentage and caused hyperglycaemia, glucose intolerance and IR, and, in mdx mice, Pred exacerbated HFHSD\u2010mediated hyperglycaemia, glucose intolerance and IR. The HFHSD augmented diaphragm fatigue and blunted the beneficial effects of Pred on specific tension in mdx mice. In C57 and mdx mice, the HFHSD increased fatty infiltration in diaphragm, but trichrome staining revealed the HFHSD and\/or Pred decreased disease\u2010related fibrosis in mdx mice. Additionally, the HFHSD altered disease and\/or Pred\u2010mediated changes to proteins associated with lipid storage, inflammatory signalling, mitochondrial\/metabolic regulation, and Sestrin signalling. These data indicate that in mdx mice, 19\u00a0weeks of a HFHSD independently impaired muscle function, altered muscle composition, and further compromised muscle cell health, and that its interaction with Pred prevented functional recovery and further exacerbated glycaemic dysregulation and cellular dysfunction.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70684-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Obesity and insulin resistance (IR) are common comorbidities of Duchenne muscular dystrophy (DMD), yet their influence on dystrophic pathology remains unknown. Additionally, the extent that obesity\/IR interact with glucocorticoids in dystrophic progression is unclear.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>To address this, mdx mice were fed a high\u2010fat, high\u2010sucrose diet (HFHSD) for 6\u00a0months, with and without glucocorticoid treatment, and outcomes related to muscle function, composition, and cell health were evaluated.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>A HFHSD decreased fatigue resistance, reduced fibrosis, increased fatty infiltration, and impaired cell health in dystrophic diaphragms.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The addition of glucocorticoids to the HFHSD did not considerably improve most outcomes, suggesting that the diet may blunt some glucocorticoid\u2010mediated benefits, but did increase specific tension, reduce fibrosis, and attenuate inflammatory signalling.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>These results demonstrate that a HFHSD impacts some parameters of dystrophic physiology and highlight the importance of considering systematic and muscle metabolism when implementing therapeutic strategies.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp289832","type":"journal-article","created":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T17:14:37Z","timestamp":1782926077000},"page":"6440-6464","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["A high\u2010fat, high\u2010sucrose diet exacerbates muscle and metabolic pathology and undermines glucocorticoid efficacy in dystrophin\u2010deficient mice"],"prefix":"10.1113","volume":"604","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-0242-7687","authenticated-orcid":false,"given":"Morgan E.","family":"Vorwald","sequence":"first","affiliation":[{"name":"Department of Animal Science Iowa State University  Ames IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6595-0862","authenticated-orcid":false,"given":"Swathy","family":"Krishna","sequence":"additional","affiliation":[{"name":"Department of Animal Science Iowa State University  Ames IA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3908-2766","authenticated-orcid":false,"given":"Ji Heun","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Kinesiology Iowa State University  Ames IA 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