PMID- 19663918
OWN - NLM
STAT- MEDLINE
DCOM- 20100730
LR  - 20220316
IS  - 1365-2362 (Electronic)
IS  - 0014-2972 (Linking)
VI  - 39
IP  - 11
DP  - 2009 Nov
TI  - Intensive insulin therapy decreases urinary MCP-1 and ICAM-1 excretions in 
      incipient diabetic nephropathy.
PG  - 980-5
LID - 10.1111/j.1365-2362.2009.02203.x [doi]
AB  - BACKGROUND: Nowadays, intensive insulin treatment has been widely used in type 2 
      diabetics who have poor control of blood glucose, to reduce the risk of chronic 
      complications of diabetes. Recently, some scholars have paid more attention to 
      the pivotal role of inflammation involved in type 2 diabetes and its 
      complications. Monocyte chemoattractant protein-1 (MCP-1) and intercellular 
      adhesion molecule-1 (ICAM-1), which are two important inflammatory chemokines, 
      have been documented to participate in the onset and development of type 2 
      diabetes and its complications, such as diabetic nephropathy (DN). DESIGN: In the 
      current study, we recruited 30 type 2 diabetics with microalbuminuria to be 
      treated with multiple insulin injections daily for 2 weeks. Random spot urine 
      samples (corrected for creatinine-Cr) were collected for the examination of 
      urinary MCP-1, ICAM-1 and albumin (Alb) levels before and after the intensive 
      insulin therapy. Changes in their levels were observed to test the hypothesis 
      that type 2 diabetes with microalbuminuria is associated with elevated urinary 
      concentrations of MCP-1 and ICAM-1, and intensive insulin therapy can result in a 
      decline of Alb by reducing the inflammatory reaction. RESULTS: The urinary 
      MCP-1/Cr and urinary ICAM-1/Cr ratios in type 2 diabetic patients with 
      microalbuminuria were much higher than those in normal controls, and intensive 
      insulin treatment could decrease significantly the urinary MCP-1/Cr, ICAM-1/Cr 
      and Alb/Cr ratios in type 2 diabetics with microalbuminuria. CONCLUSION: 
      Intensive insulin treatment may protect against renal injury in early DN by 
      reducing the urinary MCP-1 and ICAM-1 excretions.
FAU - Ye, S D
AU  - Ye SD
AD  - Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei 230001, 
      China. ysd6464@yahoo.com.cn
FAU - Zheng, M
AU  - Zheng M
FAU - Zhao, L L
AU  - Zhao LL
FAU - Qian, Y
AU  - Qian Y
FAU - Yao, X M
AU  - Yao XM
FAU - Ren, A
AU  - Ren A
FAU - Li, S M
AU  - Li SM
FAU - Jing, C Y
AU  - Jing CY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090803
PL  - England
TA  - Eur J Clin Invest
JT  - European journal of clinical investigation
JID - 0245331
RN  - 0 (Blood Glucose)
RN  - 0 (Chemokine CCL2)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Albuminuria/*urine
MH  - Blood Glucose/metabolism
MH  - Chemokine CCL2/*urine
MH  - Diabetes Mellitus, Type 2/physiopathology/*urine
MH  - Diabetic Nephropathies/physiopathology/*urine
MH  - Female
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*urine
MH  - Kidney/*metabolism/physiopathology
MH  - Male
MH  - Middle Aged
EDAT- 2009/08/12 09:00
MHDA- 2010/07/31 06:00
CRDT- 2009/08/12 09:00
PHST- 2009/08/12 09:00 [entrez]
PHST- 2009/08/12 09:00 [pubmed]
PHST- 2010/07/31 06:00 [medline]
AID - ECI2203 [pii]
AID - 10.1111/j.1365-2362.2009.02203.x [doi]
PST - ppublish
SO  - Eur J Clin Invest. 2009 Nov;39(11):980-5. doi: 10.1111/j.1365-2362.2009.02203.x. 
      Epub 2009 Aug 3.