Chronic oscillating glucose challenges disarrange innate immune homeostasis to potentiate the variation of neutrophil-lymphocyte ratio in rats with or without hidden diabetes mellitus

The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). An HD anima...

Full description

Saved in:
Bibliographic Details
Published inDiabetes, metabolic syndrome and obesity Vol. 11; pp. 277 - 288
Main Authors Yang, Gaoxiong, Yan, Rui, Tong, Huanjun, Zhang, Jitai, Chen, Bin, Xue, Xiangyang, Wang, Jue, Chu, Maoping, Jin, Shengwei, Li, Ming
Format Journal Article
LanguageEnglish
Published New Zealand Dove Medical Press Limited 01.01.2018
Taylor & Francis Ltd
Dove Medical Press
Subjects
Online AccessGet full text
ISSN1178-7007
1178-7007
DOI10.2147/DMSO.S160301

Cover

Abstract The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out. In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values. HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers.
AbstractList Gaoxiong Yang,1* Rui Yan,2* Huanjun Tong,3* Jitai Zhang,1 Bin Chen,4 Xiangyang Xue,5 Jue Wang,6 Maoping Chu,7 Shengwei Jin,8 Ming Li1 1Cardiac Regeneration Research Institute, Wenzhou Medical University, Wenzhou, China; 2School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China; 3The Second Clinical Medical College, Wenzhou Medical University, Wenzhou, China; 4Department of Medical Ultrasound, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; 5Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China; 6Department of Cardiac Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; 7Children's Heart Center, The Second Affiliated Hospital and Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, China; 8Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China *These authors contributed equally to this work Background: The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). Materials and methods: An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out. Results: In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6g/kg/6h) for 7days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50mg/kg/6h) totally blocked the glucose-induced alterations in lymphocyte and NLR values. Conclusion: HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers. Keywords: neutrophil-lymphocyte ratio, diabetes, oscillating glucose level, innate immune, rat
Background: The neutrophil--lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). Materials and methods: An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out. Results: In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values. Conclusion: HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers. Keywords: neutrophil--lymphocyte ratio, diabetes, oscillating glucose level, innate immune, rat
The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT).BACKGROUNDThe neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT).An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out.MATERIALS AND METHODSAn HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out.In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values.RESULTSIn HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values.HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers.CONCLUSIONHD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers.
Background: The neutrophil–lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). Materials and methods: An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague–Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out. Results: In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values. Conclusion: HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers.
The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated with hidden diabetes (HD), which is normal in fasting blood glucose (FBG) but abnormal in the oral glucose tolerance test (OGTT). An HD animal model for 27 days and an animal model with oscillating glucose (OG) for 7 days were applied on adult female Sprague-Dawley rats. OGTT, leukogram analysis, histology, and immunohistochemistry were carried out. In HD rats, the percentage of neutrophils increased but the percentage of lymphocytes decreased; hence, the NLR rose relative to sham. This may be a result of the OG levels often experienced by diabetic subjects, as normal rats given OG (6 g/kg/6 h) for 7 days had significantly reduced lymphocyte numbers and increased NLR compared with the values before and 1 h after oral glucose administration during OGTT. Glucose-induced disarrangement of partitions of circulating immune cells and NLR was involved in the increase in oxidative stress, as these changes were totally blocked by the antioxidant glutathione (GSH). GSH (50 mg/kg/6 h) totally blocked the glucose-induced alterations in lymphocyte and NLR values. HD associated with elevation of NLR values may be partly attributed to a homeostasis disorder of the innate inflammatory state, caused by oscillating hyperglycemia. Acute high glucose administration produced a significant decrease in lymphocyte number. OG administration potentiated this effect and increased the NLR value, which was blocked by GSH, suggesting that reactive oxygen species play a critical role in maintaining lymphocyte numbers.
