Swimming Training in a T2DM Zebrafish Model Restores Mitochondrial Function to Alleviate Anxiety-Like Behaviors and Metabolic Dysregulation

Introduction: Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dys...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in bioscience (Landmark. Print) Vol. 30; no. 5; p. 37100
Main Authors Fang, Yimeng, Qu, Junying, Zhao, Jing, Qu, Linkai, Wang, Lei, Luo, Cheng, Yang, Qinsi, Wu, Wei, Sun, Da, He, Dongjuan
Format Journal Article
LanguageEnglish
Published IMR Press 22.05.2025
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Introduction: Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dysfunction and behavioral abnormalities, the mechanism by which ST achieves this remains unclear. Objective: To investigate how ST improves T2DM and associated anxiety-like behaviors by regulating mitochondrial structure and function. Methods: T2DM was induced in zebrafish with a high-sugar diet, followed by 20 days of ST. Behavioral analysis assessed anxiety-like behaviors, while ELISA and microscopic imaging techniques were used to evaluate changes in mitochondrial structure and function in liver tissue. Results: ST significantly alleviated anxiety-like behavior and mitigated mitochondrial damage. Furthermore, ST counteracted mitochondrial dysfunction induced by oxidative stress through regulation of reactive oxygen species levels (p < 0.01), stabilization of mitochondrial membrane potential (p < 0.0001), and increasing the production of adenosine triphosphate (p < 0.01). ST also improved T2DM markers, including blood glucose regulation (p < 0.001), insulin level (p < 0.05), and lipid metabolism (p < 0.01 for low-density lipoprotein cholesterol (LDL-C), p < 0.01 for high-density lipoprotein cholesterol (HDL-C), p < 0.01 for total cholesterol (T-CHO)). Conclusions: This research provides insights into the intricate interplay between mitochondrial dysfunction in T2DM and behavioral outcomes while highlighting the potential of ST as a holistic therapeutic strategy for T2DM patients.
AbstractList Introduction: Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dysfunction and behavioral abnormalities, the mechanism by which ST achieves this remains unclear. Objective: To investigate how ST improves T2DM and associated anxiety-like behaviors by regulating mitochondrial structure and function. Methods: T2DM was induced in zebrafish with a high-sugar diet, followed by 20 days of ST. Behavioral analysis assessed anxiety-like behaviors, while ELISA and microscopic imaging techniques were used to evaluate changes in mitochondrial structure and function in liver tissue. Results: ST significantly alleviated anxiety-like behavior and mitigated mitochondrial damage. Furthermore, ST counteracted mitochondrial dysfunction induced by oxidative stress through regulation of reactive oxygen species levels (p < 0.01), stabilization of mitochondrial membrane potential (p < 0.0001), and increasing the production of adenosine triphosphate (p < 0.01). ST also improved T2DM markers, including blood glucose regulation (p < 0.001), insulin level (p < 0.05), and lipid metabolism (p < 0.01 for low-density lipoprotein cholesterol (LDL-C), p < 0.01 for high-density lipoprotein cholesterol (HDL-C), p < 0.01 for total cholesterol (T-CHO)). Conclusions: This research provides insights into the intricate interplay between mitochondrial dysfunction in T2DM and behavioral outcomes while highlighting the potential of ST as a holistic therapeutic strategy for T2DM patients.
Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dysfunction and behavioral abnormalities, the mechanism by which ST achieves this remains unclear.INTRODUCTIONAnxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dysfunction and behavioral abnormalities, the mechanism by which ST achieves this remains unclear.To investigate how ST improves T2DM and associated anxiety-like behaviors by regulating mitochondrial structure and function.OBJECTIVETo investigate how ST improves T2DM and associated anxiety-like behaviors by regulating mitochondrial structure and function.T2DM was induced in zebrafish with a high-sugar diet, followed by 20 days of ST. Behavioral analysis assessed anxiety-like behaviors, while ELISA and microscopic imaging techniques were used to evaluate changes in mitochondrial structure and function in liver tissue.METHODST2DM was induced in zebrafish with a high-sugar diet, followed by 20 days of ST. Behavioral analysis assessed anxiety-like behaviors, while ELISA and microscopic imaging techniques were used to evaluate changes in mitochondrial structure and function in liver tissue.ST significantly alleviated anxiety-like behavior and mitigated mitochondrial damage. Furthermore, ST counteracted mitochondrial dysfunction induced by oxidative stress through regulation of reactive oxygen species levels (p < 0.01), stabilization of mitochondrial membrane potential (p < 0.0001), and increasing the production of adenosine triphosphate (p < 0.01). ST also improved T2DM markers, including blood glucose regulation (p < 0.001), insulin level (p < 0.05), and lipid metabolism (p < 0.01 for low-density lipoprotein cholesterol (LDL-C), p < 0.01 for high-density lipoprotein cholesterol (HDL-C), p < 0.01 for total cholesterol (T-CHO)).RESULTSST significantly alleviated anxiety-like behavior and mitigated mitochondrial damage. Furthermore, ST counteracted mitochondrial dysfunction induced by oxidative stress through regulation of reactive oxygen species levels (p < 0.01), stabilization of mitochondrial membrane potential (p < 0.0001), and increasing the production of adenosine triphosphate (p < 0.01). ST also improved T2DM markers, including blood glucose regulation (p < 0.001), insulin level (p < 0.05), and lipid metabolism (p < 0.01 for low-density lipoprotein cholesterol (LDL-C), p < 0.01 for high-density lipoprotein cholesterol (HDL-C), p < 0.01 for total cholesterol (T-CHO)).This research provides insights into the intricate interplay between mitochondrial dysfunction in T2DM and behavioral outcomes while highlighting the potential of ST as a holistic therapeutic strategy for T2DM patients.CONCLUSIONSThis research provides insights into the intricate interplay between mitochondrial dysfunction in T2DM and behavioral outcomes while highlighting the potential of ST as a holistic therapeutic strategy for T2DM patients.
