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Ketosis is a metabolic disease of dairy cows often characterized by high concentrations of ketone bodies and fatty acids, but low milk protein and milk production. The Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5 (STAT5) and the mechanistic target of rapamycin (mTOR) signaling pathways are central for the regulation of milk protein synthesis. The effect of high levels of fatty acids on these pathways and β-casein synthesis are unknown in dairy cows with clinical ketosis. Mammary gland tissue and blood samples were collected from healthy (n = 15) and clinically-ketotic (n = 15) cows. In addition, bovine mammary epithelial cells (BMEC) were treated with fatty acids, methionine (Met) or prolactin (PRL), respectively. In vivo, the serum concentration of fatty acids was greater (P > 0.05) and the percentage of milk protein (P > 0.05) was lower in cows with clinical ketosis. The JAK2-STAT5 and mTOR signaling pathways were inhibited and the abundance of β-casein was lower in mammary tissue of cows with clinical ketosis (P > 0.05). In vitro, high levels of fatty acids inhibited the JAK2-STAT5 and mTOR signaling pathways (P > 0.05) and further decreased the β-casein synthesis (P > 0.05) in BMEC. Methionine or PRL treatment, as positive regulators, activated the JAK2-STAT5 and mTOR signaling pathways to increase the β-casein synthesis. Importantly, the high concentration of fatty acids attenuated the positive effect of Met or PRL on mTOR, JAK2-STAT5 pathways and the abundance of β-casein (P > 0.05). Overall, these data indicate that the high concentrations of fatty acids that reach the mammary cells during clinical ketosis inhibit mTOR and JAK2-STAT5 signaling pathways, and further suppress β-casein synthesis.
We established a mastitis model using exogenous infection of the mammary gland of Chinese Holstein cows with Staphylococcus aureus and extracted total RNA from S. aureus-infected and healthy mammary quarters. Differential expression of genes due to mastitis was evaluated using Affymetrix technology and results revealed a total of 1230 differentially expressed mRNAs. A subset of affected genes was verified via Q-PCR and pathway analysis. In addition, Solexa high-throughput sequencing technology was used to analyze profiles of miRNA in infected and healthy quarters. These analyses revealed a total of 52 differentially expressed miRNAs. A subset of those results was verified via Q-PCR. Bioinformatics techniques were used to predict and analyze the correlations among differentially expressed miRNA and mRNA. Results revealed a total of 329 pairs of negatively associated miRNA/mRNA, with 31 upregulated pairs of mRNA and 298 downregulated pairs of mRNA. Differential expression of miR-15a and interleukin-1 receptor-associated kinase-like 2 (IRAK2), were evaluated by western blot and luciferase reporter assays. We conclude that miR-15a and miR-15a target genes (IRAK2) constitute potential miRNA–mRNA regulatory pairs for use as biomarkers to predict a mastitis response.
The work described in this research communication aimed to investigate whether rumen-protected methionine (Met) supplementation during the periparturient period would affect the expression of galectins in blood-derived neutrophils, and secretion of galectins, IL (interleukin)-1β, IL-6, myeloperoxidase (MPO), and glucose in plasma. Because supplementation of rumen-protected Met would alleviate inflammation and oxidative stress during the peripartal period, we hypothesized that enhancing Met supply would benefit the innate immune response at least in part by altering the expression of galectin genes associated with neutrophil activity and inflammation. Galectins (Gal) have an immuno-modulating effect acting like cell-surface receptors whose activation often results in signaling cascades stimulating cells such as neutrophils. This study revealed an association between Met supplementation and galectin expression and secretion. This implies that galectin expression and secretion can be modulated by Met supplementation. Further studies are needed to evaluate the regulation of galectin gene expression for therapeutic and dietary intervention in the peripartal cow.