Audience Academic
Author Tong, Huanjun
Li, Ming
Wang, Jue
Jin, Shengwei
Xue, Xiangyang
Yan, Rui
Yang, Gaoxiong
Chen, Bin
Zhang, Jitai
Chu, Maoping
AuthorAffiliation 4 Department of Medical Ultrasound, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
8 Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
3 The Second Clinical Medical College, Wenzhou Medical University, Wenzhou, China
1 Cardiac Regeneration Research Institute, Wenzhou Medical University, Wenzhou, China
5 Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China
7 Children’s Heart Center, The Second Affiliated Hospital and Yuying Children’s Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, China
2 School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China
6 Department of Cardiac Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
AuthorAffiliation_xml – name: 3 The Second Clinical Medical College, Wenzhou Medical University, Wenzhou, China
– name: 5 Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China
– name: 4 Department of Medical Ultrasound, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
– name: 1 Cardiac Regeneration Research Institute, Wenzhou Medical University, Wenzhou, China
– name: 6 Department of Cardiac Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
– name: 2 School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China
– name: 7 Children’s Heart Center, The Second Affiliated Hospital and Yuying Children’s Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, China
– name: 8 Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
Author_xml – sequence: 1
  givenname: Gaoxiong
  orcidid: 0000-0002-6787-5827
  surname: Yang
  fullname: Yang, Gaoxiong
– sequence: 2
  givenname: Rui
  surname: Yan
  fullname: Yan, Rui
– sequence: 3
  givenname: Huanjun
  surname: Tong
  fullname: Tong, Huanjun
– sequence: 4
  givenname: Jitai
  surname: Zhang
  fullname: Zhang, Jitai
– sequence: 5
  givenname: Bin
  surname: Chen
  fullname: Chen, Bin
– sequence: 6
  givenname: Xiangyang
  surname: Xue
  fullname: Xue, Xiangyang
– sequence: 7
  givenname: Jue
  surname: Wang
  fullname: Wang, Jue
– sequence: 8
  givenname: Maoping
  surname: Chu
  fullname: Chu, Maoping
– sequence: 9
  givenname: Shengwei
  orcidid: 0000-0002-4734-8114
  surname: Jin
  fullname: Jin, Shengwei
– sequence: 10
  givenname: Ming
  orcidid: 0000-0002-7699-4502
  surname: Li
  fullname: Li, Ming
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29942142$$D View this record in MEDLINE/PubMed
BookMark eNptk01v3CAQhq0qVZOmufVcIVWqeuhuAYM_LpGi7VekVDmkPSOM8ZoVhi3gVPvL-vc63t2mu1HMYUbwzDv41fAyO3He6Sx7TfCcElZ-_PT97nZ-RwqcY_IsOyOkrGYlxuXJQX6aXcS4wtNXYkbpi-yU1jWDenqW_Vn0wTujkI_KWCuTcUu0tKPyUSPVS2u1W-qIWhNlCBJyZJyTCcIwjE6j3g_axySjiSh5tPZJu2QmIPUa3csAufEO-Q45Pabg172xM7sZ1r1XG8DCdA6iUxLRb5N65MM2-jGh3rStdtBeNjrBPQZtrUljfJU976SN-mIfz7OfXz7_WHyb3dx-vV5c3cwUz6s0U4Wuugq3XDKpWsYqplXHVdmpSjFN8oJSplvFSYtVp3hZVLzNm66pKlbUHc7z8-x6p9t6uRLrYAYZNsJLI7YbPiyFDMkoq4WShBWsJLTQlGFF64a3pJREVRXhpMGgdbnTWo_NAF3BqCDtkejxiTO9WPp7UWDMc1yCwPu9QPC_Rh2TGExU4Ih02o9RUMxrXpGcE0DfPkJXfgwOrBKUUl7WmNDyP7WU8APGdR76qklUXIEZmFOSM6DmT1CwWj0YBQPZGdg_Knh3UNBraVMfvR2nQYjH4JtDRx6s-DefAHzYASr4GIPuHhCCxfQCxPQCxP4FAE4f4cqk7fzBjY19uugvhTkL5A
CitedBy_id crossref_primary_10_1186_s12974_024_03136_1
crossref_primary_10_1007_s40520_024_02831_6
crossref_primary_10_1038_s41419_019_1552_y
ContentType Journal Article
Copyright COPYRIGHT 2018 Dove Medical Press Limited
2018. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
2018 Yang et al. This work is published and licensed by Dove Medical Press Limited 2018
Copyright_xml – notice: COPYRIGHT 2018 Dove Medical Press Limited
– notice: 2018. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: 2018 Yang et al. This work is published and licensed by Dove Medical Press Limited 2018
DBID AAYXX
CITATION
NPM
3V.