Author Qu, Linkai
Sun, Da
Qu, Junying
Zhao, Jing
Wu, Wei
Wang, Lei
He, Dongjuan
Luo, Cheng
Yang, Qinsi
Fang, Yimeng
Author_xml – sequence: 1
  givenname: Yimeng
  orcidid: 0000-0002-0859-7011
  surname: Fang
  fullname: Fang, Yimeng
– sequence: 2
  givenname: Junying
  orcidid: 0009-0004-2217-990X
  surname: Qu
  fullname: Qu, Junying
– sequence: 3
  givenname: Jing
  orcidid: 0009-0002-1306-5906
  surname: Zhao
  fullname: Zhao, Jing
– sequence: 4
  givenname: Linkai
  orcidid: 0009-0000-6583-0222
  surname: Qu
  fullname: Qu, Linkai
– sequence: 5
  givenname: Lei
  orcidid: 0000-0003-2704-9544
  surname: Wang
  fullname: Wang, Lei
– sequence: 6
  givenname: Cheng
  orcidid: 0009-0008-2257-6066
  surname: Luo
  fullname: Luo, Cheng
– sequence: 7
  givenname: Qinsi
  orcidid: 0009-0007-1707-6633
  surname: Yang
  fullname: Yang, Qinsi
– sequence: 8
  givenname: Wei
  orcidid: 0000-0003-3900-5135
  surname: Wu
  fullname: Wu, Wei
– sequence: 9
  givenname: Da
  orcidid: 0000-0001-7747-9951
  surname: Sun
  fullname: Sun, Da
– sequence: 10
  givenname: Dongjuan
  orcidid: 0009-0001-1750-127X
  surname: He
  fullname: He, Dongjuan
BookMark eNo9UcFuEzEQtVCRKKUH_sBHOCx47N2sfUxbUiolQoJw4WLNemcTF8cu9qaQb-hPs20o0kjvafTeG83Ma3YSUyTG3oL4oEBo9XFxsVQtCPGCncp2pqvZzOiTZ94KeMXOS7kVQkgDYBp9yh6-_fa7nY8bvs7o4yPxkSNfy6sV_0FdxsGXLV-lngL_SmVMmQpf-TG5bYp99hj4Yh_d6FPkY-LzEOje40h8Hv94Gg_V0v8kfkFbvPcpF46x5ysasUvBO351KJk2-4CP_jfs5YCh0Pk_PGPfF5_Wl5-r5Zfrm8v5snJKNmPVAUylEBrVQ9MPqqXOdK6DXpuaHIAA0BqNUgqUUFpqo1tV107VPSqo1Rm7Oeb2CW_tXfY7zAeb0NunRsobi3n0LpDtJn_tUGg99DUYMkaCcC1IrSeQesp6d8y6y-nXfrqP3fniKASMlPbFKglN0zailZP0_VHqcirT2sP_0SDs0__s8__UX9qAjY8
Cites_doi 10.1016/j.envpol.2024.125588.
10.3390/ijms241310635.
10.7326/0003-4819-147-6-200709180-00005.
10.1007/s10495-022-01731-2.
10.1016/j.jhazmat.2024.133953.
10.3390/biology13040209.
10.1016/j.tibs.2020.03.009.
10.1038/s41598-023-29668-9.
10.1016/j.ctim.2022.102820.
10.1016/j.scitotenv.2025.179172.
10.2147/DMSO.S243024.
