A new LePR gene knocks out the male mouse model for the study of type 2 tetanus and its complication

The concept of health management is increasingly widespread, and scientific health knowledge is becoming increasingly popular. Type 2 diabetes (T2D) is a progressive metabolic disease characterized by systemic metabolic dysfunction and multi-organ complications that greatly increase mortality and survival rates. Leptin signaling pathways through the Leptin receptor (LeprR) are essential for maintaining energy stability and insulin sensitivity; its destructiveness is strongly associated with obesity-induced type 2 diabetes.

However, the currently available mouse models do not effectively mimic the key characteristics of human T2D, in particular lipid metabolism, hypertension and progressive diabetes mellitus. The lipid metabolism and hypertension of the yellow mouse Mesocricetus auratus are similar to those of humans; therefore, they can serve as a potential improvement of the metabolic disease model. We used CRISPR/Cas9 gene editing technology to generate a model of the LePR-deficient (db/db) golden mouse to further study the role of LePR in the pathway of T2D in adult T2D patients.

LepR deficiency mouse model (db/db)) develops into chronic obesity, persistent hyperglycemia, decreased blood glucose clearance, insulin resistance, and significant lipid metabolism disorders, including significantly elevated levels of total cholesterol and low-density lipoprotein, as well as significantly reduced levels of low-density lipoprotein. It should be noted that the above information is based on international publicly available research for reference by HealthCop and does not constitute clinical advice.