Involvement of PFKFB3/iPFK2 in the suppressive effect of rosiglitazone on diet-induced intestine inflammatory response
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abstract
Overnutrition is a causal factor of metabolic syndrome. However, little attention has been paid to the regulation of overnutritionrelated intestinal inflammation as it relates to metabolic syndrome. The objective of this study is to define the role of PFKFB3/iPFK2, a master regulator of nutrient metabolism, in regulating dietinduced intestine inflammatory response in mice. For this purpose, mice were fed a highfat diet (HFD) and treated with or without rosiglitazone, an insulinsensitizer that also has an antiinflammatory effect. Compared to wildtype littermates, mice that lack one allele of PFKFB3 (PFKFB3+/ mice) displayed a significant increase in the expression of intestinal inflammatory markers such as tolllike receptor 4 and proinflammatory cytokines on a HFD. These data indicate that disruption of PFKFB3 exacerbates dietinduced intestine inflammatory response. When treated with rosiglitazone, the expression of the above inflammatory markers was markedly decreased in HFDfed wildtype mice, and, to a lesser extent, in HFDfed PFKFB3+/ mice. Additionally, treatment with rosiglitazone normalized systemic insulin sensitivity and glucose homeostasis in HFDfed wildtype mice, but not in HFDfed PFKFB3+/ mice. Therefore, PFKFB3/iPFK2 is involved in the suppressive effect of rosiglitazone on dietinduced intestine inflammatory response.
