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Research Article | Open Access

Comparative acetylome analysis reveals the potential mechanism of high fat diet function in allergic disease

Yanan Suna, Ning Liua, Huihui Wangb, Taiqi Qua, Fazheng Rena, Yixuan Lia( )
Key Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, China
College of Food Science and Engineering, Gansu Agricultural University, Lanzhou 730070, China

Peer review under responsibility of KeAi Communications Co., Ltd.

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Abstract

Modern technological lifestyles promote allergic diseases, especially food allergies. The underlying molecular mechanisms remain to be uncovered. Protein acetylation is one of the most important post-translational modifications, and it is involved in regulating multiple body metabolic processes. This study aimed to clarify the effects of a high-fat diet (HFD) on allergy risk and the underlying mechanisms. Four-week-old male C57BL/6J mice were randomly divided into two groups and fed a normal fat diet (NFD) or HFD for 24 weeks. Then, serum lipids were measured, and skeletal muscle was collected for acetylome analysis. Compared with the findings in the NFD group, HFD-fed mice were obese and hyperlipidemic. Acetylome analysis also revealed 32 differentially expressed proteins between the HFD and NFD groups. Among these, eight acetylated proteins were upregulated in the HFD group. In addition, 13 and 11 proteins were acetylated only in the HFD group and NFD group, respectively. These proteins were mainly involved in regulating energy metabolism and mitochondrial function. This study provides information regarding the underlying molecular mechanisms by which HFD promotes allergy.

Keywords

Allergic diseaseHigh fat dietSkeletal muscleAcetylome

References

[1]

S.H. Sicherer, H.A. Sampson, Food allergy: a review and update on epidemiology, pathogenesis, diagnosis, prevention, and management, J. Allergy Clin. Immun. 141 (2018) 41-58. http://dx.doi.org/10.1016/j.jaci.2017.11.003.
Crossref Google Scholar
[2]

G.H. Goossens, The metabolic phenotype in obesity: fat mass, body fat distribution, and adipose tissue function, Obesity Facts 10 (2017) 207-215. http://dx.doi.org/10.1159/000471488.
Crossref Google Scholar
[3]

M. Hussain, G.B., Rosso, C.K.C.K. Chuang, et al., High dietary fat intake induces a microbiota signature that promotes food allergy, J. Allergy Clin. Immun. 144 (2019) 157-170. http://dx.doi.org/10.1016/j.jaci.2019.01.043.
Crossref Google Scholar
[4]

S.M. Wright, L.J. Aronne, Causes of obesity, Abdom. Imaging 37 (2012) 730-732. http://dx.doi.org/10.1007/s00261-012-9862-x.
Crossref Google Scholar
[5]

B.J. Rolls, The supersizing of America: portion size and the obesity epidemic, Nutrition Today 38 (2003) 42-53. http://dx.doi.org/10.1097/00017285-200303000-00004.
Crossref Google Scholar
[6]

M. Ezzati, J. Bentham, C.M. Di, et al., Worldwide trends in body-mass index, underweight, overweight, and obesity from 1975 to 2016: a pooled analysis of 2416 population-based measurement studies in 128.9 million children, adolescents, and adults, Lancet 390 (2017) 2627-2642. http://dx.doi.org/10.1016/S0140-6736(17)32129-3.
Crossref Google Scholar
[7]

J.M. Blander, R.S. Longman, I.D. Iliev, Regulation of inflammation by microbiota interactions with the host, Nat. Immunol. 18 (2017) 851-860. http://dx.doi.org/10.1038/ni.3780.
Crossref Google Scholar
[8]

K.D. McCoy, A. Ignacio, M.B. Geuking, Microbiota and type 2 immune responses, Curr. Opin. Immunol. 54 (2018) 20-27. http://dx.doi.org/10.1016/j.coi.2018.05.009.
Crossref Google Scholar
[9]

A.J. Macpherson, M.G. Agueero, S.C. Ganal-Vonarburg, How nutrition and the maternal microbiota shape the neonatal immune system, Nat. Rev. Immunol. 17 (2017) 508-517. http://dx.doi.org/10.1038/nri.2017.58.
Crossref Google Scholar
[10]

