PMID- 36262806
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20221101
IS  - 1178-7007 (Print)
IS  - 1178-7007 (Electronic)
IS  - 1178-7007 (Linking)
VI  - 15
DP  - 2022
TI  - Association of Lipopolysaccharide-Toll-Like Receptor 4 Signaling and 
      Microalbuminuria in Patients with Type 2 Diabetes Mellitus.
PG  - 3143-3152
LID - 10.2147/DMSO.S377776 [doi]
AB  - PURPOSE: Intestinal flora imbalance has been implicated in the activation of 
      innate immunity in the kidneys. However, little is known about the potential 
      links between lipopolysaccharide (LPS)-toll-like. receptor 4 (TLR4) signaling 
      activated by intestinal barrier dysfunction and microalbuminuria in type 2 
      diabetes mellitus (T2DM). PATIENTS AND METHODS: 61 patients with T2DM were 
      stratified based on the absence (n=32) or presence (n=29) of microalbuminuria. 
      There were also 28 control subjects. Urinary albumin excretion rate (UAER), serum 
      levels of LPS, D-lactic acid (DLA), diamine oxidase (DAO), fasting blood glucose 
      (FBG), interleukin-6 (IL-6), glycosylated hemoglobin A1 (HbA1c), and 
      high-sensitivity C-reactive protein (hs-CRP), and TLR4 expression in peripheral 
      blood mononuclear cells (PBMCs) were measured. RESULTS: hs-CRP, IL-6, LPS, DLA, 
      DAO, and TLR4 were markedly increased in subjects with T2DM compared to the 
      controls (P < 0.05 for all). Moreover, LPS was positively correlated with FBG, 
      HbA1c, hs-CRP, IL-6, UAER, DLA, DAO, and TLR4 (P < 0.05 for all). In addition, 
      TLR4 was positively correlated with UAER, hs-CRP, FBG, DLA, HbA1c, and LPS (P < 
      0.05 for all). In regression analyses, TLR4, LPS, HbA1c, and hs-CRP were 
      independently associated with UAER (P < 0.05 for all), while FBG, LPS, TLR4, and 
      hs-CRP (P < 0.05 for all) were found to be risk factors for microalbuminuria in 
      T2DM. CONCLUSION: Intestinal integrity is compromised in subjects with T2DM, and 
      the activation of LPS-TLR4 signaling might play an important role in the 
      development of microalbuminuria in T2DM.
CI  - (c) 2022 Zhang et al.
FAU - Zhang, Lijuan
AU  - Zhang L
AD  - Department of Blood Transfusion, Gansu Provincial Hospital, Lanzhou, People's 
      Republic of China.
FAU - Zhang, Yuanjun
AU  - Zhang Y
AD  - Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, People's 
      Republic of China.
AD  - Key Laboratory of Endocrine and Metabolic Diseases of Gansu Province, Lanzhou, 
      People's Republic of China.
FAU - Liu, Juxiang
AU  - Liu J
AD  - Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, People's 
      Republic of China.
AD  - Key Laboratory of Endocrine and Metabolic Diseases of Gansu Province, Lanzhou, 
      People's Republic of China.
FAU - Li, Yonghong
AU  - Li Y
AD  - Institute of Clinical and Translational Medicine, Gansu Provincial Hospital, 
      Lanzhou, People's Republic of China.
FAU - Quan, Jinxing
AU  - Quan J
AUID- ORCID: 0000-0001-7103-402X
AD  - Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, People's 
      Republic of China.
AD  - Key Laboratory of Endocrine and Metabolic Diseases of Gansu Province, Lanzhou, 
      People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20221017
PL  - New Zealand
TA  - Diabetes Metab Syndr Obes
JT  - Diabetes, metabolic syndrome and obesity : targets and therapy
JID - 101515585
PMC - PMC9575588
OTO - NOTNLM
OT  - intestinal mucosal barrier
OT  - lipopolysaccharide
OT  - microalbuminuria
OT  - toll-like receptor 4
OT  - type 2 diabetes mellitus
COIS- The authors report no conflicts of interest in this work.
EDAT- 2022/10/21 06:00
MHDA- 2022/10/21 06:01
PMCR- 2022/10/17
CRDT- 2022/10/20 02:45
PHST- 2022/06/09 00:00 [received]
PHST- 2022/10/05 00:00 [accepted]
PHST- 2022/10/20 02:45 [entrez]
PHST- 2022/10/21 06:00 [pubmed]
PHST- 2022/10/21 06:01 [medline]
PHST- 2022/10/17 00:00 [pmc-release]
AID - 377776 [pii]
AID - 10.2147/DMSO.S377776 [doi]
PST - epublish
SO  - Diabetes Metab Syndr Obes. 2022 Oct 17;15:3143-3152. doi: 10.2147/DMSO.S377776. 
      eCollection 2022.