Type 2 diabetes is increasing worldwide. A research group has discovered a new gene that may be key to preventing and treating lifestyle diseases like type 2 diabetes.
The results of their research were published in the journal Nucleic Acids Research on June 18, 2021.
Selenoprotein P (SeP) is an essential plasma protein that contains the micronutrient selenium. However, too much SeP means trouble.
Excess SeP increases insulin resistance, which weakens the effects of insulin and worsens glucose metabolism.
“Excess SeP is the enemy of type 2 diabetes,” emphasizes Professor Yoshiro Saito from Tohoku University’s Graduate School of Pharmaceutical Sciences and co-author of the study. “Regulating healthy SeP levels is critical to maintaining our health.”
Together with assistant professor Yuichiro Mita from the Graduate School of Life and Medical Sciences at Doshisha University, Saito discovered the gene “CCDC152”. The gene, which is similar in structure to SeP, acts as an RNA that lowers the SeP protein.
For this reason, CCDC152 was designated as a long non-coding RNA inhibitor of selenoprotein P translation (L-IST).
A scheme of discovery. Selenoprotein P (SeP), which is synthesized and secreted by the liver, aggravates diabetes when it is in excess. The novel “L-IST” gene binds to SeP mRNA and suppresses the synthesis of SeP protein. In addition, epigallocatechin gallate, a key ingredient in green tea and known to have a preventive effect on diabetes, increases L-IST and lowers SeP protein. © Y Mita et al.
Their study also found that epigallocatechin gallate (EGCG), a herbal antioxidant commonly found in green tea, may increase L-IST.
Looking ahead, researchers believe EGCG supplements can help diabetics with high SeP levels. “Overall, our results have opened up new avenues for the prevention and treatment of lifestyle-related diseases,” added Saito.
Publication details:
Title: Identification of a new endogenous long non-coding RNA that inhibits selenoprotein P translation
Authors: Y Mita, R Uchida, S Yasuhara, K Kishi, T Hoshi, Y Matsuo, T Yokooji, Y Shirakawa, T Toyama, Y Urano, T Inada, N Noguchi and Y Saito
Journal: Nucleic Acid Research
DOI: 10.1093 / nar / gkab498
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