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Intensive insulin therapy decreases urinary MCP-1 and ICAM-1 excretions in incipient diabetic nephropathy
1Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei 230001, China. ysd6464@yahoo.com.cn
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.
Insights
Intensive insulin therapy for type 2 diabetes with microalbuminuria significantly reduces inflammatory markers monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1), potentially protecting against diabetic nephropathy.
Area of Science:
- Endocrinology and Metabolism
- Nephrology
- Inflammation Research
Background:
- Type 2 diabetes (T2D) management often involves intensive insulin treatment to control blood glucose and reduce chronic complications.
- Inflammation plays a critical role in T2D and its complications, including diabetic nephropathy (DN).
- Monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) are key inflammatory chemokines implicated in T2D pathogenesis.
Purpose of the Study:
- To investigate the association between type 2 diabetes with microalbuminuria and elevated urinary MCP-1 and ICAM-1 levels.
- To evaluate the effect of intensive insulin therapy on urinary MCP-1, ICAM-1, and albumin (Alb) in T2D patients with microalbuminuria.
- To determine if intensive insulin therapy reduces inflammation and improves renal markers in early DN.
Main Methods:
- Recruitment of 30 type 2 diabetics with microalbuminuria for a 2-week intensive insulin therapy regimen.
- Collection of serial spot urine samples for measurement of urinary MCP-1, ICAM-1, and Albumin (Alb) levels, corrected for creatinine (Cr).
- Comparison of pre- and post-treatment urinary marker levels to assess therapeutic impact.
Main Results:
- Urinary MCP-1/Cr and ICAM-1/Cr ratios were significantly elevated in type 2 diabetic patients with microalbuminuria compared to controls.
- Intensive insulin treatment led to a significant reduction in urinary MCP-1/Cr, ICAM-1/Cr, and Alb/Cr ratios.
- These findings suggest a decrease in inflammatory markers and albuminuria following intensive insulin therapy.
Conclusions:
- Intensive insulin treatment demonstrates potential in mitigating renal injury in early diabetic nephropathy.
- The renoprotective effect may be attributed to the reduction in urinary MCP-1 and ICAM-1 excretions.
- This highlights the importance of managing inflammation in T2D patients with early signs of kidney disease.
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