7RV
7XB
8C1
8FI
8FJ
8FK
8G5
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
GNUQQ
GUQSH
KB0
M2O
MBDVC
NAPCQ
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
Q9U
7X8
5PM
DOA
DOI 10.2147/DMSO.S160301
DatabaseName CrossRef
PubMed
ProQuest Central (Corporate)
Nursing & Allied Health Database
ProQuest Central (purchase pre-March 2016)
Public Health Database (ProQuest)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Research Library
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central Database Suite (ProQuest)
ProQuest One
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Central Student
ProQuest Research Library
Nursing & Allied Health Database (Alumni Edition)
Research Library
Research Library (Corporate)
Nursing & Allied Health Premium
ProQuest Central Premium
ProQuest One Academic (New)
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
ProQuest Central Basic
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
PubMed
Publicly Available Content Database
Research Library Prep
ProQuest Central Student
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
Research Library (Alumni Edition)
ProQuest Central China
ProQuest Central
ProQuest Health & Medical Research Collection
Health Research Premium Collection
ProQuest Central Korea
Health & Medical Research Collection
ProQuest Research Library
ProQuest Central (New)
ProQuest Public Health
ProQuest Central Basic
ProQuest One Academic Eastern Edition
ProQuest Nursing & Allied Health Source
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
Nursing & Allied Health Premium
ProQuest One Academic UKI Edition
ProQuest Nursing & Allied Health Source (Alumni)
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList

MEDLINE - Academic
Publicly Available Content Database

PubMed
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: BENPR
  name: ProQuest Central
  url: http://www.proquest.com/pqcentral?accountid=15518
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1178-7007
EndPage 288
ExternalDocumentID oai_doaj_org_article_ca14647126e240c29b5d17a1c88151b0
PMC6005307
A576052134
29942142
10_2147_DMSO_S160301
Genre Journal Article
GeographicLocations China
GeographicLocations_xml – name: China
GroupedDBID ---
0YH
29F
2WC
53G
5VS
7RV
8C1
8FI
8FJ
8G5
AAYXX
ABUWG
ACGFO
ADBBV
ADRAZ
AFKRA
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AOIJS
AZQEC
BAWUL
BCNDV
BENPR
BKEYQ
BPHCQ
BVXVI
C1A
CCPQU
CITATION
DIK
DWQXO
E3Z
EBD
EBS
EJD
FYUFA
GNUQQ
GROUPED_DOAJ
GUQSH
GX1
HYE
IAO
IHR
IHW
IPNFZ
ITC
KQ8
M2O
M48
M~E
NAPCQ
O5R
O5S
OK1
P2P
PGMZT
PHGZM
PHGZT
PIMPY
PQQKQ
PROAC
RIG
RNS
RPM
TDBHL
TR2
UKHRP
VDV
NPM
PMFND
3V.
