Metabolic syndrome (MetS) is a cluster of clinical manifestations including: (1) obesity, abdominal adiposity or insulin resistance, (2) impaired glucose metabolism, (3) hypertension, and (4) atherogenic dyslipidemia. Genetic factors play a significant role in MetS, which contributes to individual and interpersonal differences. The inbred genetic background of existing mouse models limits the in-depth research towards MetS, given the shared genetic background of each strain.
Gempharmatech generated wild mouse derived Chr1 substitution strains to enrich the genetic background and overcome this limitation. Using wild mouse captured from different regions of China as donors, we established 11 wild-derived chromosome 1 substitution strains in the background of C57BL/6JGpt (B6J). Introducing chromosome 1 of wild mice into inbred mice with a clear genetic background is beneficial to cloning and analysis of genes related to complex traits, and provides new resources for the analysis of noval signaling pathways and disease mechanisms.
Through phenotype screening, we have identified a specific strain called that B6-Chr1YP1 mice (D000750, abbreviated as 750), which displays obvious spontaneous MetS phenotypes. As the animals age, these mice exhibit accelerated increase in body weight and fat content, along with early hepatic steatosis, glucose intolerance and insulin resistance, which are absent among B6 mice.
Data support
1.Body weight and fat ratio
Fig 2. 750 mice showed spontaneous obesity phenotypes
There was no significant difference in body weight between male 750 and B6J before 10 weeks of age, and 750 mice displayed accelerated increase in body weight and fat content after 10 weeks of age. At 17 weeks of age and 23 weeks of age, the body fat ratio of 750 mice was significantly higher than that of control B6J males. (n=8-10/group)
2. Lipid profile on chow diet and western diet
Fig 4. 750 mice displayed higher cholesterol than B6J mice
750 mice and B6J mice of 8 weeks of age were fed the chow diet and western diet for weeks. Plasma lipids were measured at 6, 10, 14 and 18 weeks post feeding. (n=5-7/group)
3. Liver pathology on chow diet and western diet
Fig 5. 750 mice displayed more severe NASH phenotype than B6J mice
750 mice and B6J mice at 8 weeks of age were fed with chow diet and western diet for weeks. Liver pathology was checked via H&E staining at 6, 10, 14 and 18 weeks post feeding. (n=5-7/group, and the representative images were presented as above.)
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