{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T09:43:20Z","timestamp":1774518200756,"version":"3.50.1"},"reference-count":89,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,12,5]],"date-time":"2012-12-05T00:00:00Z","timestamp":1354665600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:p>Homocystinuria is a neurometabolic disease caused by a severe deficiency of cystathionine beta\u2010synthase activity, resulting in severe hyperhomocysteinemia. Affected patients present several symptoms including a variable degree of motor dysfunction. In this study, we investigated the effect of chronic hyperhomocysteinemia on the cell viability of the mitochondrion, as well as on some parameters of energy metabolism, such as glucose oxidation and activities of pyruvate kinase, citrate synthase, isocitrate dehydrogenase, malate dehydrogenase, respiratory chain complexes and creatine kinase in gastrocnemius rat skeletal muscle. We also evaluated the effect of creatine on biochemical alterations elicited by hyperhomocysteinemia. Wistar rats received daily subcutaneous injections of homocysteine (0.3\u20130.6\u2009\u00b5mol\/g body weight) and\/or creatine (50\u2009mg\/kg body weight) from the 6th to the 28th days of age. The animals were decapitated 12\u2009h after the last injection. Homocysteine decreased the cell viability of the mitochondrion and the activities of pyruvate kinase and creatine kinase. Succinate dehydrogenase was increased other evaluated parameters were not changed by this amino acid. Creatine, when combined with homocysteine, prevented or caused a synergistic effect on some changes provoked by this amino acid. Creatine <jats:italic>per se<\/jats:italic> or creatine plus homocysteine altered glucose oxidation. These findings provide insights into the mechanisms by which homocysteine exerts its effects on skeletal muscle function, more studies are needed to elucidate them. Although creatine prevents some alterations caused by homocysteine, it should be used with caution, mainly in healthy individuals because it could change the homeostasis of normal physiological functions. Copyright \u00a9 2012 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/cbf.2938","type":"journal-article","created":{"date-parts":[[2012,12,5]],"date-time":"2012-12-05T22:08:52Z","timestamp":1354745332000},"page":"575-584","source":"Crossref","is-referenced-by-count":34,"title":["Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?"],"prefix":"10.1002","volume":"31","author":[{"given":"Jana\u00edna","family":"Kolling","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Neuroprote\u00e7\u00e3o e Doen\u00e7as Neurometab\u00f3licas Universidade Federal do Rio Grande do Sul  Porto Alegre Rio Grande do Sul Brazil"},{"name":"Laborat\u00f3rio de Erros Inatos do Metabolismo, Departamento de Bioqu\u00edmica, ICBS Universidade Federal do Rio Grande do Sul  Porto Alegre Rio Grande do Sul Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emilene B. 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