PMID- 36012625
OWN - NLM
STAT- MEDLINE
DCOM- 20221227
LR  - 20221227
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 23
IP  - 16
DP  - 2022 Aug 19
TI  - SEPT9 Upregulation in Satellite Glial Cells Associated with Diabetic 
      Polyneuropathy in a Type 2 Diabetes-like Rat Model.
LID - 10.3390/ijms23169372 [doi]
LID - 9372
AB  - Despite the worldwide prevalence and severe complications of type 2 diabetes 
      mellitus (T2DM), the pathophysiological mechanisms underlying the development of 
      diabetic polyneuropathy (DPN) are poorly understood. Beyond strict control of 
      glucose levels, clinical trials for reversing DPN have largely failed. Therefore, 
      understanding the pathophysiological and molecular mechanisms underlying DPN is 
      crucial. Accordingly, this study explored biochemical and neuropathological 
      deficits in a rat model of T2DM induced through high-fat diet (HFD) feeding along 
      with two low-dose streptozotocin (STZ) injections; the deficits were explored 
      through serum lipid, neurobehavioral, neurophysiology, neuropathology, and 
      immunohistochemistry examinations. Our HFD/STZ protocol induced (1) mechanical 
      hyperalgesia and depression-like behaviors, (2) loss of intraepidermal nerve 
      fibers (IENFs) and reduced axonal diameters in sural nerves, and (3) decreased 
      compound muscle action potential. In addition to hyperglycemia, which was 
      correlated with the degree of mechanical hyperalgesia and loss of IENFs, we 
      observed that hypertriglyceridemia was the most dominant deficit in the lipid 
      profiles of the diabetic rats. In particular, SEPT9, the fourth component of the 
      cytoskeleton, increased in the satellite glial cells (SGCs) of the dorsal root 
      ganglia (DRG) in the T2DM-like rats. The number of SEPT9(+) SGCs/DRG was 
      correlated with serum glucose levels and mechanical thresholds. Our findings 
      indicate the putative molecular mechanism underlying DPN, which presumably 
      involves the interaction of SGCs and DRG neurons; nevertheless, further 
      functional research is warranted to clarify the role of SEPT9 in DPN.
FAU - Kan, Hung-Wei
AU  - Kan HW
AD  - School of Medicine for International Students, College of Medicine, I-Shou 
      University, Kaohsiung 82445, Taiwan.
FAU - Ho, Yu-Cheng
AU  - Ho YC
AD  - School of Medicine, College of Medicine, I-Shou University, Kaohsiung 82445, 
      Taiwan.
FAU - Chang, Ying-Shuang
AU  - Chang YS
AD  - Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 80708, Taiwan.
FAU - Hsieh, Yu-Lin
AU  - Hsieh YL
AUID- ORCID: 0000-0002-6380-3455
AD  - Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 80708, Taiwan.
AD  - School of Post-Baccalaureate Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 80708, Taiwan.
AD  - Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung 
      80708, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20220819
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - IY9XDZ35W2 (Glucose)
RN  - 0 (Lipids)
RN  - 0 (Septin9 protein, rat)
RN  - EC 3.6.1.- (Septins)
RN  - 5W494URQ81 (Streptozocin)
SB  - IM
MH  - Animals
MH  - Rats
MH  - *Diabetes Mellitus, Experimental/pathology
MH  - *Diabetes Mellitus, Type 2/pathology
MH  - *Diabetic Neuropathies/pathology
MH  - Ganglia, Spinal/pathology
MH  - Glucose/therapeutic use
MH  - Hyperalgesia
MH  - Lipids/therapeutic use
MH  - *Neuralgia/pathology
MH  - Neuroglia/pathology
MH  - Rats, Sprague-Dawley
MH  - *Septins/genetics
MH  - Streptozocin
MH  - Up-Regulation
PMC - PMC9409324
OTO - NOTNLM
OT  - diabetic polyneuropathy
OT  - hypertriglyceridemia
OT  - neuropathic pain
OT  - satellite glial cell
OT  - septin-9
COIS- The authors declare no conflict of interest. The funders had no role in the 
      design of the study; in the collection, analyses, or interpretation of data; in 
      the writing of the manuscript; or in the decision to publish the results.
EDAT- 2022/08/27 06:00
MHDA- 2022/08/30 06:00
PMCR- 2022/08/19
CRDT- 2022/08/26 01:24
PHST- 2022/07/31 00:00 [received]
PHST- 2022/08/16 00:00 [revised]
PHST- 2022/08/18 00:00 [accepted]
PHST- 2022/08/26 01:24 [entrez]
PHST- 2022/08/27 06:00 [pubmed]
PHST- 2022/08/30 06:00 [medline]
PHST- 2022/08/19 00:00 [pmc-release]
AID - ijms23169372 [pii]
AID - ijms-23-09372 [pii]
AID - 10.3390/ijms23169372 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Aug 19;23(16):9372. doi: 10.3390/ijms23169372.