In a pair of related studies, a team of Yale researchers has found a way to reverse type-2 diabetes and liver fibrosis in mice, and has shown that the underlying processes are conserved in humans.
In a pair of related studies, a team of Yale researchers has found a way to reverse type-2 diabetes and liver fibrosis in mice, and has shown that the underlying processes are conserved in humans.
The studies appear in the Feb. 4 edition of Cell Reports and in the Jan. 17 edition of Nature Communications.
In the earlier study, researchers found an important connection between how the body responds to fasting and type-2 diabetes. Fasting “switches on” a process in the body in which two particular proteins, TET3 and HNF4a, increase in the liver, driving up production of blood glucose. In type-2 diabetes, this “switch” fails to turn off when fasting ends, as it would in a non-diabetic person.
Researchers hypothesized that if they could “knock down” the levels of these two proteins, they could stop diabetes from developing. Yingqun Huang, M.D., Yale associate professor in Obstetrics, Gynecology, and Reproductive Sciences and her team injected mice with genetic material known as small interfering RNAs (siRNAs) packaged inside viruses that targeted TET3 or HNF4a. They found that blood glucose and insulin dropped significantly — effectively stopping diabetes in its tracks.
Read more at Yale University
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