High temperature is a major stress that negatively affects welfare, health, and productivity of dairy animals. Heat-stressed animals are more prone to disease, suggesting that their immunity is hindered. Although productive and physiologic responses of dairy animals to heat stress are well known, there is still limited information on the response at the transcriptome level. Our objective was to evaluate the changes in performance and blood transcriptomics of dairy goats under heat stress. Eight multiparous Murciano-Granadina dairy goats in mid-lactation were assigned to 1 of 2 climatic treatments for 35 d. Treatments and temperature-humidity index (THI) were: (1) thermal neutral (TN: n = 4; 15–20 °C, 40–45%, THI = 59–65), and (2) heat stress (HS: n = 4; 12 h at 37 °C–40%, THI = 86; 12 h at 30 °C–40%, THI = 77). Rectal temperature, respiratory rate, feed intake and milk yield were recorded daily. Additionally, milk composition was evaluated weekly. Blood samples were collected at d 35 and RNA was extracted for microarray analyses (Affymetrix GeneChip Bovine Genome Array). Differences in rectal temperature and respiratory rate between HS and TN goats were maximal during the first 3 d of the experiment, reduced thereafter, but remained significant throughout the 35-d experimental period. Heat stress reduced feed intake, milk yield, milk protein and milk fat contents by 29, 8, 12, and 13%, respectively. Microarray analysis of blood revealed that 55 genes were up-regulated, whereas 88 were down-regulated by HS. Bioinformatics analysis using the Dynamic Impact Approach revealed that 31 biological pathways were impacted by HS. Pathways associated with leukocyte transendothelial migration, cell adhesion, hematopoietic cell lineage, calcium signaling, and PPAR signaling were negatively impacted by HS, whereas nucleotide metabolism was activated. In conclusion, heat stress not only negatively affected milk production in dairy goats, but also resulted in alterations in the functionality of immune cells, which would make the immune system of heat-stressed goats less capable of fending-off diseases.
Madin–Darby Bovine Kidney cells cultured with 150 μm of Wy-14 643 (WY, PPARα agonist) or twelve long-chain fatty acids (LCFA; 16 : 0, 18 : 0, cis-9–18 : 1, trans-10–18 : 1, trans-11–18 : 1, 18 : 2n-6, 18 : 3n-3, cis-9, trans-11–18 : 2, trans-10, cis-12–18 : 2, 20 : 0, 20 : 5n-3 and 22 : 6n-3) were used to uncover PPAR-α target genes and determine the effects of LCFA on expression of thirty genes with key functions in lipid metabolism and inflammation. Among fifteen known PPAR-α targets in non-ruminants, ten had greater expression with WY, suggesting that they are bovine PPAR-α targets. The expression of SPP1 and LPIN3 was increased by WY, with no evidence of a similar effect in the published literature, suggesting that both represent bovine-specific PPAR-α targets. We observed the strongest effect on the expression of PPAR-α targets with 16 : 0, 18 : 0 and 20 : 5n-3.When considering the overall effect on expression of the thirty selected genes 20 : 5n-3, 16 : 0 and 18 : 0 had the greatest effect followed by 20 : 0 and c9t11–18 : 2. Gene network analysis indicated an overall increase in lipid metabolism by WY and all LCFA with a central role of PPAR-α but also additional putative transcription factors. A greater increase in the expression of inflammatory genes was observed with 16 : 0 and 18 : 0. Among LCFA, 20 : 5n-3, 16 : 0 and 18 : 0 were the most potent PPAR-α agonists. They also affected the expression of non-PPAR-α targets, eliciting an overall increase in the expression of genes related to lipid metabolism, signalling and inflammatory response. Data appear to highlight a teleological evolutionary adaptation of PPAR in ruminants to cope with the greater availability of saturated rather than unsaturated LCFA.
