Liver × receptors stimulate lipogenesis in bovine mammary epithelial cell culture but do not appear to be involved in diet-induced milk fat depression in cows

Kevin John Harvatine, Yves R. Boisclair, Dale E. Bauman

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Milk fat synthesis of ruminants can be inhibited by intermediates of ruminal fatty acid biohydrogenation including trans-10, cis-12 conjugated linoleic acid (CLA). These biohydrogenation intermediates signal a coordinated downregulation of genes involved in mammary FA synthesis, transport, and esterification. We have previously reported decreased mammary expression of sterol response element-binding protein 1 (SREBP1), SREBP1-activating proteins, and thyroid hormone-responsive spot 14 (S14) in the cow during dietinduced milk fat depression (MFD), and treatment with trans-10, cis-12 CLA. Liver × receptors (LXR) and retinoid × receptors (RXR) regulate lipogenesis and are known to bind polyunsaturated FA and LXR agonist increases lipid synthesis in mammary epithelial cell culture. The current studies investigated if biohydrogenation products of rumen origin inhibit mammary lipogenesis through LXR and/or RXR. Expression of LXRs was not different in lactating compared to nonlactating bovine mammary tissue, and expression of LXRs, RXRα, and selected LXR and RXR target genes was not changed in mammary tissue during diet-induced or CLA-induced MFD in the cow. In bovine mammary epithelial cell culture, LXR agonist stimulated lipogenesis and expression of LXRß, ATP-binding cassette 1 (ABCA1), SREBP1c, and S14, but LXR activation did not overcome CLA inhibition of lipogenesis and downregulation of LXRß, SREBP1c, and S14 expression. Lastly, expression of the LXR-regulated carbohydrate-responsive element-binding protein (ChREBP) was higher in lactating than nonlactating tissue and was decreased during CLA-induced MFD. We conclude that changes in mammary LXR expression in dairy cows are not involved in MFD and that trans-10, cis-12 CLA inhibition of lipogenesis and diet-induced MFD appears independent of direct LXR signaling.

Original languageEnglish (US)
Article numbere00266
JournalPhysiological reports
Volume2
Issue number3
DOIs
StatePublished - Jan 1 2014

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Lipogenesis
Milk
Breast
Cell Culture Techniques
Epithelial Cells
Fats
Diet
Liver
Conjugated Linoleic Acids
Carrier Proteins
Response Elements
Sterols
Down-Regulation
Esterification
Rumen
Retinoids
Ruminants
Thyroid Hormones
Genes
Fatty Acids

All Science Journal Classification (ASJC) codes

  • Physiology (medical)
  • Physiology

Cite this

@article{61c6a668cc32437eb30a0ccf0ab70fd1,
title = "Liver × receptors stimulate lipogenesis in bovine mammary epithelial cell culture but do not appear to be involved in diet-induced milk fat depression in cows",
abstract = "Milk fat synthesis of ruminants can be inhibited by intermediates of ruminal fatty acid biohydrogenation including trans-10, cis-12 conjugated linoleic acid (CLA). These biohydrogenation intermediates signal a coordinated downregulation of genes involved in mammary FA synthesis, transport, and esterification. We have previously reported decreased mammary expression of sterol response element-binding protein 1 (SREBP1), SREBP1-activating proteins, and thyroid hormone-responsive spot 14 (S14) in the cow during dietinduced milk fat depression (MFD), and treatment with trans-10, cis-12 CLA. Liver × receptors (LXR) and retinoid × receptors (RXR) regulate lipogenesis and are known to bind polyunsaturated FA and LXR agonist increases lipid synthesis in mammary epithelial cell culture. The current studies investigated if biohydrogenation products of rumen origin inhibit mammary lipogenesis through LXR and/or RXR. Expression of LXRs was not different in lactating compared to nonlactating bovine mammary tissue, and expression of LXRs, RXRα, and selected LXR and RXR target genes was not changed in mammary tissue during diet-induced or CLA-induced MFD in the cow. In bovine mammary epithelial cell culture, LXR agonist stimulated lipogenesis and expression of LXR{\ss}, ATP-binding cassette 1 (ABCA1), SREBP1c, and S14, but LXR activation did not overcome CLA inhibition of lipogenesis and downregulation of LXR{\ss}, SREBP1c, and S14 expression. Lastly, expression of the LXR-regulated carbohydrate-responsive element-binding protein (ChREBP) was higher in lactating than nonlactating tissue and was decreased during CLA-induced MFD. We conclude that changes in mammary LXR expression in dairy cows are not involved in MFD and that trans-10, cis-12 CLA inhibition of lipogenesis and diet-induced MFD appears independent of direct LXR signaling.",
author = "Harvatine, {Kevin John} and Boisclair, {Yves R.} and Bauman, {Dale E.}",
year = "2014",
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T1 - Liver × receptors stimulate lipogenesis in bovine mammary epithelial cell culture but do not appear to be involved in diet-induced milk fat depression in cows

