{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,19]],"date-time":"2026-04-19T01:14:54Z","timestamp":1776561294712,"version":"3.51.2"},"reference-count":68,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[1985,7,1]],"date-time":"1985-07-01T00:00:00Z","timestamp":489024000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Parenter Enteral Nutr"],"published-print":{"date-parts":[[1985,7]]},"abstract":"<jats:p>Carnitine is an indispensable factor for the \u03b2\u2010oxidation of medium\u2010 and long\u2010chain fatty acids, and it plays a possible role in the oxidation of branched\u2010chain amino acids. Plasma and urinary levels of free carnitine and short\u2010chain acyl\u2010carnitines were studied in 67 surgical patients, after non\u2010septic surgical procedures or during sepsis. The septic state was associated with increased urinary excretion of free carnitine (p &lt; 0.001), as well as with lower plasma levels of short\u2010chain acyl\u2010carnitines (p &lt; 0.001); the latter feature correlated with the level of hypermetabolism, as evaluated by the metabolic rate and by the arterial\u2010mixed venous O<jats:sub>2<\/jats:sub> difference. In 26 patients during total parenteral nutrition D, L\u2010acetyl\u2010carnitine was administered (100 mg\/kg\/24 hrs, in continous iv infusion) and was associated, in septic patients only, with a significant decrease in the respiratory quotient, suggesting enhanced oxidation of low respiratory quotient substrates (fatty acids and\/ or branched\u2010chain amino acids). Carnitine supplementation during total parenteral nutrition might be of theoretical benefit in some clinical conditions, such as sepsis, in which the following conditions coexist (1) enhanced utilization of substrates whose oxidation is partially or totally carnitine dependent; (2) prolonged absence of exogenous intake of carnitine (as in long\u2010term total parenteral nutrition); (3) eventual impairment of carnitine synthesis due to hepatic dysfunction; (4) increased, massive urinary loss of carnitine. <jats:italic>(Journal of Parenteral and Enteral Nutrition<\/jats:italic> <jats:bold>9<\/jats:bold>:483\u2013490, 1985)<\/jats:p>","DOI":"10.1177\/0148607185009004483","type":"journal-article","created":{"date-parts":[[2008,5,14]],"date-time":"2008-05-14T19:51:26Z","timestamp":1210794686000},"page":"483-490","source":"Crossref","is-referenced-by-count":43,"title":["Plasma Carnitine Levels and Urinary Carnitine Excretion during 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