7XB
8FK
MBDVC
PJZUB
PKEHL
PPXIY
PQEST
PQUKI
PRINS
Q9U
7X8
PUEGO
5PM
ID FETCH-LOGICAL-c538t-c6e8f80d5a4acd4484ecf5c7fc8c4e136224edc51d0cfc57685d3bfb88469f033
IEDL.DBID M48
ISSN 1178-7007
IngestDate Wed Aug 27 01:27:47 EDT 2025
Thu Aug 21 13:36:01 EDT 2025
Fri Sep 05 00:11:36 EDT 2025
Fri Jul 25 23:07:07 EDT 2025
Tue Jun 17 21:07:54 EDT 2025
Tue Jun 10 20:40:39 EDT 2025
Thu May 22 21:22:14 EDT 2025
Thu Jan 02 22:54:58 EST 2025
Thu Apr 24 23:11:48 EDT 2025
Tue Jul 01 01:45:11 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Keywords innate immune
rat
neutrophil–lymphocyte ratio
diabetes
oscillating glucose level
Language English
License http://creativecommons.org/licenses/by-nc/3.0
The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c538t-c6e8f80d5a4acd4484ecf5c7fc8c4e136224edc51d0cfc57685d3bfb88469f033
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
These authors contributed equally to this work
ORCID 0000-0002-7699-4502
0000-0002-6787-5827
0000-0002-4734-8114
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.2147/DMSO.S160301
PMID 29942142
PQID 2225790127
PQPubID 3933170
PageCount 12
ParticipantIDs doaj_primary_oai_doaj_org_article_ca14647126e240c29b5d17a1c88151b0
pubmedcentral_primary_oai_pubmedcentral_nih_gov_6005307
proquest_miscellaneous_2059581351
proquest_journals_2225790127
gale_infotracmisc_A576052134
gale_infotracacademiconefile_A576052134
gale_healthsolutions_A576052134
pubmed_primary_29942142
crossref_primary_10_2147_DMSO_S160301
crossref_citationtrail_10_2147_DMSO_S160301
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2018-01-01
PublicationDateYYYYMMDD 2018-01-01
PublicationDate_xml – month: 01
  year: 2018
  text: 2018-01-01
  day: 01
PublicationDecade 2010
PublicationPlace New Zealand
PublicationPlace_xml – name: New Zealand
– name: Macclesfield
PublicationTitle Diabetes, metabolic syndrome and obesity
PublicationTitleAlternate Diabetes Metab Syndr Obes
PublicationYear 2018
Publisher Dove Medical Press Limited
Taylor & Francis Ltd
Dove Medical Press
Publisher_xml – name: Dove Medical Press Limited
– name: Taylor & Francis Ltd
– name: Dove Medical Press
SSID ssj0000070422
Score 2.1052222
Snippet The neutrophil-lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is also elevated...
Background: The neutrophil--lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is...
Background: The neutrophil–lymphocyte ratio (NLR) has been considered as an inflammatory marker in various disorders, but it is not clear whether the NLR is...
Gaoxiong Yang,1* Rui Yan,2* Huanjun Tong,3* Jitai Zhang,1 Bin Chen,4 Xiangyang Xue,5 Jue Wang,6 Maoping Chu,7 Shengwei Jin,8 Ming Li1 1Cardiac Regeneration...
SourceID doaj
pubmedcentral
proquest
gale
pubmed
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 277
SubjectTerms Antioxidants (Nutrients)
Apoptosis
Blood glucose
Care and treatment
Control
Development and progression
Diabetes
