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Review
. 2023 Jul 6;29(1):93.
doi: 10.1186/s10020-023-00684-9.

Roles of protein post-translational modifications in glucose and lipid metabolism: mechanisms and perspectives

Affiliations
Review

Roles of protein post-translational modifications in glucose and lipid metabolism: mechanisms and perspectives

Yu-Hang Yang et al. Mol Med. .

Abstract

The metabolism of glucose and lipids is essential for energy production in the body, and dysregulation of the metabolic pathways of these molecules is implicated in various acute and chronic diseases, such as type 2 diabetes, Alzheimer's disease, atherosclerosis (AS), obesity, tumor, and sepsis. Post-translational modifications (PTMs) of proteins, which involve the addition or removal of covalent functional groups, play a crucial role in regulating protein structure, localization function, and activity. Common PTMs include phosphorylation, acetylation, ubiquitination, methylation, and glycosylation. Emerging evidence indicates that PTMs are significant in modulating glucose and lipid metabolism by modifying key enzymes or proteins. In this review, we summarize the current understanding of the role and regulatory mechanisms of PTMs in glucose and lipid metabolism, with a focus on their involvement in disease progression associated with aberrant metabolism. Furthermore, we discuss the future prospects of PTMs, highlighting their potential for gaining deeper insights into glucose and lipid metabolism and related diseases.

Keywords: Glucose metabolism; Lipid metabolism; Metabolic disease; Post-translational modification.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Functions and effect of post-translational modifications in physiology and pathology
Fig. 2
Fig. 2
Roles of post-translational modifications in glucose metabolism
Fig. 3
Fig. 3
Roles of post-translational modifications in lipid metabolism
Fig. 4
Fig. 4
Roles of PTMs in metabolic diseases

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References

    1. Abrams AJ, Farooq A, Wang G. S-nitrosylation of apoe in Alzheimer’s disease. Biochemistry. 2011;50(17):3405–3407. doi: 10.1021/bi200266v. - DOI - PMC - PubMed
    1. Ahmed SA, Sarma P, Barge SR, Swargiary D, Devi GS, Borah JC. Xanthosine, a purine glycoside mediates hepatic glucose homeostasis through inhibition of gluconeogenesis and activation of glycogenesis via regulating the ampk/ foxo1/akt/gsk3beta signaling cascade. Chem Biol Interact. 2023;371:110347. doi: 10.1016/j.cbi.2023.110347. - DOI - PubMed
    1. Akasu R, Miyazaki T, Elhussiny MZ, Sugiura Y, Tomitsuka Y, Haraguchi S, et al. Calpain-mediated proteolytic production of free amino acids in vascular endothelial cells augments obesity-induced hepatic steatosis. J Biol Chem. 2022;298(6):101953. doi: 10.1016/j.jbc.2022.101953. - DOI - PMC - PubMed
    1. Anand S, Khan MA, Zubair H, Sudan SK, Vikramdeo KS, Deshmukh SK, et al. Myb sustains hypoxic survival of pancreatic cancer cells by facilitating metabolic reprogramming. EMBO Rep. 2023;24(3):e55643. doi: 10.15252/embr.202255643. - DOI - PMC - PubMed
    1. Andrew RJ, Fernandez CG, Stanley M, Jiang H, Nguyen P, Rice RC, et al. Lack of bace1 s-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer’s disease. Proc Natl Acad Sci U S A. 2017;114(45):E9665–E9674. doi: 10.1073/pnas.1708568114. - DOI - PMC - PubMed