Effects of dietary mannanoligosaccharide on performance, some blood parameters, IgG levels and antibody response of lambs to parenterally administered E. coli O157:H7

Forty-eight male lambs were used to evaluate the effect of dietary supplementation of mannanoligosaccharide (MOS) with or without parenteral Escherichia coli injection on their growth performance, feed conversion efficiency, blood metabolites, total serum immunoglobulin G (IgG) levels and antibody response. Lambs were randomly assigned to four groups of 12 animals each. In groups C (control) and CE (E. coli challenged), animals were fed commercial concentrate pellets and hay (50:50), and in groups M (MOS) and ME (MOS + E. coli challenged), animals were fed commercial concentrate pellets including MOS at 0.2% and hay (50:50). At day 15 and 30, animals in groups CE and ME were injected subcutaneously with 1 ml of phosphate buffered saline (PBS) suspension containing 10(6) cfu of heat inactivated non-toxigenic E. coli O157:H7, while animals in C and M groups were injected subcutaneously with 1 ml of PBS. The experimental period was 45 days. Data indicated that body weight of lambs at the end of the study were statistically non-significant among the groups. Blood metabolites, i.e. total protein, albumin, calcium and phosphorus concentrations were not affected significantly by MOS supplementation. However, administration E. coli lowered (p < 0.05) total protein, albumin and calcium concentrations in the serum on day 30. The IgG level was not different between groups. However, on day 45, the total IgG level was found to be higher (p < 0.05) in lambs that had received MOS and E. coli than in other groups. Application of MOS did not have any effect on the antibody response to E. coli as OD values.     

Combined metabolic activators therapy ameliorates liver fat in nonalcoholic fatty liver disease patients

Nonalcoholic fatty liver disease (NAFLD) refers to excess fat accumulation in the liver. In animal experiments and human kinetic study, we found that administration of combined metabolic activators (CMAs) promotes the oxidation of fat, attenuates the resulting oxidative stress, activates mitochondria, and eventually removes excess fat from the liver. Here, we tested the safety and efficacy of CMA in NAFLD patients in a placebo‐controlled 10‐week study. We found that CMA significantly decreased hepatic steatosis and levels of aspartate aminotransferase, alanine aminotransferase, uric acid, and creatinine, whereas found no differences on these variables in the placebo group after adjustment for weight loss. By integrating clinical data with plasma metabolomics and inflammatory proteomics as well as oral and gut metagenomic data, we revealed the underlying molecular mechanisms associated with the reduced hepatic fat and inflammation in NAFLD patients and identified the key players involved in the host–microbiome interactions. In conclusion, we showed that CMA can be used to develop a pharmacological treatment strategy in NAFLD patients.     

The protection by heme oxygenase‐1 induction against thioacetamide‐induced liver toxicity is associated with changes in arginine and asymmetric dimethylarginine

This study was designed to investigate the role of HO‐1 induction in prevention of thioacetamide (TAA)‐induced oxidative stress, inflammation and liver damage. The changes in hepatic dimethylarginine dimethylaminohydrolase (DDAH) activity as well as plasma arginine and asymmetric dimethylarginine (ADMA) levels were also measured to evaluate nitric oxide (NO) bioavailability. Rats were divided into four groups as control, hemin, TAA and hemin + TAA groups. Hemin (50 mg kg^?1, i.p.) was injected to rats 18 h before TAA treatment to induce HO‐1 enzyme expression. Rats were given TAA (300 mg kg^?1, i.p.) and killed 24 h after treatment. Although TAA treatment produced severe hepatic injury, upregulation of HO‐1 ameliorated TAA‐induced liver damage up to some extent as evidence by decreased serum alanine transaminase, aspartate transaminase and arginase activities and histopathological findings. Induction of HO‐1 stimulated antioxidant system and decreased lipid peroxidation in TAA‐treated rats. Myeloperoxidase activity and inducible NO synthase protein expression were decreased, whereas DDAH activity was increased by hemin injection in TAA‐treated rats. Induction of HO‐1 was associated with increased arginine levels and decreased ADMA levels, being the main determinants of NO production, in plasma of TAA‐treated rats. In conclusion, our results indicate that HO‐1 induction alleviated increased oxidative stress and inflammatory reactions together with deterioration in NO production in TAA‐induced liver damage in rats. Copyright © 2012 John Wiley & Sons, Ltd.