Special Issue "Molecular Nutrition: Methods, Advances, and Practical Applications to Improve Health and Performance of Livestock and Pets"

A special issue of Veterinary Sciences (ISSN 2306-7381).

Deadline for manuscript submissions: 31 July 2019

Special Issue Editor

Guest Editor
A/Prof. Dr. Massimo Bionaz

Animal and Rangeland Sciences, Oregon State University, 561 Weniger Hall, Corvallis, OR 97331, USA
Website | E-Mail
Interests: Nutrigenomics in ruminants, effect of milk on human health, system biology, and dairy management and welfare

Special Issue Information

Dear Colleagues,

Molecular nutrition is a relatively new branch of research in livestock with great potential to face the challenges of improving the efficiency of food production and animal health ahead of us. The research into molecular nutrition appears to face a challenge in livestock science, where immediate practical applications are expected. Molecular studies can take several years before any practical application can be developed. Classical approaches to nutritional science in livestock have allowed us to make tremendous progress to the point where we can feed our herds with high accuracy; however, further advances require us to go deeper and understand the intricate and complex molecular crosstalk that is happening inside the cells and between cells (both near and far). Fortunately, we are in an era where we can benefit from the tremendous technological advances—such as RNA sequencing, gene editing (e.g., CRISPR-Cas9), and bioinformatics—that are essential to stepping into the abyss of the molecular relationships that allow life in an organism and allow the organism to respond harmoniously (or not) to molecules coming from its diet. We are also in the era of personalized medicine and personalized diets. This implies the necessity to account for and valorize the diversity among organisms and use such diversity to maximize the effect of the diet. For this reason, the use of technologies such as DNA sequencing and techniques to study the epigenome are also essential.

The aim of this Special Issue is to capture the advances in molecular nutrition in livestock and pets encompassing the development of new methods (e.g., techniques, cell lines, or protocols) and studies performed in vitro, ex vivo, in vivo or in silico to investigate the role of dietary molecules or to use the molecular effects of these to improve the performance of animals and their response to health problems.

A/Prof. Dr. Massimo Bionaz
Guest Editor

Manuscript Submission Information

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Keywords

  • molecular nutrition
  • nutrigenomics
  • epigenenomics
  • livestock
  • pets

Published Papers (4 papers)