AU - Harvatine, Kevin John

AU - Boisclair, Yves R.

AU - Bauman, Dale E.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Milk fat synthesis of ruminants can be inhibited by intermediates of ruminal fatty acid biohydrogenation including trans-10, cis-12 conjugated linoleic acid (CLA). These biohydrogenation intermediates signal a coordinated downregulation of genes involved in mammary FA synthesis, transport, and esterification. We have previously reported decreased mammary expression of sterol response element-binding protein 1 (SREBP1), SREBP1-activating proteins, and thyroid hormone-responsive spot 14 (S14) in the cow during dietinduced milk fat depression (MFD), and treatment with trans-10, cis-12 CLA. Liver × receptors (LXR) and retinoid × receptors (RXR) regulate lipogenesis and are known to bind polyunsaturated FA and LXR agonist increases lipid synthesis in mammary epithelial cell culture. The current studies investigated if biohydrogenation products of rumen origin inhibit mammary lipogenesis through LXR and/or RXR. Expression of LXRs was not different in lactating compared to nonlactating bovine mammary tissue, and expression of LXRs, RXRα, and selected LXR and RXR target genes was not changed in mammary tissue during diet-induced or CLA-induced MFD in the cow. In bovine mammary epithelial cell culture, LXR agonist stimulated lipogenesis and expression of LXRß, ATP-binding cassette 1 (ABCA1), SREBP1c, and S14, but LXR activation did not overcome CLA inhibition of lipogenesis and downregulation of LXRß, SREBP1c, and S14 expression. Lastly, expression of the LXR-regulated carbohydrate-responsive element-binding protein (ChREBP) was higher in lactating than nonlactating tissue and was decreased during CLA-induced MFD. We conclude that changes in mammary LXR expression in dairy cows are not involved in MFD and that trans-10, cis-12 CLA inhibition of lipogenesis and diet-induced MFD appears independent of direct LXR signaling.

AB - Milk fat synthesis of ruminants can be inhibited by intermediates of ruminal fatty acid biohydrogenation including trans-10, cis-12 conjugated linoleic acid (CLA). These biohydrogenation intermediates signal a coordinated downregulation of genes involved in mammary FA synthesis, transport, and esterification. We have previously reported decreased mammary expression of sterol response element-binding protein 1 (SREBP1), SREBP1-activating proteins, and thyroid hormone-responsive spot 14 (S14) in the cow during dietinduced milk fat depression (MFD), and treatment with trans-10, cis-12 CLA. Liver × receptors (LXR) and retinoid × receptors (RXR) regulate lipogenesis and are known to bind polyunsaturated FA and LXR agonist increases lipid synthesis in mammary epithelial cell culture. The current studies investigated if biohydrogenation products of rumen origin inhibit mammary lipogenesis through LXR and/or RXR. Expression of LXRs was not different in lactating compared to nonlactating bovine mammary tissue, and expression of LXRs, RXRα, and selected LXR and RXR target genes was not changed in mammary tissue during diet-induced or CLA-induced MFD in the cow. In bovine mammary epithelial cell culture, LXR agonist stimulated lipogenesis and expression of LXRß, ATP-binding cassette 1 (ABCA1), SREBP1c, and S14, but LXR activation did not overcome CLA inhibition of lipogenesis and downregulation of LXRß, SREBP1c, and S14 expression. Lastly, expression of the LXR-regulated carbohydrate-responsive element-binding protein (ChREBP) was higher in lactating than nonlactating tissue and was decreased during CLA-induced MFD. We conclude that changes in mammary LXR expression in dairy cows are not involved in MFD and that trans-10, cis-12 CLA inhibition of lipogenesis and diet-induced MFD appears independent of direct LXR signaling.

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