{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T20:09:32Z","timestamp":1781899772329,"version":"3.54.5"},"reference-count":18,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,12,26]],"date-time":"2016-12-26T00:00:00Z","timestamp":1482710400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Introduction<\/jats:italic>: Human fibroblast growth factor 21 (FGF21) is a regulator of lipid and glucose metabolism. It is expressed in skeletal muscle and may be a sensitive and specific marker for mitochondrial diseases and other neuromuscular disorders. <jats:italic>Methods<\/jats:italic>: Serum FGF21 levels were determined in 71 human samples. Thirty patients with mitochondrial disease, 16 patients with myotonic dystrophy type 1 (DM1), 5 patients with facioscapulohumeral dystrophy, and 20 healthy controls were enrolled. <jats:italic>Results<\/jats:italic> Serum FGF21 levels were significantly elevated in patients with progressive external ophthalmoplegia and DM1 compared with patients with facioscapulohumeral dystrophy, other types of mitochondrial diseases, and controls. In the mitochondrial disorder group, serum FGF21 levels were related to the number of ragged blue fibers. Significant insulin resistance was found in DM1 that might be responsible for FGF21 elevation. <jats:italic>Conclusions<\/jats:italic> FGF21 elevation may be associated with certain types of mitochondrial disease, and it is influenced by insulin resistance. <jats:italic>Muscle Nerve<\/jats:italic> <jats:bold>55<\/jats:bold>: 564\u2013569, 2017<\/jats:p>","DOI":"10.1002\/mus.25364","type":"journal-article","created":{"date-parts":[[2016,8,4]],"date-time":"2016-08-04T22:47:33Z","timestamp":1470350853000},"page":"564-569","source":"Crossref","is-referenced-by-count":29,"title":["Elevated FGF 21 in myotonic dystrophy type 1 and mitochondrial diseases"],"prefix":"10.1002","volume":"55","author":[{"given":"Emese","family":"Lovadi","sequence":"first","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M\u00e1rta","family":"Csereklyei","sequence":"additional","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajnalka","family":"Merkli","sequence":"additional","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krisztina","family":"F\u00fcL\u00f6p","sequence":"additional","affiliation":[{"name":"Neuropathology Unit Department of Pathology, University of P\u00e9cs  Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c1gnes","family":"Seb\u0151k","sequence":"additional","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veronika","family":"Karcagi","sequence":"additional","affiliation":[{"name":"Department of Molecular Genetics National Institute of Environmental Health Budapest Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00e1muel","family":"Komoly","sequence":"additional","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Endre","family":"P\u00e1l","sequence":"additional","affiliation":[{"name":"Department of Neurology University of P\u00e9cs P\u00e9cs R\u00e9t u. 2 Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,12,26]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/MOP.0b013e3283557d22"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2792"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.11.001"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-12-0357"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2012-1221"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2007.05.002"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddq310"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(11)70155-7"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2012.09.019"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1212\/01.wnl.0000436068.43384.ef"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3014"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1212\/01.WNL.0000033795.17156.00"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00645.2007"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2011.03.015"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.3109\/07435800.2011.558550"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng704"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1093\/jnen\/60.3.217"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1111\/cen.12095"}],"container-title":["Muscle &amp; 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