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Research

Open AccessArticle
Nutrigenomic Effect of Saturated and Unsaturated Long Chain Fatty Acids on Lipid-Related Genes in Goat Mammary Epithelial Cells: What Is the Role of PPARγ?
Vet. Sci. 2019, 6(2), 54; https://doi.org/10.3390/vetsci6020054
Received: 17 April 2019 / Revised: 17 May 2019 / Accepted: 5 June 2019 / Published: 11 June 2019
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Abstract
A prior study in bovine mammary (MACT) cells indicated that long-chain fatty acids (LCFA) C16:0 and C18:0, but not unsaturated LCFA, control transcription of milk fat-related genes partly via the activation of peroxisome proliferator-activated receptor gamma (PPARγ). However, in that study, the activation [...] Read more.
A prior study in bovine mammary (MACT) cells indicated that long-chain fatty acids (LCFA) C16:0 and C18:0, but not unsaturated LCFA, control transcription of milk fat-related genes partly via the activation of peroxisome proliferator-activated receptor gamma (PPARγ). However, in that study, the activation of PPARγ by LCFA was not demonstrated but only inferred. Prior data support a lower response of PPARγ to agonists in goat mammary cells compared to bovine mammary cells. The present study aimed to examine the hypothesis that LCFA alter the mRNA abundance of lipogenic genes in goat mammary epithelial cells (GMEC) at least in part via PPARγ. Triplicate cultures of GMEC were treated with a PPARγ agonist (rosiglitazone), a PPARγ inhibitor (GW9662), several LCFA (C16:0, C18:0, t10,c12-CLA, DHA, and EPA), or a combination of GW9662 with each LCFA. Transcription of 28 genes involved in milk fat synthesis was measured using RT-qPCR. The data indicated that a few measured genes were targets of PPARγ in GMEC (SCD1, FASN, and NR1H3) while more genes required a basal activation of PPARγ to be transcribed (e.g., LPIN1, FABP3, LPL, and PPARG). Among the tested LCFA, C16:0 had the strongest effect on upregulating transcription of measured genes followed by C18:0; however, for the latter most of the effect was via the activation of PPARγ. Unsaturated LCFA downregulated transcription of measured genes, with a lesser effect by t10,c12-CLA and a stronger effect by DHA and EPA; however, a basal activation of PPARγ was essential for the effect of t10,c12-CLA while the activation of PPARγ blocked the effect of DHA. The transcriptomic effect of EPA was independent from the activation of PPARγ. Data from the present study suggest that saturated LCFA, especially C18:0, can modulate milk fat synthesis partly via PPARγ in goats. The nutrigenomic effect of C16:0 is not via PPARγ but likely via unknown transcription factor(s) while PPARγ plays an indirect role on the nutrigenomic effect of polyunsaturated LCFA (PUFA) on milk fat related genes, particularly for CLA (permitting effect) and DHA (blocking effect). Full article
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Open AccessArticle
2,4-Thiazolidinedione in Well-Fed Lactating Dairy Goats: II. Response to Intra-Mammary Infection
Vet. Sci. 2019, 6(2), 52; https://doi.org/10.3390/vetsci6020052
Received: 28 March 2019 / Revised: 17 May 2019 / Accepted: 1 June 2019 / Published: 5 June 2019
PDF Full-text (2857 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
In a prior experiment, treatment of goats with the putative PPARγ agonist 2,4-thiazolidinedione (2,4-TZD) ameliorated the response to intramammary infection without evidence of PPARγ activation. The lack of PPARγ activation was possibly due to deficiency of vitamin A and/or a poor body condition [...] Read more.
In a prior experiment, treatment of goats with the putative PPARγ agonist 2,4-thiazolidinedione (2,4-TZD) ameliorated the response to intramammary infection without evidence of PPARγ activation. The lack of PPARγ activation was possibly due to deficiency of vitamin A and/or a poor body condition of the animals. Therefore, the present study hypothesized that activation of PPARγ by 2,4-TZD in goats supplemented with adequate amounts of vitamin A can improve the response to sub-clinical mastitis. Lactating goats receiving a diet that met National Research Council requirements, including vitamin A, were injected with 8 mg/kg BW of 2,4-TZD (n = 6) or saline (n = 6; control (CTR)) daily. Two weeks into treatment, all goats received Streptococcus uberis (IMI) in the right mammary gland. Blood biomarkers of metabolism, inflammation, and oxidative status plus leukocytes phagocytosis were measured. Mammary epithelial cells (MEC) and macrophages were isolated from milk and liver tissue collected for gene expression analysis. Milk fat was maintained by treatment with 2,4-TZD, but decreased in CTR, after IMI. Haptoglobin was increased after IMI only in 2,4-TZD without any effect on negative acute phase proteins, indicating an improved liver function. 2,4-TZD vs. CTR had a greater amount of globulin. The expression of inflammation-related genes was increased by IMI in both macrophages and MEC. Except for decreasing expression of SCD1 in MEC, 2,4-TZD did not affect the expression of measured genes. Results confirmed the successful induction of sub-clinical mastitis but did not confirm the positive effect of 2,4-TZD on the response to IMI in well-fed goats. Full article
