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 HNF4 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. Huang and team injected mice with genetic material known as small interfering RNAs (siRNAs) packaged inside viruses that targeted TET3 or HNF4?. They found that blood glucose and insulin dropped significantly -- effectively stopping diabetes in its tracks.
In the Feb. 4 Cell Reports study, researchers looked at how TET3 contributed to the development of fibrosis in the liver, and found that the protein was involved in fibrosis on multiple levels. Almost all fibrosis, regardless of the organ involved, starts from abnormal protein signaling, Huang said.
She and colleagues discovered that TET3 plays a role in the fibrosis signaling pathway in three different locations -- and acts as an important regulator in fibrosis development. This means there are likely opportunities to develop drugs that inhibit TET3 to slow or reverse fibrosis, said Da Li, associate research scientist in genetics and co-author on both studies. Related Stories
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