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Curcumin Supplementation May Reduce Glycemia and Risk of Vascular Inflammation in Diabetics
In this study, involving a cell culture study and an animal study (diabetic rat model), results found that the detrimental effects of high glucose on lipid peroxidation, IL-6, IL-8, MCP-1, and TNF-alpha secretion were inhibited by curcumin in cultured monocytes. In rats, diabetes was found to increase blood levels of IL-6, MCP-1, TNF-alpha, glucose, HbA(1), and oxidative stress. These levels significantly decreased in rats treated with curcumin. The authors conclude, "Thus, curcumin can decrease markers of vascular inflammation and oxidative stress levels in both a cell-culture model and in the blood of diabetic rats. This suggests that curcumin supplementation can reduce glycemia and the risk of vascular inflammation in diabetes." Additional research is warranted.
Reference:
"Curcumin Supplementation Lowers TNF-alpha, IL-6, IL-8, and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-alpha, IL-6, MCP-1, Glucose, and Glycosylated Hemoglobin in Diabetic Rats," Jain SK, Rains J, et al, Antioxi Redox Signal, 2008 Oct 31
Reference:
"Curcumin Supplementation Lowers TNF-alpha, IL-6, IL-8, and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-alpha, IL-6, MCP-1, Glucose, and Glycosylated Hemoglobin in Diabetic Rats," Jain SK, Rains J, et al, Antioxi Redox Signal, 2008 Oct 31
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Dr. Derrick DeSilva is on the Attending Staff at the Raritan Bay Medical Center in Perth Amboy, N.J., and on the teaching faculty at JFK Medical Center in Edison, N.J.
He has lectured on various topics in medicine --nationally and internationally-- and has his own talk show called Ask the Doctor which airs on WCTC in New Jersey (1450 AM) as well as his own television show, "To Your ...
He has lectured on various topics in medicine --nationally and internationally-- and has his own talk show called Ask the Doctor which airs on WCTC in New Jersey (1450 AM) as well as his own television show, "To Your ...
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