A potential treatment target for type 2 diabetes may have been discovered by researchers at IDIBELL, a Spanish research foundation.
In a study published in the Journal of Clinical Investigatio, a team led by Sara Kozma at the Laboratory of Cancer Metabolism found that inhibiting the S6K1 protein increased insulin sensitivity in mice.
Insulin resistance can lead to type 2 diabetes, which occurs due to increased insulin production as the body looks to compensate for the impaired ability to respond to insulin.
Kozma’s team observed that animals that lacked S6K1 – a protein kinase – were more sensitive to insulin and did not develop diabetes.
They also observed that S6K1 deficient mice had decreased beta cell growth, decreased insulin circulation and were smaller in size.
The team subsequently combined S6K1 deficient embryonic stem cells with mice placentas. While the embryos developed normally, beta cells still remained decreased.
The absence of S6K1 increased insulin sensitivity in the mice, with the research team concluding that deleting S6K1 could protect against insulin sensitivity and treat type 2 diabetes.
“We also showed that in the absence of S6K1, peripheral tissues of the animal became more sensitive to insulin and did not develop diabetes,” Kozma concluded.

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