Diabetes mellitus
Genetic aspects
Glucose
Glucose tolerance test
Health aspects
High definition television
Homeostasis
Hospitals
Hyperglycemia
Hypotheses
Immunohistochemistry
Immunology
Inflammation
innate immune
Lymphocytes
Neutrophil/lymphocyte ratio
Neutrophils
Original Research
oscillating glucose level
Oxidative stress
Pancreas
rat
Reactive oxygen species
Urine
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQD4gL4k1KASOBOKDQZGPncSyPqkJaOJRKvVmJY7ORtvYqj0r9Zf17zMROtBFCXDjtI7NR7BnPfOMdf0PI2zSudRqnPOSKs5ClqQ6LOoHlnmmVKK4hhuPh5PX39OyCfbvkl3utvrAmzNEDu4k7liWsZfCgq1RB8JGrouJ1nJWxzHMIVtWYrUMY20umHPDNkNzKdVbJwww-u6p3bMtz_GV9_uPjOTZY9r1gpng00vb_6Zz3otOycnIvFJ0-IPc9hqQn7tkfkjvKPCJ31_5f8sfk1jPeUiSq3GKxm_lFfW06lVP3lI7WTVe2LZ4uoI0xADppg6dFFN3YK2UBNnZNR3tLd7bHmiIUALhIryG9HvVJraZGDX1rd5tmG25vwDKsvAGx0azgpvimo7jXS207vtqhpxukLTF02valV0gK2g_dE3Jx-vXn57PQN2gIJfjJPpSpynUe1bxkpawh0WNKai4zLXPJVAyxccVgrnhcR1JLzGx4nVS6ygH0FDpKkqfkwFijnhMqoxgUCnCFJZLFGnAn3DcrKskjFWWlDsiHSU1CevZybKKxFZDFoFIFKlV4pQbk3Sy9c6wdf5H7hBqfZZBre_wCLFB4CxT_ssCAvEZ7Ee7g6uwxxAkMGI9GJywg70cJ9Bnw0LL0Rx9g6Mi-tZA8WkjCWpfLy5NNCu9rOoEZe1ZgCUFA3syX8ZdYP2eUHUAGUDTPsRtjQJ45E54HDYCEIfFeQLKFcS9mZXnFNJuRiTxFHx5lh_9jGl-QewBGc7e9dUQO-nZQLwHw9dWrcW3_BoDQVEg
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: ProQuest Central Database Suite (ProQuest)
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3NbtQwELbKVkJcEP8NFDASiAMKzY-dnwNCLbSqkHZBlEq9RYljdyNt7SXJIvXGO_A0vA5PwkzihEYITrtaz0Z2PJ75bM98Q8jzyC9V5Efc5ZIzl0WRctMyhOUeKxlKrsCHY3LyfBEdn7IPZ_xsiyyGXBgMqxxsYmeoSyPwjHwP9yVxihelb9dfXawahberQwmN3JZWKN90FGPXyHaAVZVnZPvgcPHp83jqguw2LAj6CHgs0bP3fn7y8fUJFlu2dWEG39RR-P9tqK94qmkU5RW3dHSL3LR4ku73CnCbbEl9h1yf2xvzu-SnZb-lSFq5wsA3fU5tnDoVQyWVhpZVk9c1ZhrQSmsAoLTCzBFJl-ZCGoCQTdXQ1tC1aTG-CAUAOtJvsNXu5pYaRbXctLVZL6vVr-8_VpegJ0ZcgmCnZPBY_NJQPPmlpu4-zaalSyQx0XQ4BKYXSBHabpp75PTo8Mu7Y9eWa3AFWM3WFZFMVOKVPGe5KGHbx6RQXMRKJIJJHzxlwOBtcb_0hBK4z-FlWKgiAQiUKi8M75OZNlruECo8P0l8AC8sFMxXgELhuXFaCO5JL86VQ14NE5UJy2WOJTVWGexpcFoznNbMTqtDXozS657D4x9yBzjnowwyb3c_mPo8sws5Ezn4FvDoQSQBDIkgLXjpx7kvoMPcLzyHPEWNyfo01tF-ZPswYEyUDplDXnYSaEGg0yK3iRAwdOTimkjuTiRh5Ytp86CVmbU8TfZnnTjk2diM_8RoOi3NBmQAU_MEazM65EGvxOOgAZ4wpOFzSDxR78lbmbboatnxkkdo0b344f-79YjcANCZ9MdYu2TW1hv5GIBdWzyxq_U3qJVTcw
  priority: 102
  providerName: ProQuest
Title Chronic oscillating glucose challenges disarrange innate immune homeostasis to potentiate the variation of neutrophil-lymphocyte ratio in rats with or without hidden diabetes mellitus
URI https://www.ncbi.nlm.nih.gov/pubmed/29942142
https://www.proquest.com/docview/2225790127
https://www.proquest.com/docview/2059581351
https://pubmed.ncbi.nlm.nih.gov/PMC6005307
https://doaj.org/article/ca14647126e240c29b5d17a1c88151b0
Volume 11
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAFT
  databaseName: Open Access Digital Library
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: KQ8
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html
