Document Detail


CCR2 antagonism improves insulin resistance, lipid metabolism, and diabetic nephropathy in type 2 diabetic mice.
MedLine Citation:
PMID:  20686445     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chemokine ligand 2 (CCL2) binds to its receptor C-C chemokine receptor 2 (CCR2), initiating tissue inflammation, and recent studies have suggested a beneficial effect of a blockade of this pathway in diabetic nephropathy. To investigate the mechanism of protection, we studied the effect of RS504393, a CCR2 antagonist, on insulin resistance and diabetic nephropathy in db/db mice. Administering this antagonist improved insulin resistance as confirmed by various biomarkers, including homeostasis model assessment index levels, plasma insulin levels, and lipid abnormalities. Mice treated with the antagonist had a significant decrease in epididymal fat mass as well as phenotypic changes of adipocytes into small differentiated forms with decreased CCL2 expression and lipid hydroperoxide levels. In addition, treatment with the CCR2 antagonist markedly decreased urinary albumin excretion, mesangial expansion, and suppressed profibrotic and proinflammatory cytokine synthesis. Furthermore, the CCR2 antagonist improved lipid metabolism, lipid hydroperoxide, cholesterol, and triglyceride contents of the kidney, and decreased urinary 8-isoprostane levels. Hence, our findings suggest that CCR2 antagonists can improve insulin resistance by modulation of the adipose tissue and restore renal function through both metabolic and anti-fibrotic effects in type 2 diabetic mice.
Authors:
Young Sun Kang; Mi Hwa Lee; Hye Kyoung Song; Gang Jee Ko; Oh Sung Kwon; Tae Kyung Lim; Sung Hwan Kim; Sang Youb Han; Kum Hyun Han; Ji Eun Lee; Jee Young Han; Hyoung Kyu Kim; Dae Ryong Cha
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-04
Journal Detail:
Title:  Kidney international     Volume:  78     ISSN:  1523-1755     ISO Abbreviation:  Kidney Int.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-15     Completed Date:  2011-02-09     Revised Date:  2012-04-09    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  883-94     Citation Subset:  IM    
Affiliation:
Division of Nephrology, Department of Internal Medicine, Korea University, Ansan City, Korea.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / drug effects,  metabolism
Adiponectin / blood
Adipose Tissue / drug effects*,  metabolism,  pathology
Albuminuria / drug therapy,  metabolism
Animals
Anti-Inflammatory Agents / pharmacology*
Biological Markers / blood
Blood Glucose / metabolism
Cells, Cultured
Cytokines / genetics,  metabolism
Diabetes Mellitus, Type 2 / complications,  drug therapy*,  metabolism,  physiopathology
Diabetic Nephropathies / drug therapy*,  etiology,  metabolism,  physiopathology
Disease Models, Animal
Fibrosis
Gene Expression Regulation
Hemoglobin A, Glycosylated / metabolism
Hypoglycemic Agents / pharmacology*
Inflammation Mediators / metabolism
Insulin / blood
Insulin Resistance*
Kidney / drug effects*,  metabolism,  pathology
Lipid Metabolism / drug effects*
Lipid Peroxidation / drug effects
Male
Mice
Mice, Inbred C57BL
Receptors, CCR2 / antagonists & inhibitors*,  metabolism
Time Factors
Chemical
Reg. No./Substance:
0/Adiponectin; 0/Adipoq protein, mouse; 0/Anti-Inflammatory Agents; 0/Biological Markers; 0/Blood Glucose; 0/Ccr2 protein, mouse; 0/Cytokines; 0/Hemoglobin A, Glycosylated; 0/Hypoglycemic Agents; 0/Inflammation Mediators; 0/Insulin; 0/Receptors, CCR2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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