Attenuation of acute and chronic liver injury in rats by iron-deficient diet.
Am J Physiol Regul Integr Comp Physiol. 2008 Feb;294(2):R311-20. Epub 2007 Nov 21. PMID: 18032466
Kohji Otogawa, Tomohiro Ogawa, Ryoko Shiga, Kazuki Nakatani, Kazuo Ikeda, Yuji Nakajima, Norifumi Kawada
Oxidative stress due to iron deposition in hepatocytes or Kupffer cells contributes to the initiation and perpetuation of liver injury. The aim of this study was to clarify the association between dietary iron and liver injuries in rats. Liver injury was initiated by the administration of thioacetamide or ligation of the common bile duct in rats fed a control diet (CD) or iron-deficient diet (ID). In the acute liver injury model induced by thioacetamide, serum levels of aspartate aminotransferase and alanine aminotransferase, as well as hepatic levels of lipid peroxide and 4-hydroxynonenal, were significantly decreased in the ID group. The expression of 8-hydroxydeoxyguanosine and terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling positivity showed a similar tendency. The expression of interleukin-1beta and monocyte chemotactic protein-1 mRNA was suppressed in the ID group. In liver fibrosis induced by an 8-wk thioacetamide administration, ID suppressed collagen deposition and smooth muscle alpha-actin expression. The expressions of collagen 1A2, transforming growth factor beta, and platelet-derived growth factor receptor beta mRNA were all significantly decreased in the ID group. Liver fibrosis was additionally suppressed in the bile-duct ligation model by ID. In culture experiments, deferoxamine attenuated the activation process of rat hepatic stellate cells, a dominant producer of collagen in the liver. In conclusion, reduced dietary iron is considered to be beneficial in improving acute and chronic liver injuries by reducing oxidative stress. The results obtained in this study support the clinical usefulness of an iron-reduced diet for the improvement of liver disorders induced by chronic hepatitis C and alcoholic/nonalcoholic steatohepatitis.
Article Published Date : Feb 01, 2008
Effects of Fe-YM1504 on iron deficiency anemia in rats.
Food Funct. 2016 Jul 13;7(7):3184-92
Authors: Zhang XG, Wei GX, Wang WN, Ma GD, Tang P, Chen XQ
Iron deficiency anemia (IDA) is one of the most serious forms of malnutrition. It is possible that some strains present in the natural environment possess a higher tolerance to inorganic iron and a higher ability to convert and accumulate iron compared with Saccharomyces cerevisiae wild-type strain. In the present study, the strain no. YM1504, able to grow in an iron-rich environment, was used as a potential organic iron supplement, and its efficacy in alleviating IDA in rats was investigated. Sixty female weanling Sprague-Dawley rats were randomly divided into a normal control group fed with a standard diet and a model group fed with an iron-deficient diet to create the IDA model. After the model was established, IDA rats were further randomly divided into five subgroups: the IDA group, the ferrous sulfate (FeSO4) group and Fe-YM1504 low-, medium- or high-dose groups receiving different concentrations of Fe-YM1504 supplements. Our results showed that Fe-YM1504 has an effective restorative function by returning the hemoglobin (Hb), hematocrit (HCT), mean corpuscular hemoglobin (MCH), mean corpuscular volume (MCV), serum iron (SI), total iron binding capacity (TIBC), serum ferritin (SF), etc. in IDA animals to the normal level. Moreover, malondialdehyde and the enzyme activities of superoxide dismutase and glutathione peroxidase in both plasma and liver homogenate were improved. Finally, compared with the FeSO4 group, the Fe-YM1504 middle-dose was more effective in alleviating IDA and fewer side effects were observed. The present study indicated that iron-enriched strain no. YM1504 might play a significant role in ameliorating IDA rats and might be exploited as a new iron supplement.
PMID: 27326788 [PubMed - indexed for MEDLINE]