About: Monensin is a research topic. Over the lifetime, 2457 publications have been published within this topic receiving 56629 citations. The topic is also known as: monensic acid & monensin A.
TL;DR: Evidence is provided that in normal fibroblasts about 50% of surface LDL receptors absence of LDL can be induced to recycle by the presence of LDL; and monensin interrupts this recycling by preventing the receptor from returning to the surface, thereby causing the receptors to accumulate within the cell.
TL;DR: It is demonstrated that sunflower oil, ionophores, and possibly some yeast products can be used to decrease the GE lost as methane from cattle, but fiber digestibility is impaired with oil supplementation.
Abstract: Methane emitted from the livestock sector contributes to greenhouse gas (GHG) emissions. Understanding the effects of diet on enteric methane production can help refine GHG emission inventories and identify viable GHG reduction strategies. Our study focused on measuring methane and carbon dioxide emissions, total-tract digestibility, and ruminal fermentation in growing beef cattle fed a diet supplemented with various additives or ingredients. Two experiments, each designed as a 4 x 4 Latin square with 21-d periods, were conducted using 16 Holstein steers (initial BW 311.6 +/- 12.3 kg). In Exp. 1, treatments were control (no additive), monensin (Rumensin, Elanco Animal Health, Indianapolis, IN; 33 mg/kg DM), sunflower oil (400 g/d, approximately 5% of DMI), and proteolytic enzyme (Protex 6-L, Genencor Int., Inc., CA; 1 mL/kg DM). In Exp. 2, treatments were control (no additive), Procreatin-7 yeast (Prince Agri Products, Inc., Quincy, IL; 4 g/d), Levucell SC yeast (Lallemand, Inc., Rexdale, Ontario, Canada; 1 g/d), and fumaric acid (Bartek Ingredients Inc., Stoney Creek, Ontario, Canada; 80 g/d). The basal diet consisted of 75% barley silage, 19% steam-rolled barley grain, and 6% supplement (DM basis). Four large chambers (two animals per chamber) were equipped with lasers and infrared gas analyzers to measure methane and carbon dioxide, respectively, for 3 d each period. Total-tract digestibility was determined using chromic oxide. Approximately 6.5% of the GE consumed was lost in the form of methane emissions from animals fed the control diet. In Exp. 1, sunflower oil decreased methane emissions by 22% (P = 0.001) compared with the control, whereas monensin (P = 0.44) and enzyme had no effect (P = 0.82). However, oil decreased (P = 0.03) the total-tract digestibility of NDF by 20%. When CH(4) emissions were corrected for differences in energy intake, the loss of GE to methane was decreased by 21% (P = 0.002) using oil and by 9% (P = 0.09) using monensin. In Exp. 2, Procreatin-7 yeast (P = 0.72), Levucell SC yeast (P = 0.28), and fumaric acid (P = 0.21) had no effect on methane emissions, although emissions as a percentage of GE intake were 3% (non-significant, P = 0.39) less for steers fed Procreatin-7 yeast compared with the control. This study demonstrates that sunflower oil, ionophores, and possibly some yeast products can be used to decrease the GE lost as methane from cattle, but fiber digestibility is impaired with oil supplementation.
TL;DR: Energy metabolism data suggested that monensin improved digestibility of DM, reduced fasting heat production and increased dietary net energy maintenance (NEm) values more than it increased net energy gain (NEg) values.
Abstract: Performance data on nearly 16,000 head of cattle that were used in trials to document effects of monensin on feedlot cattle were summarized. Cattle fed monensin-containing diets gained 1.6% faster, consumed 6.4% less feed and required 7.5% less feed/100 kg gain than cattle fed control diets. Monensin resulted in the greatest improvement in feed/gain at 2.9 Mcal metabolizable energy (ME)/kg diet dry matter (DM). Within the range of monensin concentrations used in the trials that were summarized (31.8 +/- 7.5 mg/kg DM), high monensin concentrations did not improve feed/gain over that obtained with lower concentrations. Carcass characteristics were not significantly influenced by monensin. Responses of cattle to monensin and implants were additive. Energy metabolism data suggested that monensin improved digestibility of DM, reduced fasting heat production and increased dietary net energy maintenance (NEm) values more than it increased net energy gain (NEg) values. Data showing the response of cattle to monensin when fed various dietary protein concentrations or sources of supplemental N suggested that monensin had a protein sparing effect. Monensin has also been shown to reduce lactic acid production, aid in the control of coccidia and bloat and to be toxic to face and horn fly larva in feces of monensin-fed cattle. In pasture trials, monensin improved daily gains. When fed to beef cows, monensin reduced amounts of feed required to maintain cow weight.
TL;DR: Overall, this study provides a more comprehensive glimpse of the chicken cecum microbial community, the modulations of this community in response to growth promoters, and targets for future efforts to mimic these effects using alternative approaches.
Abstract: With increasing pressures to reduce or eliminate the use of antimicrobials for growth promotion purposes in production animals, there is a growing need to better understand the effects elicited by these agents in order to identify alternative approaches that might be used to maintain animal health. Antibiotic usage at subtherapeutic levels is postulated to confer a number of modulations in the microbes within the gut that ultimately result in growth promotion and reduced occurrence of disease. This study examined the effects of the coccidiostat monensin and the growth promoters virginiamycin and tylosin on the broiler chicken cecal microbiome and metagenome. Using a longitudinal design, cecal contents of commercial chickens were extracted and examined using 16S rRNA and total DNA shotgun metagenomic pyrosequencing. A number of genus-level enrichments and depletions were observed in response to monensin alone, or monensin in combination with virginiamycin or tylosin. Of note, monensin effects included depletions of Roseburia, Lactobacillus and Enterococcus, and enrichments in Coprococcus and Anaerofilum. The most notable effect observed in the monensin/virginiamycin and monensin/tylosin treatments, but not in the monensin-alone treatments, was enrichments in Escherichia coli. Analysis of the metagenomic dataset identified enrichments in transport system genes, type I fimbrial genes, and type IV conjugative secretion system genes. No significant differences were observed with regard to antimicrobial resistance gene counts. Overall, this study provides a more comprehensive glimpse of the chicken cecum microbial community, the modulations of this community in response to growth promoters, and targets for future efforts to mimic these effects using alternative approaches.