Obesity is one of the main risk factors for the development of type 2 diabetes as it leads to excessive production of free radicals, disruptions in glucose and fatty acid metabolism, and insulin resistance.

The study focuses on understanding the role of the NUDT16L1 protein, which is a key regulator of TP53 activity. Deletion or silencing of the NUDT16L1 gene results in excessive activation of TP53, which may influence the development of insulin resistance and type 2 diabetes.

The research project focuses on a molecular analysis of serum and adipose tissue samples obtained during bariatric surgery procedures, and it’s relation to data on insulin resistance, body weight, and lipid profile before and after the surgery.

Through RNA sequencing, signaling pathways dependent on the expression of the NUDT16L1 gene in adipose tissue will be identified, along with their impact on insulin resistance. Additionally, molecular differences between patients presenting different degrees of insulin resistance before and after bariatric interventions will be determined.

The results of this project will shed light on the significance of the NUDT16L1-TP53BP1-TP53 axis in human metabolism, allowing for potential future use of the NUDT16L1 protein as a therapeutic target. The project will also involve collaborations with Dana-Farber Cancer Institute and Harvard Medical School, providing a unique opportunity for further research on this intriguing topic related to cancer biology and metabolism.

The project is funded by the Ministry of Science and Education, under the “Pearls of Science” program, grant number PN/01/0025/2022. More information is available here.

Importance of the NUDT16L1-TP53BP1-TP53 axis in obesity and type 2 diabetes
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