{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T23:06:33Z","timestamp":1768259193805,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[1996,7,1]]},"abstract":"<jats:p> In this study, we investigated the effects of a glycine-containing diet (5%) on mortality and liver injury due to intravenous injection of endotoxin [Escherichia coli lipopolysaccharide (LPS)] in Sprague-Dawley rats in vivo. Fifty percent of the rats fed control diet died within 24 h after an intravenous injection of LPS (10 mg\/kg), whereas feeding the rats glycine totally prevented mortality and markedly reduced an LPS-induced elevation of serum transaminase levels, hepatic necrosis, and lung injury. The elevation in serum tumor necrosis factor-alpha (TNF-alpha) due to LPS was also blunted and delayed significantly by glycine feeding. In a two-hit model (hepatic ischemia-reperfusion and injection of sublethal LPS), all rats fed control diet died, whereas 83% of glycine-fed animals survived with a significant reduction in transaminases and improved liver and lung histology. LPS elevated intracellular Ca2+ concentration ([Ca2+]i) in cultured Kupffer cells, an effect blocked almost completely by glycine. Glycine most likely reduces injury and mortality by preventing the LPS-induced elevation of [Ca2+]i in Kupffer cells, thereby minimizing toxic eicosanoid and cytokine production. <\/jats:p>","DOI":"10.1152\/ajpgi.1996.271.1.g97","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T11:36:48Z","timestamp":1514115408000},"page":"G97-G103","source":"Crossref","is-referenced-by-count":41,"title":["A diet containing glycine improves survival in endotoxin shock in the rat"],"prefix":"10.1152","volume":"271","author":[{"given":"K.","family":"Ikejima","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of North Carolina, Chapel Hill27599-7365, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Iimuro","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of North Carolina, Chapel Hill27599-7365, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. T.","family":"Forman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of North Carolina, Chapel Hill27599-7365, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. G.","family":"Thurman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of North Carolina, Chapel Hill27599-7365, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajpgi.1996.271.1.G97","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:20:23Z","timestamp":1567988423000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajpgi.1996.271.1.G97"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,7,1]]}},"alternative-id":["10.1152\/ajpgi.1996.271.1.G97"],"URL":"https:\/\/doi.org\/10.1152\/ajpgi.1996.271.1.g97","relation":{},"ISSN":["0193-1857","1522-1547"],"issn-type":[{"value":"0193-1857","type":"print"},{"value":"1522-1547","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,7,1]]}}}