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Effect of INSIG1 on the milk fat synthesis of buffalo mammary epithelial cells

Published online by Cambridge University Press:  10 September 2020

Xinyang Fan
Affiliation:
Faculty of Animal Science and Technology, Yunnan Agricultural University, Kunming, Yunnan, 650201, China
Lihua Qiu
Affiliation:
Faculty of Animal Science and Technology, Yunnan Agricultural University, Kunming, Yunnan, 650201, China
Xiaohong Teng
Affiliation:
Faculty of Animal Science and Technology, Yunnan Agricultural University, Kunming, Yunnan, 650201, China
Yongyun Zhang
Affiliation:
Teaching Demonstration Center of the Basic Experiments of Agricultural Majors, Yunnan Agricultural University, Kunming, Yunnan, 650201, China
Yongwang Miao*
Affiliation:
Faculty of Animal Science and Technology, Yunnan Agricultural University, Kunming, Yunnan, 650201, China
*
Author for correspondence: Yongwang Miao, Email: yongwangmiao1@126.com

Abstract

We hypothesized that insulin-induced gene 1 (INSIG1) affects milk fat synthesis in buffalo. For this reason, the protein abundance of INSIG1 in the mammary tissue of buffalo during the peak period of lactation and dry-off period was evaluated. The results showed that the expression of INSIG1 at the peak of lactation was lower than that in the dry-off period. To explore the role of INSIG1 in milk fat synthesis, the buffalo mammary epithelial cells (BMECs) were isolated and purified from buffalo mammary tissue, and INSIG1 gene were overexpressed and knocked down by constructing the recombinant lentivirus vector of INSIG1 gene and transfecting into BMECs. Results revealed that INSIG1 overexpression decreased the expression of INSIG2, SREBP, PPARG, SCD, GPAM, DGAT2 and AGPAT6, which led to reduction of triglycerides (TAG) content in the cell. In contrast, knockdown of INSIG1 had a positive effect on mRNA expression of the above genes. Overall, the data provide strong support for a key role of INSIG1 in the regulation of milk fat synthesis in BMECs.

Type
Research Article
Copyright
Copyright © The Author(s), 2020. Published by Cambridge University Press on behalf of Hannah Dairy Research Foundation.

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Footnotes

*

These authors contributed equally to this paper.

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