10.1126/science.abq5209.
10.1007/s00125-016-4164-4.
10.1002/alz.037238.
10.1038/nrm.2017.95.
10.1016/j.diabres.2019.107843.
10.1111/obr.12317.
10.1016/j.brainresbull.2023.110725.
10.32598/bcn.9.10.450.
10.1073/pnas.1214364110.
10.1016/j.cegh.2022.101016.
10.1016/j.bbadis.2016.11.010.
10.1016/j.physbeh.2021.113665.
10.3389/fphar.2024.1407200.
10.2337/db16-0556.
10.1249/MSS.0000000000002800.
10.1371/journal.pcbi.1008644.
10.1080/21691401.2019.1641509.
10.1038/s42255-019-0124-x.
10.1038/s41420-018-0109-7.
10.1186/s12864-018-4647-4.
10.1155/2023/6663141.
10.1016/j.tins.2019.07.002.
10.1136/bmjopen-2019-031612.
10.1016/j.chemosphere.2022.136431.
ContentType Journal Article
Copyright 2025 The Author(s). Published by IMR Press.
Copyright_xml – notice: 2025 The Author(s). Published by IMR Press.
DBID AAYXX
CITATION
7X8
DOA
DOI 10.31083/FBL37100
DatabaseName CrossRef
MEDLINE - Academic
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE - Academic
DatabaseTitleList
CrossRef
MEDLINE - Academic
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 2768-6698
ExternalDocumentID oai_doaj_org_article_b0384ca088fd419e99210c712880c728
10_31083_FBL37100
GroupedDBID 3IV
53G
AAFWJ
AAYXX
AFPKN
ALMA_UNASSIGNED_HOLDINGS
CITATION
GROUPED_DOAJ
7X8
EMOBN
ID FETCH-LOGICAL-c325t-b11b113a153d15df37eb9bcb1d894ec1101188a93331303828987344c34da3143
IEDL.DBID DOA
ISSN 2768-6701
2768-6698
IngestDate Wed Aug 27 01:26:37 EDT 2025
Wed Jul 02 02:46:55 EDT 2025
Thu Jul 03 08:22:31 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 5
Language English
License https://creativecommons.org/licenses/by/4.0
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c325t-b11b113a153d15df37eb9bcb1d894ec1101188a93331303828987344c34da3143
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0009-0004-2217-990X
0000-0002-0859-7011
0009-0002-1306-5906
0000-0003-2704-9544
0000-0003-3900-5135
0009-0007-1707-6633
0009-0001-1750-127X
0000-0001-7747-9951
0009-0000-6583-0222
0009-0008-2257-6066
OpenAccessLink https://doaj.org/article/b0384ca088fd419e99210c712880c728
PQID 3215575072
PQPubID 23479
ParticipantIDs doaj_primary_oai_doaj_org_article_b0384ca088fd419e99210c712880c728
proquest_miscellaneous_3215575072
crossref_primary_10_31083_FBL37100
PublicationCentury 2000
PublicationDate 2025-05-22
PublicationDateYYYYMMDD 2025-05-22
PublicationDate_xml – month: 05
  year: 2025
  text: 2025-05-22
  day: 22
PublicationDecade 2020
PublicationTitle Frontiers in bioscience (Landmark. Print)
PublicationYear 2025
Publisher IMR Press
Publisher_xml – name: IMR Press
References ref13
ref35
ref12
ref34
ref15
ref14
ref36
ref31
ref30
ref11
ref33
ref10
ref32
ref2
ref1
ref17
ref16
ref19
ref18
ref24
ref23
ref26
ref25
ref20
ref22
ref21
ref28
ref27
ref29
ref8
ref7
ref9
ref4
ref3
ref6
ref5
References_xml – ident: ref27
  doi: 10.1016/j.envpol.2024.125588.
– ident: ref24
  doi: 10.3390/ijms241310635.
– ident: ref11
  doi: 10.7326/0003-4819-147-6-200709180-00005.
– ident: ref28
  doi: 10.1007/s10495-022-01731-2.
– ident: ref20
  doi: 10.1016/j.jhazmat.2024.133953.
– ident: ref22
  doi: 10.3390/biology13040209.
– ident: ref3
  doi: 10.1016/j.tibs.2020.03.009.
– ident: ref25
  doi: 10.1038/s41598-023-29668-9.
– ident: ref29
  doi: 10.1016/j.ctim.2022.102820.
– ident: ref21
  doi: 10.1016/j.scitotenv.2025.179172.
– ident: ref9
  doi: 10.2147/DMSO.S243024.
– ident: ref33
  doi: 10.1126/science.abq5209.
– ident: ref31
  doi: 10.1007/s00125-016-4164-4.
