Obesity and Type 2 diabetes are associated with an increased risk of developing cardiovascular
disease. Reports have suggested that the chemokine, interleukin-8, may be involved
in the development of diabetic macroangiopathy as well as in the pathogenesis of atherosclerosis.
Two classes of drugs, the biguanides and the insulin-sensitizing thiazolidinediones
seem to have additional beneficial effects on cardiovascular risk-factors besides
their effects on glucose homeostasis. In this study, we investigated the effects of
the thiazolidinedione, Ciglitazone, the peroxisome proliferator-activated receptor
alpha-agonist 5,8,11,14-eicosatetraynoic acid (ETYA) and the biguanide, Metformin
on interleukin-8 gene expression and production in human adipose tissue in vitro . Ciglitazone 10-100 M inhibited interleukin-8 release by 25-33% (p < 0.05) and mRNA
expression by 33-60% (p < 0.05). Metformin 0.1-10 mM inhibited interleukin-8 release
by 20-50% (p < 0.05) and mRNA expression by 20-90% (p < 0.05). However, ETYA did not
effect the production of interleukin-8 in the adipose tissue. In conclusion, we demonstrate
the ability of two anti-diabetic compounds to decrease the release of interleukin-8
from human adipose tissue in vitro . These findings open the possibility that the beneficial effects on cardiovascular
risk-factors of these anti-diabetic compounds might involve a reduction in the interleukin-8
produced in human adipose tissue.
Key words
Ciglitazone - Metformin - Chemokines - Human Adipose Tissue - Obesity - Atherosclerosis
