{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T23:38:06Z","timestamp":1780097886603,"version":"3.54.0"},"reference-count":27,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,3,15]],"date-time":"2006-03-15T00:00:00Z","timestamp":1142380800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Proliferation"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:p><jats:bold>Abstract.\u2002<\/jats:bold> We previously reported that a subnecrogenic dose (20\u00a0mg\/kg) of diethylnitrosamine (DENA) can induce the development of liver cancer when rats undergo a fasting\u2013re\u2010feeding regimen. The present study was undertaken to establish whether fasting followed by re\u2010feeding builds up mechanisms able to trigger liver fibrosis, eventually leading to cirrhosis and cancer. Adult male rats, for fasted 4\u00a0days, were given 20\u00a0mg\/kg of DENA after 1\u00a0day of re\u2010feeding; in parallel, consistently fed animals receiving 20\u00a0mg\/kg (subnecrogenic) or 200\u00a0mg\/kg (necrogenic dose) of DENA were used as negative and positive controls, respectively. All three groups were then subjected to the 2\u2010acetylaminofluorene\/carbon tetrachloride promoting regimen. Fasting induced moderate apoptosis in liver tissue, as evidenced by increased levels of transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21) and Bax proteins and by a dramatic drop in the level of Bcl\u20102. Subsequent re\u2010feeding caused all changes to revert except TGF\u2010\u03b21 up\u2010regulation. Histological findings of inflammation and fibrosis were consistently associated with increased production of TGF\u2010\u03b21, the inflammatory cytokine with the most pronounced profibrogenic action. Thus, up\u2010regulation of TGF\u2010\u03b21 expression appears as a major mechanism by which the fasting\u2013re\u2010feeding regimen predisposes to initiation and promotion of liver carcinogenesis in rats. Avoiding fasting\u2013re\u2010feeding could be considered in the nutritional status of patients with liver fibrosis.<\/jats:p>","DOI":"10.1111\/j.1365-2184.2006.00371.x","type":"journal-article","created":{"date-parts":[[2006,3,15]],"date-time":"2006-03-15T17:09:24Z","timestamp":1142442564000},"page":"105-116","source":"Crossref","is-referenced-by-count":12,"title":["Early induction of TGF\u2010\u03b21 through a fasting\u2013re\u2010feeding regimen promotes liver carcinogenesis by a sub\u2010initiating dose of diethylnitrosamine"],"prefix":"10.1111","volume":"39","author":[{"given":"L.","family":"Tessitore","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Bollito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,3,15]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"109","article-title":"Hepatocellular carcinoma: an overview","volume":"39","author":"Anthony PP","year":"2001","journal-title":"Hepatology"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/emm.2001.31"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00432-003-0460-8"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/path.1451"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/18.10.1921"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/23.2.245"},{"key":"e_1_2_6_8_1","first-page":"4","article-title":"Hepatocarcinogenesis: a dynamic cellular perspective","volume":"56","author":"Farber E","year":"1987","journal-title":"Lab. 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