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 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).
Highlights
Fat is an important component of milk that accounts for many physical properties and manufacturing characteristics of milk and dairy products [1]
Unsaturated long-chain fatty acids (LCFA) downregulated transcription of measured genes, with a lesser effect by t10,c12-CLA and a stronger effect by DHA and EPA; a basal activation of PPARγ was essential for the effect of t10,c12-CLA while the activation of PPARγ blocked the effect of DHA
Milk fat is primarily composed of triacylglycerol (TAG) including fatty acids that originate from two sources: De novo synthesis within the mammary gland and the uptake of long-chain fatty acids (LCFA) from circulation [2]
Summary
Fat is an important component of milk that accounts for many physical properties and manufacturing characteristics of milk and dairy products [1]. Milk fat production is regulated by many factors including the availability of precursors and the abundance of proteins involved in milk fat synthesis, fatty acid (FA) activation, FA transport, FA desaturation, TAG synthesis, and milk fat globule formation and secretion [3,4]. A recent review of the literature highlighted a complex and still partially known network of transcription regulators responsible for the regulation of genes involved in milk fat synthesis [5]. Gene network analysis revealed that the transcription of PPARG and its putative target genes was upregulated during lactation, suggesting a role for this nuclear receptor in the concerted regulation of genes that are responsible for the control of milk fat synthesis and secretion [4].
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