Plasma leptinconcentrationsaregreaterintypeIIdiabeticpatientsand stimulatemonocytechemotacticpeptide-1synthesisviathemitogen-activatedproteinkinase/extracellularsignal-regulatedkinasepathway
Background: Leptin isanadipokinethatisrecentlyreportedtobeabiomarkerof systemic inflammation.Althoughatherosclerosiscausescardiovasculardiseases,it is notclearwhetherleptincontributestotheaccelerationofthisprocess.Inthis study, weinvestigatedwhetheralterationsofplasmaleptinlevelswererelatedto diabet...
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| Published in: | Kidney research and clinical practice pp. 177 - 185 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
대한신장학회
01-09-2012
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| Subjects: | |
| Online Access: | Get full text |
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| Summary: | Background: Leptin isanadipokinethatisrecentlyreportedtobeabiomarkerof systemic inflammation.Althoughatherosclerosiscausescardiovasculardiseases,it is notclearwhetherleptincontributestotheaccelerationofthisprocess.Inthis study, weinvestigatedwhetheralterationsofplasmaleptinlevelswererelatedto diabetic nephropathyandsystemicinflammation.Inaddition,weexaminedthe physiologic actionofleptininculturedvascularsmoothmusclecells(VSMCs).
Methods: A totalof126type2diabeticparticipantsand37healthycontrolswere studied. Thediabeticparticipantsweredividedintothreegroupsaccordingto stage ofnephropathy.Weinvestigatedwhetherleptininducedmonocytechemo-tactic peptide-1(MCP-1)synthesisthroughthemitogen-activatedproteinkinase (MAPK) pathwayusingculturedVSMCs.
Results: Plasma leptinconcentrationsweresignificantlyhigherinthediabetic group thaninthecontrols.Plasmaleptinlevelswerepositivelycorrelatedwith body massindex,fastingandpostprandialbloodglucose,hemoglobinA1c,total cholesterol, urinaryalbuminexcretion,high-sensitivityC-reactiveprotein(hsCRP),and MCP-1plasmalevels,andnegativelycorrelatedwithcreatinineclearance values. InculturedVSMCs,leptinincreasedMCP-1productioninadose-dependent manner, andthisstimulatingeffectofleptinonMCP-1expressionwasreversedby the MAPK(MEK)inhibitorPD98059.Inaddition,leptinstimulatedthephosphor-ylation ofMEK,extracellularsignal–regulatedkinase,andE26-liketranscription factor, whicharecomponentsoftheMAPKpathway.
Conclusions: Overall, thesefindingssuggestthatactivationofleptinsynthesis may promoteMCP-1activationinadiabeticenvironmentviatheMAPKpathway in VSMCsandthatitpossiblycontributestotheaccelerationofatherosclerosis. KCI Citation Count: 1 |
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| Bibliography: | G704-000889.2012.31.3.011 |
| ISSN: | 2211-9132 2211-9140 |