The effects of cell death-inducing DNA fragmentation factor-α-like effector C (CIDEC) on milk lipid synthesis in mammary glands of dairy cows

ABSTRACT Adequate lipid synthesis by the mammary gland during lactation is essential for the survival of mammalian offspring. Cell death-inducing DNA fragmentation factor-α-like effector C (CIDEC) is a lipid droplet-associated protein and functions to promote lipid accumulation and inhibit lipolysis in mice and human adipocytes. However, the function of CIDEC in regulation of milk lipid synthesis in dairy cow mammary gland remains largely unknown. In this study, 6 multiparous Holstein cows (parity = 3) in early lactation were allocated to high-fat milk (milk yield 33.9 ± 2.1 kg/d, milk fat >3.5%, n=3) and low-fat milk (milk yield 33.7 ± 0.5 kg/d, milk fat CIDEC in cultured bovine mammary epithelial cells decreased milk lipid content and reduced expression of genes associated with mammary de novo fatty acid synthesis, short- and long-chain intracellular fatty acid activation, triacylglycerol synthesis, and transcription regulation. These genes included those for acetyl-CoA carboxylase (ACC, −60%), fatty acid synthase (FASN, −65%), acyl-CoA synthetase short-chain family member 2 (ACSS2, −50%), acyl-CoA synthetase long-chain family member 1 (ACSL1, −30%), diacylglycerol acyltransferase 1 (DGAT1, −60%), sterol regulatory element-binding protein 1 (SREBP1, −45%), and SREBP cleavage activating protein (SCAP, −66%). Conversely, in cells overexpressing CIDEC , triacylglycerol content was increased, and transcription of those genes involved in milk lipid synthesis was coordinately upregulated. These results suggest that CIDEC plays an important role in regulating milk lipid synthesis in dairy cow mammary gland via a mechanism involving gene expression, which provides further insight into the mechanisms regulating mammary lipogenesis in ruminants.