Adipose tissues of MPC1± mice display altered lipid metabolism-related enzyme expression levels

Shiying Zou; Liye Zhu; Kunlun Huang; Haoshu Luo; Wentao Xu; Xiaoyun He

doi:10.7717/peerj.5799

Adipose tissues of MPC1^± mice display altered lipid metabolism-related enzyme expression levels

PeerJ. 2018 Oct 30:6:e5799. doi: 10.7717/peerj.5799. eCollection 2018.

Authors

Shiying Zou^{1

2}, Liye Zhu^{1

2}, Kunlun Huang^{1

2}, Haoshu Luo³, Wentao Xu^{1

2}, Xiaoyun He^{1

2}

Affiliations

¹ China Agricultural University, Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, Beijing, China.
² Key Laboratory of Safety Assessment of Genetically Modified Organism (Food Safety), Ministry of Agriculture, Beijing, China.
³ China Agricultural University, College of Biological Sciences, Beijing, China.

Abstract

Mitochondrial pyruvate carrier 1 (MPC1) is a component of the MPC1/MPC2 heterodimer that facilitates the transport of pyruvate into mitochondria. Pyruvate plays a central role in carbohydrate, fatty, and amino acid catabolism. The present study examined epididymal white adipose tissue (eWAT) and intrascapular brown adipose tissue (iBAT) from MPC1^± mice following 24 weeks of feeding, which indicated low energy accumulation as evidenced by low body and eWAT weight and adipocyte volume. To characterize molecular changes in energy metabolism, we analyzed the transcriptomes of the adipose tissues using RNA-Sequencing (RNA-Seq). The results showed that the fatty acid oxidation pathway was activated and several genes involved in this pathway were upregulated. Furthermore, qPCR and western blotting indicated that numerous genes and proteins that participate in lipolysis were also upregulated. Based on these findings, we propose that the energy deficiency caused by reduced MPC1 activity can be alleviated by activating the lipolytic pathway.

Keywords: Energy metabolism; Mitochondrial pyruvate carrier 1; Pyruvate; RNA-Sequencing; White adipose tissue.

Grants and funding

This work was supported by the Genetically Modified Organisms Breeding Major Projects of the People’s Republic of China (2016ZX08011-005). There were no additional external funding received for this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.