Response: effects of rosiglitazone on inflammation in Otsuka long-evans Tokushima Fatty rats (korean diabetes j 2010;34:191-9).

Abstract

matory cytokines such as TNF-α, interleukin (IL)-1β and IL6, and α-smooth muscle actin (SMA) in the pancreas [7,8]. In our study, we investigated the effects of the insulin-sensitizing anti-diabetic agent rosiglitazone on the progression of skeletal muscle inflammation in OLETF rats. We found that rosigli tazone decreased the concentrations of glucose, insulin and inflammatory cytokines in the sera of OLETF rats. Rosiglitazone also inhibited mRNA expression of inflammatory cyto kines in skeletal muscle by blocking the NF-κB pathway. There fore, our findings suggest that rosiglitazone may improve in sulin sensitivity with its anti-inflammatory activity in the skel etal muscle of diabetic rats. Our results concur with the findings of previous studies that PPAR-γ agonists can improve inflammation in peripheral tis sues (including the muscle and pancreas) via the inhibition of inflammatory signaling pathways [9,10]. Recently, TZD was discovered to have anti-inflammatory effects, and its potential was reevaluated for treating diabetes. Several studies have reported that TZD including rosiglitazone decreases serum levels of inflammatory makers TNF- α, IL-6, C-reactive protein (CRP), and FFAs in an experimental model of induced type 2 diabetes in high-fat-diet albino rats [11,12]. In our study, FFA levels were lower in the OLETF group compared to the LETO group at the 40th week (Fig. 1). In contrast, we observed no decrease in FFA levels in the group treated with rosiglitazone. We still do not know why rosiglitazone did not decrease se