Y. Sanz, A. Moya-Perez, Microbiota, inflammation and obesity, Adv. Exp. Med. Biol. 817 (2014) 291-317. http://dx.doi.org/10.1007/978-1-4939-0897-4_14.
Crossref Google Scholar
[11]

A.T. Stefka, T. Feehley, P. Tripathi, et al., Commensal bacteria protect against food allergen sensitization, PNAS 111 (2014) 13145-13150. http://dx.doi.org/10.1073/pnas.1412008111.
Crossref Google Scholar
[12]

M.N. Rivas, O.T. Burton, P. Wise, et al., A microbiota signature associated with experimental food allergy promotes allergic sensitization and anaphylaxis, J. Allergy Clin. Immun. 131 (2013) 201-212. http://dx.doi.org/10.1016/j.jaci.2012.10.026.
Crossref Google Scholar
[13]

D. Iyer, N. Mishra, A. Agrawal, Mitochondrial function in allergic disease, Curr. Allergy Asthm. R. 17 (2017) 29. http://dx.doi.org/10.1007/s11882-017-0695-0.
Crossref Google Scholar
[14]

C. Lipina, H.S. Hundal, Lipid modulation of skeletal muscle mass and function, J. Cachexia Sarcopeni. 8 (2017) 190-201. http://dx.doi.org/10.1002/jcsm.12144.
Crossref Google Scholar
[15]

J. Tumova, M. Andel, J. Trnka, Excess of free fatty acids as a cause of metabolic dysfunction in skeletal muscle. Physiol. Res. 6 (2016) 193-207. http://dx.doi.org/10.33549/physiolres.932993.
Crossref Google Scholar
[16]

S.R. Kim, D.I. Kim, S.H. Kim, et al., NLRP3 inflammasome activation by mitochondrial ROS in bronchial epithelial cells is required for allergic inflammation, Cell Death Dis. 5 (2014) e1498. http://dx.doi.org/10.1038/cddis.2014.460.
Crossref Google Scholar
[17]

P.H. Reddy, Mitochondrial dysfunction and oxidative stress in Asthma: implications for mitochondria-targeted antioxidant therapeutics, Pharmaceuticals 4 (2011) 429-456. http://dx.doi.org/10.3390/ph4030429.
Crossref Google Scholar
[18]

N.S. Nagaraj, O.V. Singh, N.B. Merchant, Proteomics: a strategy to understand the novel targets in protein misfolding and cancer therapy, Exp. Rev. Proteomic. 7 (2010) 613-623. http://dx.doi.org/10.1586/epr.10.70.
Crossref Google Scholar
[19]

C. Choudhary, B.T. Weinert, Y. Nishida, et al., The growing landscape of lysine acetylation links metabolism and cell signalling, Nat. Rev. Mol. Cell Bio. 15 (2014) 536-550. http://dx.doi.org/10.1038/nrm3841.
Crossref Google Scholar
[20]

A. Lundby, K. Lage, B.T. Weinert, et al., Proteomic analysis of lysine acetylation sites in rat tissues reveals organ specificity and subcellular patterns, Cell Rep. 2 (2012) 419-431. http://dx.doi.org/10.1016/j.celrep.2012.07.006.
Crossref Google Scholar
[21]

J.M. Thompson, J. Nagel, S. Hoving, et al.,Quantitative Lys-epsilon-Gly-Gly (diGly) proteomics coupled with inducible RNAi reveals ubiquitin-mediated proteolysis of DNA damage-inducible transcript 4 (DDIT4) by the E3 ligase HUWE1, J. Biol. Chem. 289 (2014) 28942-28955. http://dx.doi.org/10.1074/jbc.M114.573352.
Crossref Google Scholar
[22]

S. Pendyala, J.M. Walker, P.R. Holt, A high-fat diet is associated with endotoxemia that originates from the gut, Gastroenterology 142 (2012) 1100-1101. http://dx.doi.org/10.1053/j.gastro.2012.01.034.
Crossref Google Scholar
[23]

Y. Nie, F. Luo, Q. Lin, Dietary nutrition and gut microflora: a promising target for treating diseases, Trends Food Sci. Tech. 75 (2018) 72-80. http://dx.doi.org/10.1016/j.tifs.2018.03.002.
Crossref Google Scholar
[24]

