PMID- 25277804
OWN - NLM
STAT- MEDLINE
DCOM- 20150330
LR  - 20211021
IS  - 1476-511X (Electronic)
IS  - 1476-511X (Linking)
VI  - 13
DP  - 2014 Oct 2
TI  - Involvement of CSE/ H2S in high glucose induced aberrant secretion of adipokines 
      in 3T3-L1 adipocytes.
PG  - 155
LID - 10.1186/1476-511X-13-155 [doi]
LID - 155
AB  - BACKGROUND: Deregulated secretion of adipokines contributes to subclinical 
      systemic inflammation associated with type 2 diabetes mellitus (T2DM). However, 
      the mechanisms underlying are not fully understood. Hydrogen sulfide (H2S), as an 
      endogenous gasotransmitter, possesses an anti-inflammation activity. The aim of 
      this study was to examine the possible involvement of H2S in high glucose induced 
      adipokine secretion in 3T3-L1 adipocytes. METHODS: The expression of 
      cystathionine-gamma-lyase (CSE), the H2S-forming enzyme, was evaluated by 
      Western-blotting and real-time PCR. The secretion of TNF-alpha, MCP-1 and adiponectin 
      was determined by radioimmunoassay and enzyme-linked immunosorbent assay (ELISA), 
      respectively. Lentiviral empty vector and vector expressing mouse CSE were used 
      for in vitro transduction. RESULTS: High glucose (HG) significantly decreased CSE 
      expression at both protein and mRNA levels in mature 3T3-L1 adipocytes. In 
      parallel, HG significantly increased secretion of MCP-1 while decreasing 
      secretion of adiponectin, but had no effect on secretion of TNF-alpha. HG induced 
      changes in MCP-1 and adiponectin secretion were partly attenuated by forced 
      expression of CSE or sodium hydrosulfide (NaHS), a source of exogenous H2S. 
      CONCLUSION: High glucose induces aberrant secretion of adipokines in mature 
      3T3-L1 adipocytes, favoring inflammation. The mechanism is partly related to 
      inhibition of CSE/ H2S system.
FAU - Pan, Zhe
AU  - Pan Z
FAU - Wang, Hanbo
AU  - Wang H
FAU - Liu, Yuantao
AU  - Liu Y
FAU - Yu, Chunxiao
AU  - Yu C
FAU - Zhang, Yuchao
AU  - Zhang Y
FAU - Chen, Jicui
AU  - Chen J
FAU - Wang, Xiangdong
AU  - Wang X
FAU - Guan, Qingbo
AU  - Guan Q
AD  - Department of Endocrinology, Shandong Provincial Hospital affiliated to Shandong 
      University; Shandong Clinical Medical Center of Endocrinology and Metabolism; 
      Institute of Endocrinology and Metabolism; Shandong Academy of Clinical Medicine, 
      324 Jing 5 Rd, Jinan, Shandong 250021, P, R, China. guanqingbo163@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141002
PL  - England
TA  - Lipids Health Dis
JT  - Lipids in health and disease
JID - 101147696
RN  - 0 (Adipokines)
RN  - 0 (RNA, Messenger)
RN  - EC 4.4.1.1 (Cystathionine gamma-Lyase)
RN  - IY9XDZ35W2 (Glucose)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipogenesis
MH  - Adipokines/*metabolism
MH  - Animals
MH  - Cystathionine gamma-Lyase/genetics/*metabolism
MH  - Down-Regulation
MH  - Enzyme Repression
MH  - Glucose/*physiology
MH  - Hydrogen Sulfide/*metabolism
MH  - Mice
MH  - RNA, Messenger/genetics/metabolism
PMC - PMC4271437
EDAT- 2014/10/04 06:00
MHDA- 2015/03/31 06:00
PMCR- 2014/10/02
CRDT- 2014/10/04 06:00
PHST- 2014/06/29 00:00 [received]
PHST- 2014/09/28 00:00 [accepted]
PHST- 2014/10/04 06:00 [entrez]
PHST- 2014/10/04 06:00 [pubmed]
PHST- 2015/03/31 06:00 [medline]
PHST- 2014/10/02 00:00 [pmc-release]
AID - 1476-511X-13-155 [pii]
AID - 1167 [pii]
AID - 10.1186/1476-511X-13-155 [doi]
PST - epublish
SO  - Lipids Health Dis. 2014 Oct 2;13:155. doi: 10.1186/1476-511X-13-155.