Effects of maternal supplementation with rumen-protected methionine and niacin on gene expression: the role of fetal programming on growing beef cattle
Type of DegreePhD Dissertation
MetadataShow full item record
The role of supplementation with dietary rumen-protected methionine (RPM), and niacin (RPN) on beef cattle was assessed in two different, 2-year studies. In the first study, Angus × Simmental dams (n = 44) were divided based on parities, either primiparous (PRIM) or multiparous (second calf; MULT). Simultaneously, parity groups were split based on two nutritional treatments: control (CTRL) and RPM groups. Control group received bermudagrass hay, and corn gluten and soybean hulls pellets supplementation (base diet); whereas RPM group received the base diet in addition to 8 g/hd/day of RPM at a fixed rate the last trimester of gestation and the first ~85 days of lactation, in which calves were early weaned. Only male calves were included in this study. After weaning, calves born to RPM dams also received RPM from weaning (Day 1) to Day 100. Blood sampling and skeletal muscle biopsies for subsequent quantitative PCR analysis were conducted at Day 1, 25, 50, and 100 on calves. There was no difference in maternal body weight (BW), body condition score, and milk production by the inclusion of RPM. Similarly, offspring BW and average daily gain were similar within each parity category. Glucose and blood metabolites that served as biomarkers for liver health (e.g., aspartate transaminase, albumin, alkaline phosphatase, and alanine transaminase) were in the normal levels for all calves. Calves in the PRIM-RPM group had a greater expression of adipogenic genes (e.g., PPARg, LPL, and CEBPD) at Day 100 compared with PRIM-CTRL. In addition, DNA methylation (DNMT1) and oxidative stress-related genes (SOD2 and NOS3) in PRIM-RPM group were upregulated at Day 100 compared with PRIM-CTRL. These results may suggest that calves born to PRIM dams exposed to RPM supplementation are more prone to develop greater adipose tissue than CTRL calves. Furthermore, RPM supplementation may improve methylation processes in addition to a possible hypertrophy acceleration due to greater free radicals in skeletal muscle cells. However, the mechanisms in which methionine executes these nutrigenetic changes only in calves born to PRIM dams remain to be elucidated. In the second study, a total of 28 Angus × Simmental pregnant dams (11 cows and 17 heifers) were selected based on genetic resistance to fescue toxicosis based on a commercial genetic test (T-snip™, Ag. Botanica, Columbia, MO). Subsequently, dams were divided based on genetic resistance to fescue toxicosis and randomly assigned to dietary treatments: 1) Susceptible Control (SC; n = 7); 2) Susceptible Niacin (SN; n = 7); 3) Tolerant Control (TC; n = 7); and 4) Tolerant Niacin (TN; n = 7). All animals received 1.16 kg of endophyte-infected (E+) tall fescue (Schedonorus arundinaceus (Schreb.) Dumort.) seeds for a period of 30 days. Ergovaline concentration in fescue seeds was ~5,000 ppb on a DM basis. Dams in SN and TN groups received 6 g/hd/day as-fed of top-dressed rumen-protected niacin (RPN), following manufacturer’s maximum dose recommendation. Dams in the TN group experienced an accelerated reduction in BW as compared to the rest of the treatments. However, TN offspring did not show BW differences at birth or weaning as compared to those born to dams in other treatments. Milk production was estimated by the weigh-suckle-weigh method, and no difference was observed among treatments. All dams had a reduction in circulating prolactin concentration, indicating that all animals were experiencing fescue toxicosis. In addition, blood metabolites that indicate liver health were markedly decreased at the end of the study. Overall, these results suggest that dams receiving E+ tall fescue seeds effectively are exposed to fescue toxicosis symptoms. Therefore, neither RPN supplementation nor genetic test for fescue toxicosis tolerance could be used as an effective mechanism of dampening these symptoms. In addition, steers and heifers born to dams receiving E+ tall fescue seeds were also exposed to 30 days feeding trial period following maternal dietary treatments. A total of 20 μg/kg BW/day was the daily dietary dose of ergovaline offered to the animals under study to produce characteristic signs of fescue toxicosis. Complete blood count analysis was performed in the offspring to identify hematological changes of ergovaline consumption. Animals in the SC group presented low mean corpuscular hemoglobin and mean corpuscular volume at the end of the study, which is indicative of anemia; whereas animals in the TN group presented signs of inflammation or infection due to a high level of white blood cells and basophils, and low neutrophil to lymphocytes ratio. Furthermore, there was a reduction in rectal temperature in SC animals. The utilization of RPN supplementation or genetic test did not improve performance parameters (i.e., BW and average daily gain). Lastly, we performed RNA-sequencing on liver samples of steers (n = 4) and heifers (n = 2) receiving E+ tall fescue seeds and born to cows exposed to E+ tall fescue during mid-gestation; and a total of 3 animals (2 steers and 1 heifer) receiving endophyte-free (E-) tall fescue seeds. All animals received tall fescue seeds (E+ or E-) for a period of 30 days. Results showed an overall downregulation in KEGG pathways in E+ group compared with E- group. More specifically, a downregulation in ‘Cellular processes’ showed that liver cells may experience less senescence due to ergot alkaloids consumption. There was a lower expression of ‘Environmental information processes’, which is related to several endocrinal and immune pathways. In addition, ‘Organismal system’ KEGG category was also downregulated in E+ group, in which the most impacted pathway was ‘B cell receptor signaling pathway’. Thus, a possible immunosuppression may exist in cattle exposed to E+. Based on our results, future research could be aimed at developing pharmacological strategies to dampen fescue toxicosis.