– ident: ref18
  doi: 10.1002/alz.037238.
– ident: ref34
  doi: 10.1038/nrm.2017.95.
– ident: ref1
  doi: 10.1016/j.diabres.2019.107843.
– ident: ref12
  doi: 10.1111/obr.12317.
– ident: ref10
  doi: 10.1016/j.brainresbull.2023.110725.
– ident: ref35
  doi: 10.32598/bcn.9.10.450.
– ident: ref6
  doi: 10.1073/pnas.1214364110.
– ident: ref8
  doi: 10.1016/j.cegh.2022.101016.
– ident: ref32
  doi: 10.1016/j.bbadis.2016.11.010.
– ident: ref36
  doi: 10.1016/j.physbeh.2021.113665.
– ident: ref30
  doi: 10.3389/fphar.2024.1407200.
– ident: ref5
  doi: 10.2337/db16-0556.
– ident: ref13
  doi: 10.1249/MSS.0000000000002800.
– ident: ref14
  doi: 10.1371/journal.pcbi.1008644.
– ident: ref23
– ident: ref26
  doi: 10.1080/21691401.2019.1641509.
– ident: ref4
  doi: 10.1038/s42255-019-0124-x.
– ident: ref17
  doi: 10.1038/s41420-018-0109-7.
– ident: ref15
  doi: 10.1186/s12864-018-4647-4.
– ident: ref16
  doi: 10.1155/2023/6663141.
– ident: ref7
  doi: 10.1016/j.tins.2019.07.002.
– ident: ref2
  doi: 10.1136/bmjopen-2019-031612.
– ident: ref19
  doi: 10.1016/j.chemosphere.2022.136431.
SSID ssj0002911958
Score 2.2992325
Snippet Introduction: Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming...
Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST)...
SourceID doaj
proquest
crossref
SourceType Open Website
Aggregation Database
Index Database
StartPage 37100
SubjectTerms anxiety
mitochondrial damage
oxidative stress
swimming training
t2dm
Title Swimming Training in a T2DM Zebrafish Model Restores Mitochondrial Function to Alleviate Anxiety-Like Behaviors and Metabolic Dysregulation
URI https://www.proquest.com/docview/3215575072
https://doaj.org/article/b0384ca088fd419e99210c712880c728
Volume 30
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Na9wwEBUlEOiltElLt0nDNPQqYmvktXzcfCyhZHNoNxB6MbI-WtONN2Qd2vyG_OnM2N6Q0kMvAYPBGGyPR_PeIOk9IT7nGE0ekyB95aIk_m-lURFlCKn1hBAhj7zBeXY-Pr3QXy6zyydWX7wmrJcH7gN3UCVotLM0GKLXaRGKgpoUl1NZNXRS3TZfwrwnzRTXYFWwlFlnR0d8Wo7zJO1lhYjNGDyYHp4hy9r8BUadZv8_JbnDmelr8WogiDDpX-yNeBGaLbHZW0bebYv7b7_rqyvCG5gP5g5QN2Bhro5n8J1ngWO9-glscbaAr51tTFjBjMYt1bnGc7rBlLCM_we0S5gseH85EU6YNH94_aY8q38FGGQTb1ZgGw-z0FKuLGoHx3f0FT8Gy6-34mJ6Mj86lYOhgnSoslZWaUoHWqpyPs18xDxUReWq1JtCB0dMgNoNYwtEZGjjZszkqLVD7S0Ss3onNpplE94LSIPRBm3mvM-0JdYzTqJDp4tKRau9GYn9dWTL6143o6R-owt_uQ7_SBxyzB9vYKnr7gIlQDkkQPm_BBiJT-s_VtLQ4PkO24Tl7apEojPERpNcfXiOB-2Il4rNf5NMKrUrNtqb2_CRGElb7XXJ9wCOzduq
linkProvider Directory of Open Access Journals
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Swimming+Training+in+a+T2DM+Zebrafish+Model+Restores+Mitochondrial+Function+to+Alleviate+Anxiety-Like+Behaviors+and+Metabolic+Dysregulation&rft.jtitle=Frontiers+in+bioscience+%28Landmark.+Print%29&rft.au=Yimeng+Fang&rft.au=Junying+Qu&rft.au=Jing+Zhao&rft.au=Linkai+Qu&rft.date=2025-05-22&rft.pub=IMR+Press&rft.issn=2768-6701&rft.volume=30&rft.issue=5&rft.spage=37100&rft_id=info:doi/10.31083%2FFBL37100&rft.externalDBID=DOA&rft.externalDocID=oai_doaj_org_article_b0384ca088fd419e99210c712880c728
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2768-6701&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2768-6701&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2768-6701&client=summon