Research Profile

Insulin resistance is a key metabolic dysfunction associated with obesity and type 2 diabetes. It happens when fat cells and tissue become inflamed. We know about things that cause inflammation and insulin resistance, but we don't know much about things that protect against them. In studies with mice, we found that when a specific gene called Dnmt3a was missing in their fat cells, they became better at using insulin and handling glucose, even on a high-fat diet. We also discovered a new secreted protein that is found a lot in fat tissue without the Dnmt3a gene. This protein helps reduce inflammation and makes insulin work better in lab tests and animal studies. Interestingly, obese mice had less of this protein compared to normal-weight mice. By increasing the levels of this protein in obese mice, we improved their insulin resistance and glucose intolerance. Now we want to learn more about how this protein fights inflammation and helps insulin work better. We'll also study how it affects fat tissue and the body's overall metabolism. If everything goes well, this research could lead to new treatments for insulin resistance and help improve metabolic health and human health.

Inflammation is considered a contributing factor causing insulin resistance. Particularly in fat tissue, inflammation is believed to play a substantial role in insulin resistance associated with obesity and type 2 diabetes. Thus, improving insulin resistance can be helpful in ameliorating insulin resistance and other metabolic impairments. Our studies have identified a novel molecular factor that plays a critical role in preserving insulin sensitivity by suppressing inflammatory responses in fat tissue. Our research suggests that the protein levels of this novel factor are significantly suppressed by the inflammatory mediators of insulin resistance in obesity. Therefore, weight loss through the reduction of fat mass could be helpful in maintaining the levels of this novel factor, thereby preserving insulin sensitivity. We are hoping that successful completion of our studies could lead to the identification of a novel drug target promoting insulin sensitivity.

Metabolic issues, such as insulin resistance, are key defining features of diabetes. However, they are often associated with a wide range of pathologic and physiological issues, such as obesity, cardiovascular problems, aging, and pregnancy. Therefore, I believe that researching this topic and metabolism can have a larger impact than one might think. Moreover, metabolic regulation is highly complex, involving both cell-autonomous and cell nonautonomous input, and intricate cross-talk between various metabolic and non-metabolic tissues. These aspects have captured my enthusiasm for this field. This award holds immense importance in catalyzing my research efforts, providing the necessary financial support and resources to explore innovative avenues in diabetes research. I will be able to validate the therapeutic potential of this novel factor as an insulin-sensitizing molecular agent in animal models. Furthermore, it reinforces my confidence and belief that my work has the potential to make meaningful contributions to the field of diabetes research.

Diabetes research is entering a transformative phase driven by technological advancements, personalized medicine, and a deeper grasp of genetic, environmental, and lifestyle factors. Cutting-edge techniques allow for a more nuanced exploration of diabetes complexities at a molecular level. However, managing the vast datasets generated presents a challenge. To tackle this, the integration of artificial intelligence and big data analytics is pivotal. These technologies extract meaningful insights from immense datasets, aiding in the identification of biomarkers, prediction of disease trajectories, and personalized treatment strategies. The synergy of technology, personalized approaches, and advanced analytics is shaping a future where diabetes research is more targeted, precise, and effective.