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Open AccessArticle
2,4-Thiazolidinedione in Well-Fed Lactating Dairy Goats: I. Effect on Adiposity and Milk Fat Synthesis
Vet. Sci. 2019, 6(2), 45; https://doi.org/10.3390/vetsci6020045
Received: 28 March 2019 / Revised: 29 April 2019 / Accepted: 14 May 2019 / Published: 17 May 2019
Cited by 1 | PDF Full-text (1575 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Background: In a prior experiment, treatment of goats with the putative PPARγ agonist 2,4-thiazolidinedione (2,4-TZD) did not affect milk fat or expression of milk-fat related genes. The lack of response was possibly due to deficiency of vitamin A and/or a poor body [...] Read more.
Background: In a prior experiment, treatment of goats with the putative PPARγ agonist 2,4-thiazolidinedione (2,4-TZD) did not affect milk fat or expression of milk-fat related genes. The lack of response was possibly due to deficiency of vitamin A and/or a poor body condition of the animals. In the present experiment, we tested the hypothesis that PPARγ activation affects milk fat synthesis in goats with a good body condition and receiving adequate levels of vitamin A. Methods: Lactating goats receiving a diet that met NRC requirements, including vitamin A, were injected with 8 mg/kg BW of 2,4-TZD (n = 6) or saline (n = 6; CTR) daily for 26 days. Blood metabolic profiling and milk yield and components were measured including fatty acid profile. Expression of genes related to glucose and lipid metabolism was measured in adipose tissue and in mammary epithelial cells (MEC). Size of adipocytes was assessed by histological analysis. Results: NEFA, BHBA, and fatty acids available in plasma decreased while glucose increased in 2,4-TZD vs. CTR. Size of cells and expression of insulin signaling and glucose metabolism-related genes were larger in 2,4-TZD vs. CTR in adipose tissue. In MEC, expression of SCD1 and desaturation of stearate was lower in 2,4-TZD vs. CTR. Conclusions: Overall data revealed a lack of PPARγ activation by 2,4-TZD and no effect on milk fat synthesis despite a strong anti-lipolysis effect on adipose tissue. Full article
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Open AccessArticle
Flaxseed and Carbohydrase Enzyme Supplementation Alters Hepatic n-3 Polyunsaturated Fatty Acid Molecular Species and Expression of Genes Associated with Lipid Metabolism in Broiler Chickens
Vet. Sci. 2019, 6(1), 25; https://doi.org/10.3390/vetsci6010025
Received: 17 January 2019 / Revised: 19 February 2019 / Accepted: 5 March 2019 / Published: 8 March 2019
PDF Full-text (881 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Flaxseed is rich in α-linolenic acid and is used in broiler chicken diets to enrich tissues with n-3 fatty acids (FA). However, non-starch polysaccharides (NSP) in flaxseed decreases nutrient digestibility and limits the availability of n-3 FA. Addition of carbohydrase enzymes to flaxseed-based [...] Read more.
Flaxseed is rich in α-linolenic acid and is used in broiler chicken diets to enrich tissues with n-3 fatty acids (FA). However, non-starch polysaccharides (NSP) in flaxseed decreases nutrient digestibility and limits the availability of n-3 FA. Addition of carbohydrase enzymes to flaxseed-based diets can decrease the anti-nutritive effects of NSP. We hypothesized that flaxseed and enzyme supplementation affect lipid content and alter expression of genes related to lipid metabolism in broiler liver. Five day-old broiler chicks were fed a corn-soybean basal diet with 0% flaxseed, a basal diet with 10% of flaxseed, or 10% flaxseed + 0.05% enzyme diet up to day 42 of growth. Total lipids, including long-chain (≥20C) n-3 FA and monounsaturated FA, were increased in flax-fed broiler livers. Enzyme addition reduced arachidonic acid and total long chain n-6 FA. These changes were similarly reflected in phosphatidylcholine lipid species. Dietary flax and enzyme treatments up-regulated PPARα target genes CPT1A and ACOX1 while reducing expression of de novo FA synthesis-related genes. This study concludes that flaxseed and enzyme supplementation in broiler diets enhances LC n-3 FA species, while reducing n-6 FA species in hepatic phospholipids (PL). Flaxseed-based diets changes the expression of genes involved in FA lipid metabolism without affecting growth or production performance in broilers. Full article
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