P.D. Cani, R. Bibiloni, C. Knauf, et al., Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice, Diabetes 57 (2008) 1470-1481. http://dx.doi.org/10.2337/db07-1403.
Crossref Google Scholar
[25]

J.R. Pieklik, R.W. Guynn, Equilibrium-constants of reactions of choline-acetyltransferase, carnitine acetyltransferase, and acetylcholinesterase under physiological conditions, J. Biol. Chem. 250 (1975) 4445-4450.
Crossref Google Scholar
[26]

D.M. Muoio, R.C. Noland, J.P. Kovalik, et al., Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility, Cell Metab. 15 (2012) 764-777. http://dx.doi.org/10.1016/j.cmet.2012.04.005.
Crossref Google Scholar
[27]

L.M. Hinder, C. Figueroa-Romero, C. Pacut, et al., Long-chain Acyl coenzyme A synthetase 1 overexpression in primary cultured Schwann cells prevents long chain fatty acid-induced oxidative stress and mitochondrial dysfunction, Antioxid. Redox Sign. 21 (2014) 558-600. http://dx.doi.org/10.1089/ars.2013.5248.
Crossref Google Scholar
[28]

V. Skop, M. Cahova, H. Dankova, et al., Autophagy inhibition in early but not in later stages prevents 3T3-L1 differentiation: effect on mitochondrial remodeling, Differentiation 87 (2014) 220-229. http://dx.doi.org/10.1016/j.diff.2014.06.002.
Crossref Google Scholar
[29]

D. Wang, J. Wang, G.M.C. Bonamy, et al., A small molecule promotes mitochondrial fusion in mammalian cells, Angewandte Chemie-International Edition 51 (2012) 9302-9305. http://dx.doi.org/10.1002/anie.201204589.
Crossref Google Scholar
[30]

A.I. Jonckheere, J.A.M. Smeitink, R.J.T. Rodenburg, Mitochondrial ATP synthase: architecture, function and pathology, J. Inherit. Metab. Dis. 35 (2012) 211-225. http://dx.doi.org/10.1007/s10545-011-9382-9.
Crossref Google Scholar
[31]

S.L. Wu, M.J. Sampson, W.K. Decker, et al., Each mammalian mitochondrial outer membrane porin protein is dispensable: effects on cellular respiration, BBA-Mol. Cell. Res. 1452 (1999) 68-78. http://dx.doi.org/10.1016/s0167-4889(99)00120-2.
Crossref Google Scholar
[32]

G. Bathori, G. Csordas, C. Garcia-Perez, et al., Ca2+-dependent control of the permeability properties of the mitochondrial outer membrane and voltage-dependent anion-selective channel (VDAC), J. Biol. Chem. 281 (2006) 17347-17358. http://dx.doi.org/10.1074/jbc.M600906200.
Crossref Google Scholar
[33]

V. Shoshan-Barmatz, E.N. Maldonado, Y. Krelin, VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress, Cell Stress 1 (2017) 11-36. http://dx.doi.org/10.15698/cst2017.10.104.
Crossref Google Scholar
[34]

F. Baertling, L. Sanchez-Caballero, M.A.M. van den Brand, et al., NDUFA9 point mutations cause a variable mitochondrial complex Ⅰ assembly defect, Clin. Genet. 93 (2018) 111-118. http://dx.doi.org/10.1111/cge.13089.
Crossref Google Scholar
[35]

B.J.C. van den Bosch, M. Gerards, W. Sluiter, et al., Defective NDUFA9 as a novel cause of neonatally fatal complex Ⅰ disease, J. Med. Genet. 49 (2012) 10-15. http://dx.doi.org/10.1136/jmedgenet-2011-100466.
Crossref Google Scholar
Food Science and Human Wellness
Volume 12 Issue 3,
May 2023
Pages 889-894
DOI: 10.1016/j.fshw.2022.09.019
Cite this article:
Sun Y, Liu N, Wang H, et al. Comparative acetylome analysis reveals the potential mechanism of high fat diet function in allergic disease. Food Science and Human Wellness, 2023, 12(3): 889-894. https://doi.org/10.1016/j.fshw.2022.09.019

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Received: 19 June 2021
Revised: 14 October 2021
Accepted: 07 December 2021
Published: 15 October 2022
© 2023 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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