  providerName: Colorado Alliance of Research Libraries
– providerCode: PRVAON
  databaseName: DOAJ Directory of Open Access Journals
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: DOA
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVBFR
  databaseName: Free Medical Journals - Free Access to All
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: DIK
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: http://www.freemedicaljournals.com
  providerName: Flying Publisher
– providerCode: PRVFQY
  databaseName: Free Medical Journals
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: GX1
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: http://www.gfmer.ch/Medical_journals/Free_medical.php
  providerName: Geneva Foundation for Medical Education and Research
– providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: M~E
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVAQN
  databaseName: PubMed Central (WRLC)
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: RPM
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/
  providerName: National Library of Medicine
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl: http://www.proquest.com/pqcentral?accountid=15518
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: BENPR
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Public Health Database (ProQuest)
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: 8C1
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/publichealth
  providerName: ProQuest
– providerCode: PRVFZP
  databaseName: Scholars Portal Open Access Journals
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 20250131
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: M48
  dateStart: 20081001
  isFulltext: true
  titleUrlDefault: http://journals.scholarsportal.info
  providerName: Scholars Portal
– providerCode: PRVAWR
  databaseName: Taylor & Francis Open Access
  customDbUrl:
  eissn: 1178-7007
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000070422
  issn: 1178-7007
  databaseCode: 0YH
  dateStart: 20081001
  isFulltext: true
  titleUrlDefault: https://www.tandfonline.com
  providerName: Taylor & Francis
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3dbtMwFLb2IyFu0PgPG8VIIC5QRtzYSXqB0DY2JqQOxKjUuyhx7DVSF3dJiugd78DT8Do8CeckTrVowE1bxaeW7XPs8x3n_BDyImCZDlggXKEEd3kQaHeU-bDdQ618JTTocAxOHp8FpxP-cSqmG6Tzn7cLWP3VtMN6UpNyvv_9avUONvxbdGNmPHzzfnz-af8c6yWDXby4crGkFL56tfU1Nsk2qKkhivzYYv8WG4eY_6p1hr_RT09NNdn8b57Z15RW36HymoY62SF3LLSkB60s3CUbqrhHbo3ty_P75JdNhEsxf-UcfeCKC2pd1qnsiqpUNMurpCwx6IDmRQFYlOYYRKLozFwqA2iyyitaG7owNboaIQGgSPoNrO6GzdRoWqhlXZrFLJ___vFzvgKRMXIFhI28Qbf4o6J4CUxN2XybZU1nmM-koN19ML3EbKH1snpAJifHX49OXVu5wZVwgNauDFSkIy8TCU9kBhYgV1ILGWoZSa4YKM0hh9USLPOklmjyiMxPdRoBGhppz_cfkq3CFOoxodJjUcQAx3BfcqYBkEK_4SiVwlNemGiHvO4YFUub1hyra8xjMG-QrTGyNbZsdcjLNfWiTefxD7pD5PmaBpNwNw9MeRHbPR3LBNQMKPdhoAAXyeEoFRkLEyZhwIKlnkOeocTEbUTr-iiJD2DCGDPtc4e8aihQvGHQMrExETB1TMvVo9zrUcIhIPvNnVTG3R6K0ZQPR-hb4JDn62b8JzrWFcosgQbgtYiwTKNDHrVCvJ40IBWOGfkcEvbEu7cq_ZYinzUpygM83L3wyf-HtUtuA_6M2hutPbJVl0v1FDBenQ7IZnTEBmT78Pjs85dBc1MCnx-m8Ax38R_Jp1r3
