Dataset Information

Sodium acetate regulates milk fat synthesis through the activation of GPR41/GPR43 signaling pathway.

ABSTRACT:

Background

Fat is a critical component in milk, which provided energy for the early growth and development of mammals. Milk fat is positively related to the concentration of acetate in the blood, while the underlying mechanism is still unclear.

Objective

This study is to investigate the effects of sodium acetate (NaAc) on milk fat synthesis in the mammary gland, and explored the underlying mechanism.

Methods

In vitro experiments were carried out in mouse mammary epithelial cell line (HC11) cells cultured with NaAc to explore the potential pathway of NaAc on milk fat synthesis. Furthermore, 24 pregnant mice (from d 18.5 of gestation to d 7 of lactation, exposed to 200 mM NaAc drinking water) were used as an in vivo model to verify the results.

Results

In this study, we found that NaAc promoted milk fat synthesis and the expression of related genes and proteins in HC11 mammary epithelial cells with the activation of GPCR and mTORC1 signaling pathways (p < 0.05). Pretreatment with the mTORC1 inhibitors and G protein inhibitors attenuated the NaAc-induced milk fat synthesis in HC11 mammary epithelial cells (p < 0.05). Importantly, the effect of NaAc on milk synthesis was attenuated in GPR41 and GPR43 knockdown HC11 mammary epithelial cells (p < 0.05). This evidence indicates that NaAc might regulate milk fat synthesis through the GPR41/GPR43-mTORC1 pathway. Consistently, in in vivo experiment, dietary supplementation with NaAc significantly increased milk fat content and fat synthesis-related proteins in mice mammary glands with the activation of mTORC1 and GPCR signaling pathways at peak lactation (p < 0.05).

Conclusion

The addition of NaAc promoted the increase of milk fat synthesis in HC11 mammary epithelial cells and mice mammary glands at peak lactation. Mechanistically, NaAc activates GPR41 and GPR43 receptors, leading to the activation of the mTORC1 signaling pathway to promote the synthesis of milk fat.Graphical abstract.

SUBMITTER: Qi Y

PROVIDER: S-EPMC10035050 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Publications

Sodium acetate regulates milk fat synthesis through the activation of GPR41/GPR43 signaling pathway.

Qi Yingao Y Zheng Tenghui T Liu Xinghong X Yang Siwang S Li Qihui Q Shao Jiayuan J Zeng Xiangfang X Guan Wutai W Zhang Shihai S

Frontiers in nutrition 20230216

<h4>Background</h4>Fat is a critical component in milk, which provided energy for the early growth and development of mammals. Milk fat is positively related to the concentration of acetate in the blood, while the underlying mechanism is still unclear.<h4>Objective</h4>This study is to investigate the effects of sodium acetate (NaAc) on milk fat synthesis in the mammary gland, and explored the underlying mechanism.<h4>Methods</h4><i>In vitro</i> experiments were carried out in mouse mammary epit ...[more]

PMID: 36969813

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Project description:Supplementation with sodium acetate (NaAcet) increases milk fat production through an apparent stimulation of de novo lipogenesis in the mammary gland. Sodium acetate increases acetate supply to the mammary gland, but it also increases dietary cation-anion difference, which can also increase milk fat yield. The objective of this study was to determine if the effect of NaAcet on milk fat production was due to an increase in acetate supply or an increase in dietary cation-anion difference. The study included 12 multiparous cows in a replicated 3 × 3 Latin square design balanced for carryover effects, with 14-d experimental periods. Treatments were a basal total mixed ration (31.8% neutral detergent fiber, 14.8% crude protein, 25.5% starch, and 4.4% fatty acids on a dry matter basis) as a no-supplement control, acetate supplemented at 3.25% of dry matter as NaAcet, and sodium bicarbonate (NaHCO3) providing an equal amount of sodium to the NaAcet treatment. The NaAcet and NaHCO3 were mixed into the basal diet before feeding. Milk samples were taken at each milking during the last 3 d of each period. Plasma samples were taken every 9 h during the last 3 d (a total of 8 times) to determine concentrations of plasma metabolites and hormones. Eating behavior was monitored during the last week of each period using an automated system. The NaAcet and NaHCO3 treatments increased milk fat concentration and yield compared to the no-supplement control. The NaAcet treatment increased milk fat production predominantly by increasing the yield of de novo and mixed-source fatty acids. The NaHCO3 treatment increased the yield of preformed and de novo fatty acids, suggesting different mechanisms for the 2 treatments. The NaAcet treatment increased plasma acetate concentration in a period of the day concurrent with the highest dry matter intake. The NaAcet treatment increased milk fat production by stimulating the production of de novo fatty acids, a mechanism consistent with previous reports, possibly by increasing acetate supply to the mammary gland. The NaHCO3 treatment increased milk fat production by increasing the production of all biological categories of fatty acids, except for odd and branched-chain fatty acids, possibly by increasing overall diet digestibility.

Dataset Information

Sodium acetate regulates milk fat synthesis through the activation of GPR41/GPR43 signaling pathway.

Background

Objective

Methods

Results

Conclusion

Publications

Sodium acetate regulates milk fat synthesis through the activation of GPR41/GPR43 signaling pathway.

Similar Datasets

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