PMID- 26894024
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160219
LR  - 20200930
IS  - 2211-9132 (Print)
IS  - 2211-9140 (Electronic)
IS  - 2211-9132 (Linking)
VI  - 31
IP  - 3
DP  - 2012 Sep
TI  - Plasma leptin concentrations are greater in type II diabetic patients and 
      stimulate monocyte chemotactic peptide-1 synthesis via the mitogen-activated 
      protein kinase/extracellular signal-regulated kinase pathway.
PG  - 177-85
LID - 10.1016/j.krcp.2012.06.004 [doi]
AB  - BACKGROUND: Leptin is an adipokine that is recently reported to be a biomarker of 
      systemic inflammation. Although atherosclerosis causes cardiovascular diseases, 
      it is not clear whether leptin contributes to the acceleration of this process. 
      In this study, we investigated whether alterations of plasma leptin levels were 
      related to diabetic nephropathy and systemic inflammation. In addition, we 
      examined the physiologic action of leptin in cultured vascular smooth muscle 
      cells (VSMCs). METHODS: A total of 126 type 2 diabetic participants and 37 
      healthy controls were studied. The diabetic participants were divided into three 
      groups according to stage of nephropathy. We investigated whether leptin induced 
      monocyte chemotactic peptide-1 (MCP-1) synthesis through the mitogen-activated 
      protein kinase (MAPK) pathway using cultured VSMCs. RESULTS: Plasma leptin 
      concentrations were significantly higher in the diabetic group than in the 
      controls. Plasma leptin levels were positively correlated with body mass index, 
      fasting and postprandial blood glucose, hemoglobin A1c, total cholesterol, 
      urinary albumin excretion, high-sensitivity C-reactive protein (hsCRP), and MCP-1 
      plasma levels, and negatively correlated with creatinine clearance values. In 
      cultured VSMCs, leptin increased MCP-1 production in a dose-dependent manner, and 
      this stimulating effect of leptin on MCP-1 expression was reversed by the MAPK 
      (MEK) inhibitor PD98059. In addition, leptin stimulated the phosphorylation of 
      MEK, extracellular signal-regulated kinase, and E26-like transcription factor, 
      which are components of the MAPK pathway. CONCLUSIONS: Overall, these findings 
      suggest that activation of leptin synthesis may promote MCP-1 activation in a 
      diabetic environment via the MAPK pathway in VSMCs and that it possibly 
      contributes to the acceleration of atherosclerosis.
FAU - Cha, Jin Joo
AU  - Cha JJ
AD  - Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Korea.
FAU - Hyun, Young Youl
AU  - Hyun YY
AD  - Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Korea.
FAU - Jee, Yi Hwa
AU  - Jee YH
AD  - Medical Research Institute, Korea University, Ansan, Korea.
FAU - Lee, Mi Jin
AU  - Lee MJ
AD  - Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Korea.
FAU - Han, Kum Hyun
AU  - Han KH
AD  - Department of Internal Medicine, Inje University Ilsan-Paik Hospital, Ilsan, 
      Korea.
FAU - Kang, Young Sun
AU  - Kang YS
AD  - Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Korea.
FAU - Han, Sang Youb
AU  - Han SY
AD  - Department of Internal Medicine, Inje University Ilsan-Paik Hospital, Ilsan, 
      Korea.
FAU - Cha, Dae Ryong
AU  - Cha DR
AD  - Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Korea.
LA  - eng
PT  - Journal Article
DEP - 20120626
PL  - Korea (South)
TA  - Kidney Res Clin Pract
JT  - Kidney research and clinical practice
JID - 101586778
PMC - PMC4716089
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Diabetes mellitus
OT  - Leptin
OT  - Monocyte chemotactic peptide-1
OT  - Vascular smooth muscle cell
EDAT- 2012/09/01 00:00
MHDA- 2012/09/01 00:01
PMCR- 2012/06/26
CRDT- 2016/02/20 06:00
PHST- 2012/04/15 00:00 [received]
PHST- 2012/05/02 00:00 [revised]
PHST- 2012/05/15 00:00 [accepted]
PHST- 2016/02/20 06:00 [entrez]
PHST- 2012/09/01 00:00 [pubmed]
PHST- 2012/09/01 00:01 [medline]
PHST- 2012/06/26 00:00 [pmc-release]
AID - S2211-9132(12)00698-5 [pii]
AID - 10.1016/j.krcp.2012.06.004 [doi]
PST - ppublish
SO  - Kidney Res Clin Pract. 2012 Sep;31(3):177-85. doi: 10.1016/j.krcp.2012.06.004. 
      Epub 2012 Jun 26.