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3NbtQwELaqIgEXxD-BQo1ExQGFxlk7yR4QKi1VS7vl0FbqLSSO3Y20jZckC9ob78B7cOd1eBJmEic0QnDraVfr2cjOjGc-j-eHkBcBy3TAAuEKJbjLg0C742wE2z3UaqSEBhuOycmTo2DvlH84E2cr5EeXC4NhlZ1ObBR1ZiT6yDfxXBKO8aL07fyzi12j8Ha1a6HRisWBWn6FI1v1Zn8H-Lvh-7vvT7b3XNtVwJWwuWtXBirSkZeJhCcyg9MJV1ILGWoZSa4YKHSfq0wKlnlSS4TjIhulOo3AUo-1hw5QUPnXMNMI91W0zXqfDtbO4b7fxtdjA6DNncnxx9fH2MrZdp3pLF_TIOBvM3DJDg5jNC8Zvd3b5JZFq3SrFa87ZEUVd8n1ib2Pv0d-2tq6FEtizjCsrjinNgqeyq5PS0WzvErKEvMYaF4UAG9pjnkpik7NhTIAUKu8orWhc1Nj9BISADClX-Ag30gONZoWalGXZj7NZ7--fZ8tQQqNXAJhI8LwWPxSUfQrU1M2n2ZR0ymWSClo52KmF1iAtF5U98nplbDtAVktTKEeESo9FkUMoBEfSc40YFx4bjhOpfCUFybaIa86RsXSVkrHhh2zGE5MyNYY2Rpbtjpko6eetxVC_kH3Dnne02Bd7-YHU57HVk3EMgHLBXjBDxRALemPU5GxMGESJixY6jlkHSUmbpNke-0Ub8GCMQ17xB3ysqFA_QSTlolNs4ClY6WvAeXagBL0ihwOd1IZW71WxX92oUOe98P4T4zVK5RZAA0gdhFh50eHPGyFuF80gB-ORf4cEg7Ee_BWhiNFPm2qngdoL7zw8f-ntU5u7J1MDuPD_aODJ-QmwNuodZitkdW6XKinACHr9Fmzbyn5dNWK4jfkiIr7
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3NbtNAEF5VqVRxQfxjKHSRqDggE9vZtZ1DhVrSqKUkVJRKvRl7vdtYSr3BdkC98Q48Da_AY_AkzNjrUAvBradE2Ym165md-XZ2fgh57rup8l2f21xyZjPfV_YwHcB2D5QcSK7AhmNy8mTqH5yyt2f8bI38bHNhMKyy1Ym1ok61QB95H88lwRAvSvvKhEUcj8avF59t7CCFN61tO43YtFlId-pyYybJ40hefoXjXLlzOALeb3veeP_jmwPbdBywBWz8yha-DFXopDxmsUjh5MKkUFwESoSCSReUvcdkKribOkIJhOo8HSQqCcGKD5WDzlEwB-sB5ov2yPre_vT4w8rjg5V1mOc10ffYHqg_mpy8f3WCjZ5NT5rWLtbtA_42ElesZDeC84pJHN8iNw2WpbuN8N0mazK_QzYm5rb-LvlhKu9SLJg5x6C7_JyaGHkq2i4uJU2zMi4KzHKgWZ4D-KUZZq1IOtMXUgN8LbOSVpoudIWxTUgAsJV-gWN-LVdUK5rLZVXoxSyb__r2fX4JMqrFJRDWAg6PxS8lRa8z1UX9qZcVnWEBlZy2Dmh6geVJq2V5j5xeC-Puk16uc_mQUOG4YegCcGIDwVwFCBieGwwTwR3pBLGyyMuWUZEwddSxncc8gvMUsjVCtkaGrRbZXlEvmvoh_6DbQ56vaLDqd_2DLs4jo0QiEYNdAzTh-RKAmPCGCU_dIHYFTJi7iWORLZSYqEmhXemuaBcWjEnaA2aRFzUFai-YtIhNEgYsHeuAdSg3O5SgdUR3uJXKyGi9MvqzRy3ybDWM_8RIvlzqJdAAnuch9oW0yINGiFeLBmjEsASgRYKOeHfeSnckz2Z1TXQfrYkTPPr_tLbIBiiN6N3h9OgxuQHYN2y8aZukVxVL-QTwZZU8NRuXkk_XrSt-A_qPlgo
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=Chronic+oscillating+glucose+challenges+disarrange+innate+immune+homeostasis+to+potentiate+the+variation+of+neutrophil%E2%80%93lymphocyte+ratio+in+rats+with+or+without+hidden+diabetes+mellitus&rft.jtitle=Diabetes%2C+metabolic+syndrome+and+obesity&rft.au=Yang%2C+Gaoxiong&rft.au=Yan%2C+Rui&rft.au=Tong%2C+Huanjun&rft.au=Zhang%2C+Jitai&rft.date=2018-01-01&rft.pub=Taylor+%26+Francis+Ltd&rft.eissn=1178-7007&rft.volume=11&rft.spage=277&rft_id=info:doi/10.2147%2FDMSO.S160301&rft.externalDBID=HAS_PDF_LINK
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1178-7007&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1178-7007&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1178-7007&client=summon