EEF1D facilitates milk lipid synthesis by regulation of PI3K‐Akt signaling in mammals

2021 ◽  
Vol 35 (5) ◽  
Author(s):  
Dongxiao Sun ◽  
Yali Hou ◽  
Yan Xie ◽  
Shaohua Yang ◽  
Bo Han ◽  
...  
2007 ◽  
Vol 28 (3) ◽  
pp. 323-336 ◽  
Author(s):  
Michael C. Rudolph ◽  
James L. McManaman ◽  
TzuLip Phang ◽  
Tanya Russell ◽  
Douglas J. Kominsky ◽  
...  

The mammary gland of the lactating mouse synthesizes and secretes milk lipid equivalent to its entire body weight in a single 20-day lactation cycle, making it one of the most active lipid synthetic organs known. We test the hypothesis that multiple control points and potential regulatory mechanisms regulate milk lipid synthesis at the level of gene expression. The mammary transcriptome of 130 genes involved in glucose metabolism was examined at late pregnancy and early lactation, utilizing data obtained from microarray analysis of mammary glands from quadruplicate FVB mice at pregnancy day 17 and lactation day 2. To correlate changes with physiological parameters, the metabolome obtained from magnetic resonance spectroscopy of flash-frozen glands at day 17 of pregnancy was compared with that at day 2 of lactation. A significant increase in carbohydrates (glucose, lactose, sialic acid) and amino acids (alanine, aspartate, arginine, glutamate) with a moderate increase in important osmolytes ( myo-inositol, betaine, choline derivatives) were observed in the lactating gland. In addition, diets containing 8% or 40% lipid were fed from lactation days 5–10 and mammary glands and livers of triplicate FVB mice prepared for microarray analysis. The results show that substantial regulation of lipid synthesis occurs at the level of mRNA expression and that some of the regulation points differ substantially from the liver. They also implicate the transcription factor SREBP-1c in regulation of part of the pathway.


1986 ◽  
Vol 116 (9) ◽  
pp. 1789-1797 ◽  
Author(s):  
Murray R. Grigor ◽  
Zygmunt Poczwa ◽  
Peter G. Arthur
Keyword(s):  

1992 ◽  
Vol 281 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K J Heesom ◽  
P F A Souza ◽  
V Ilic ◽  
D H Williamson

The effects of a series of medium-chain fatty acids (C6-C12) on glucose metabolism in isolated acini from lactating rat mammary glands have been studied. Hexanoate (C6) octanoate (C8) and decanoate (C10), but not laurate (C12), decreased [1-14C]glucose conversion into [14C]lipid and the production of 14CO2 (an index of the pentose phosphate pathway). With hexanoate and octanoate, glucose utilization was decreased, whereas decanoate had a slight stimulatory effect on glucose utilization, but there was a large accumulation of lactate. Addition of dichloroacetate (an inhibitor of pyruvate dehydrogenase kinase) decreased this accumulation of lactate and stimulated the conversion of [1-14C]glucose into [14C]lipid and 14CO2. Insulin had no effect on the rate of glucose utilization in the presence of hexanoate. It stimulated the rate in the presence of octanoate and laurate and increased the conversion of [1-14C]glucose into [14C]lipid in the presence of octanoate, decanoate or laurate. The major fate of 1-14C-labelled medium-chain fatty acids (C6, C8 and C12) was conversion into [14C]lipid. The proportion converted into 14CO2 decreased with increasing chain length, whereas the rate of [14C]lipid formation increased. It is concluded that the interactions between medium-chain fatty acids and glucose metabolism represent a feed-back mechanism to control milk lipid synthesis, and this may be important when milk accumulates in the gland.


2012 ◽  
Vol 3 (6) ◽  
pp. 581-591 ◽  
Author(s):  
James L. McManaman

AbstractNeonates of most species depend on milk lipids for calories, fat-soluble vitamins, and bioactive lipid components for growth and development during the postnatal period. To meet neonatal nutrition and development needs, the mammary gland has evolved efficient mechanisms for synthesizing and secreting large quantities of lipid during lactation. Although the biochemical steps involved in milk lipid synthesis are understood, the identities of the genes mediating these steps and the molecular physiology of milk lipid production and secretion have only recently begun to be understood in detail through advances in mouse genetics, gene expression analysis, protein structural properties, and the cell biology of lipid metabolism. This review discusses emerging data about the molecular, cellular, and structural determinants of milk lipid synthesis and secretion within the context of physiological functions.


2017 ◽  
Vol 100 (5) ◽  
pp. 4014-4024 ◽  
Author(s):  
Yang Yang ◽  
Ye Lin ◽  
Xiaoyu Duan ◽  
He Lv ◽  
Weinan Xing ◽  
...  

2020 ◽  
Vol 87 (3) ◽  
pp. 344-348
Author(s):  
Hang Zhang ◽  
Ni Dan ◽  
Changjin Ao ◽  
Sizhen Wang ◽  
Khas Erdene ◽  
...  

AbstractWe determined the effects of a combination of C18 unsaturated fatty acids (C18-UFAs) consisting of oleic, linoleic, and linolenic acids on milk lipogenesis in bovine mammary epithelial cells (BMECs). By orthogonal experiments to determine cellular triacylglycerol (TAG) accumulation, a combination of 200 μmol/l C18 : 1, 50 μmol/l C18 : 2, and 2 μmol/l C18 : 3 was selected as C18-UFAs combination treatment, and culture in medium containing fatty acid-free bovine serum albumin was used as the control. The expression of genes related to milk lipid synthesis and intracellular FA composition was measured. The results showed that cytosolic TAG formation was higher under C18-UFAs treatment than under control treatment. The mRNA expression of acetyl-CoA carboxylase-α (ACACA), fatty acid synthase (FASN), and peroxisome proliferator-activated receptor gamma (PPARG) did not differ between treatments. The abundance of stearoyl-CoA desaturase (SCD) and acyl-CoA synthetase long-chain family member 1 (ACSL1) was higher, whereas that of sterol regulatory element binding transcription factor 1 (SREBF-1) was lower after C18-UFAs treatment compared to control treatment. The C16 : 0 and SFA content was decreased following C18-UFAs treatment compared to control treatment, while the cis-9 C18 : 1 and UFA content was increased. In conclusion, C18-UFAs could stimulate triglyceride accumulation, increase the cellular UFA concentration, and regulate lipogenic genes in BMECs.


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