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To investigate the role and mechanism of CREG in high fat diet induced mouse obesity.
A high fat diet induced mouse obesity model was established in both C57 wild type mouse (CREG+/+) and CREG heterozygote mouse (CREG+/-). Mice fed with normal chow were used as control. After 12 weeks of feeding, body weight, white fat weight, size of hepatocyte and fatty liver degeneration were detected. Glucose tolerance and insulin tolerance were also assessed by injecting glucose and insulin. Differential gene expression was screened by using a lipid metabolism related gene microarray. Expression of genes screened in white fat tissue was further confirmed by Western blot.
Calories intake of CREG+/- mouse was comparable to CREG+/+ mouse. Compared to CREG+/+ group, CREG+/- mice had much higher body weight and white fat tissue weight, larger adipocytes and more severe fatty liver after 12 weeks of high fat diet feeding. Glucose tolerance and insulin tolerance were more severely impaired in CREG+/- mice than CREG+/- mice. Lipid related gene microarray assay showed that Alox12 and PPARδwere significantly decreased on transcription level. Western blot identified that expression of PPARδ were decreased on protein level.
CREG was involved in high fat induce mouse obesity, which might be a potential therapeutic target for obesity.