Evidence map›Paper›PMID 39483005›Full record

ArticleAnimal bioscience2025

Guanidinoacetic acid regulated postmortem muscle glycolysis associated with AMPK signaling and protein acetylation.

Ning Liu, Bolin Zhang, Shubai Wang, Qingzhen Zhong, Zewei Sun

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Article in Animal bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Ning LiuCollege of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
Bolin ZhangCollege of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109, China.
Shubai WangCollege of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109, China.
Qingzhen ZhongCollege of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
Zewei SunCollege of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.

Funding

Lu-Yu Cooperation Project of Shandong Province 23-2-8-cspz-1-nshNational Natural Science Foundation of China 31760674National Natural Science Foundation of China 32360838Wellcome Trust 202201
6 · The paper itself

Abstract

objectiveAntemortem stress accelerated muscle energy consumption in postmortem muscle. The objective of our study was to investigate the regulation of guanidinoacetic acid (GAA) administration on the postmortem glycolysis and protein acetylation in postmortem muscle of antemortem stress.

methodsForty C57BL/6 male mice were chosen and randomly assigned to four treatment groups (A, B, C and D), each treatment consisted of 10 replicates. Mice in group B, C and D were treated with 0.05% GAA oral administration for 6 days. On the 7th day of the experiment, the mice in group A and B were injected with saline, and mice in group C and D were injected with 5-aminoimidazole-4-carboxamide1-β-D-ribofuranoside (AICAR; 50 μg/g body weight) and a combined injection with AICAR (50 μg/g body weight) and histone acetylase inhibitor II (HAT II; 185 μg/g body weight), respectively.

resultsThe results showed that the values of pH45min and pH24h of postmortem muscle in GAA administration were higher than those in the control group. However, the opposite result was observed in AICAR group. Moreover, the activities of pyruvate kinase, hexokinase and fruc-tose-2,6-diphosphatase, combined with the protein abundance of phosphorylated liver kinase, phosphorylated AMPKα2 and total acetylated protein were all decreased by GAA administration and HAT II treatment.

conclusionTaken together, adenosine 5'-monophosphate-activated protein kinase signaling and protein acetylation could mediate the regulation of GAA administration on postmortem glycolysis of antemortem stress-muscle.

Indexed as

Adenosine 5'-Monophosphate-Activated Protein Kinase (AMPK) SignalingAntemortem StressGlycolysisGuanidinoacetic AcidProtein Acetylation

Identifiers

PMID39483005
PMCPMC11917429

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