Adipocyte differentiation is probably controlled by transcriptional and post-transcriptional regulation. Longissimus lumborum from Angus steers (aged 155 d; seven animals per diet) fed high-starch or low-starch diets for 112 d (growing phase) followed by a common high-starch diet for an additional 112 d (finishing phase) was biopsied at 0, 56, 112 and 224 d for transcript profiling via quantitative PCR of twenty genes associated with adipogenesis and energy metabolism. At 56 d steers fed high starch had greater expression of PPARγ as well as the lipogenic enzymes ATP citrate lyase (ACLY), glucose-6-phosphate dehydrogenase (G6PD), fatty acid synthase (FASN), fatty acid binding protein 4 (FABP4), stearoyl-CoA desaturase (SCD), glycerol-3-phosphate acyltransferase, mitochondrial (GPAM), and diacylglycerol O-acyltransferase homologue 2 (DGAT2), and the adipokine adiponectin (ADIPOQ). Expression of insulin-induced gene 1 (INSIG1) was also greater with high starch at 56 d. Steers fed low starch experienced a marked increase in FASN, FABP4, SCD, DGAT2 and thyroid hormone-responsive (SPOT14 homologue, rat) (THRSP) between 56 and 112 d of feeding. A greater expression of the transcription factors sterol regulatory element-binding transcription factor 1 (SREBF1) and MLX interacting protein-like (MLXIPL) was observed at 224 d in steers fed high starch, suggesting a nutritional imprinting effect. Carryover effects of low starch feeding were discerned by greater expression at 224 d of THRSP, FABP4, SCD and DGAT2. These steers also had greater PPARγ at 224 d. Despite these responses, low starch led to greater expression at 224 d of nuclear receptor subfamily 2, group F, member 2 (NR2F2), a known repressor of rodent adipocyte differentiation through its negative effects on PPARγ, ADIPOQ and FABP4. Results suggested that early exposure to high starch induced precocious intramuscular adipocyte proliferation and metabolic imprinting of lipogenic transcription regulators. Low starch might have blunted the PPARγ-driven adipogenic response through up-regulation of NR2F2 but the endogenous ligand for this nuclear receptor remains unknown.
Cis 9, trans 11 (c 9, t11)-18: 2 and trans 10, cis 12 (t10, c12)-18: 2 are the major conjugated linoleic acid (CLA) isomers in dietary supplements which reduce milk fat content in nursing women. The present study evaluated the effects of each CLA isomer or vaccenic acid on body composition and tissue fatty acids during lactation in mice. Dams were fed 30 g rapeseed oil (control)/kg diet or 20 g control plus 10 g 18: 0, trans 11–18: 1 (t11–18: 1), c 9, t11–18: 2, or t10, c12–18: 2. Dietary t10, c12–18: 2 reduced food intake by 18 % and carcass fat weight of the dams by 49 % compared with the other treatments. Milk fat percentage ranked by treatment was 18: 0>t11–18: 1=c 9, t11–18: 2>t10, c12–18: 2. The sum of saturated 12: 0 to 16: 0 in milk fat was lower when c 9, t11–18: 2 was fed compared with the control, 18: 0, or t11–18: 1 treatments. Dietary t10, c12–18: 2 caused further reductions in milk fat 12: 0 to 16: 0. The proportion of CLA isomers was 3-fold greater in milk fat than in the carcasses of the dams. The pups nursing from the dams fed t10, c12–18: 2 had the lowest body weights and carcass fat, protein, and ash contents. Nursing from the dams fed c 9, t11–18: 2 also resulted in lower carcass fat compared with the 18: 0 or t11–18: 1 treatments. The ratios of cis 9–16: 1:16: 0 or cis 9–18: 1:18: 0, proxies for Δ9-desaturase activity, were markedly lower in the carcasses of the dams and pups fed t10, c12–18: 2. The ratio of 20: 4n-6:18: 2n-6, a proxy for Δ6- and Δ5-desaturase and elongase activity, in the liver of the dams and pups fed t10, c12–18: 2 also was lower. Dietary t11–18: 1 enhanced the content of c 9, t11–18: 2 in milk fat and carcasses. As in previous studies, the reduction in food intake by t10, c12–18: 2 could not entirely account for the marked decrease in carcass fat content and milk fat concentration. T10, c12–18: 2 probably had a negative effect on Δ9-desaturase and mammary de novo fatty acid synthesis. Although these effects need to be confirmed in lactating women, the results suggest that the consumption of supplements containing t10, c12–18: 2 should be avoided during the nursing period.
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