Overnutrition causes many metabolic diseases including type 2 diabetes. PFKFB3/iPFK2 is a master regulator of adipocyte and intestinal nutrient metabolism. Using PFKFB3/iPFK2+/– mice and adipocyte-specific PFKFB3 over-expression mice, the present study investigated the role of PFKFB3/iPFK2 in regulating diet-induced adiposity, inflammation in adipose tissue and intestine, and systemic insulin resistance.
On a high-fat diet (HFD), PFKFB3+/– mice gained much less body weight than did wild-type littermates. However, HFD-induced systemic insulin resistance in PFKFB3+/– mice was more severe than in wild-type littermates. In contrast, adipocyte-specific PFKFB3 over-expression increased adiposity but suppressed overnutrition induced adipose tissue inflammatory response and improved insulin sensitivity. In addition to adipose tissue, PFKFB3/iPFK2 also played a role in intestine events. Compared to wild-type littermates, PFKFB3+/– mice displayed a significant increase in the expression of intestinal inflammatory markers on a HFD.
In conclusion, PFKFB3 protects against overnutrition-induced adipose tissue and intestine inflammatory response and systemic insulin resistance in an adiposity-independent manner. Selective PFKFB3 activation may be viable for treating and/or preventing insulin resistance and type 2 diabetes.
| Identifer | oai:union.ndltd.org:tamu.edu/oai:repository.tamu.edu:1969.1/149413 |
| Date | 03 October 2013 |
| Creators | Guo, Xin |
| Contributors | Wu, Chaodong, Morgan, Caurnel, Sturino, Joseph M, Awika, Joseph M |
| Source Sets | Texas A and M University |
| Language | English |
| Detected Language | English |
| Type | Thesis, text |
| Format | application/pdf |
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