PMID- 36902049
OWN - NLM
STAT- MEDLINE
DCOM- 20230410
LR  - 20230410
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 24
IP  - 5
DP  - 2023 Feb 27
TI  - Oral Administration of Lipopolysaccharide Enhances Insulin Signaling-Related 
      Factors in the KK/Ay Mouse Model of Type 2 Diabetes Mellitus.
LID - 10.3390/ijms24054619 [doi]
LID - 4619
AB  - Lipopolysaccharide (LPS), an endotoxin, induces systemic inflammation by 
      injection and is thought to be a causative agent of chronic inflammatory 
      diseases, including type 2 diabetes mellitus (T2DM). However, our previous 
      studies found that oral LPS administration does not exacerbate T2DM conditions in 
      KK/Ay mice, which is the opposite of the response from LPS injection. Therefore, 
      this study aims to confirm that oral LPS administration does not aggravate T2DM 
      and to investigate the possible mechanisms. In this study, KK/Ay mice with T2DM 
      were orally administered LPS (1 mg/kg BW/day) for 8 weeks, and blood glucose 
      parameters before and after oral administration were compared. Abnormal glucose 
      tolerance, insulin resistance progression, and progression of T2DM symptoms were 
      suppressed by oral LPS administration. Furthermore, the expressions of factors 
      involved in insulin signaling, such as insulin receptor, insulin receptor 
      substrate 1, thymoma viral proto-oncogene, and glucose transporter type 4, were 
      upregulated in the adipose tissues of KK/Ay mice, where this effect was observed. 
      For the first time, oral LPS administration induces the expression of adiponectin 
      in adipose tissues, which is involved in the increased expression of these 
      molecules. Briefly, oral LPS administration may prevent T2DM by inducing an 
      increase in the expressions of insulin signaling-related factors based on 
      adiponectin production in adipose tissues.
FAU - Yamamoto, Kazushi
AU  - Yamamoto K
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
FAU - Yamashita, Masashi
AU  - Yamashita M
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
FAU - Oda, Masataka
AU  - Oda M
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
FAU - Tjendana Tjhin, Vindy
AU  - Tjendana Tjhin V
AUID- ORCID: 0000-0002-3558-3678
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
FAU - Inagawa, Hiroyuki
AU  - Inagawa H
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
AD  - Research Institute for Healthy Living, Niigata University of Pharmacy and Applied 
      Life Sciences, Niigata 956-0841, Japan.
FAU - Soma, Gen-Ichiro
AU  - Soma GI
AD  - Control of Innate Immunity, Technology Research Association, Takamatsu 761-0301, 
      Japan.
AD  - Research Institute for Healthy Living, Niigata University of Pharmacy and Applied 
      Life Sciences, Niigata 956-0841, Japan.
LA  - eng
GR  - N/A/Control of Innate Immunity Collaborative Innovation Partnership/
GR  - SIP-No. 14533073/Council for Science from Technology and Innovation (CSTI) and 
      National Agriculture and Food Research Organization (NARO)/
PT  - Journal Article
DEP - 20230227
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Adiponectin)
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Adiponectin/metabolism
MH  - Administration, Oral
MH  - Blood Glucose/metabolism
MH  - *Diabetes Mellitus, Type 2/metabolism/therapy
MH  - Insulin/metabolism
MH  - Insulin Resistance/physiology
MH  - *Lipopolysaccharides/administration & dosage/pharmacology
MH  - *Diabetes Mellitus, Experimental/metabolism/therapy
PMC - PMC10003108
OTO - NOTNLM
OT  - adipose tissue
OT  - glucose tolerance
OT  - insulin resistance
OT  - lipopolysaccharide
OT  - oral administration
COIS- The authors declare no conflict of interest.
EDAT- 2023/03/12 06:00
MHDA- 2023/03/15 06:00
PMCR- 2023/02/27
CRDT- 2023/03/11 01:17
PHST- 2023/01/31 00:00 [received]
PHST- 2023/02/16 00:00 [revised]
PHST- 2023/02/21 00:00 [accepted]
PHST- 2023/03/11 01:17 [entrez]
PHST- 2023/03/12 06:00 [pubmed]
PHST- 2023/03/15 06:00 [medline]
PHST- 2023/02/27 00:00 [pmc-release]
AID - ijms24054619 [pii]
AID - ijms-24-04619 [pii]
AID - 10.3390/ijms24054619 [doi]
PST - epublish
SO  - Int J Mol Sci. 2023 Feb 27;24(5):4619. doi: 10.3390/ijms24054619.