New hope for type 2 diabetes treatment emerges from Nanjing University study

Previous research suggests that insulin resistance is caused by reactive oxygen species (ROS), unstable molecules produced by mitochondria within our cells. Excessive ROS production can result in DNA, protein, and RNA damage and cell death.

Scientists have identified a class of drugs called "mitochondrial uncouplers" that can inhibit ROS production at its source. This is significant because traditional antioxidant-based treatments can only address already formed unstable molecules.

Another method to reduce excess ROS production involves using ultrasmall platinum nanoparticles, known for their antimicrobial, anticancer, and antioxidant properties. However, their small size clears these nanoparticles from the liver too quickly.

The Nanjing research team combined these two treatments to restore insulin sensitivity and treat type 2 diabetes effectively.

The team developed "nano scavengers" by coating a mold with platinum particles and a layer of silica. They conducted their study using an animal model, testing the nano scavengers on mice with diabetes. The results revealed that the nano scavengers effectively traveled to the liver and reduced fat content, helping the liver function usually and showing promise in treating insulin resistance.

The researchers believe that this breakthrough could have a significant impact on reducing the incidence of type 2 diabetes.

Research on nanoscavengers

According to the study's abstract, the team designed liver-targeted biodegradable silica nanoshells embedded with platinum nanoparticles.

These nanoshells acted as reactive oxygen species (ROS) nanoscavengers and functional hollow nanocarriers.

They loaded 2,4-dinitrophenol-methyl ether (DNPME), a mitochondrial uncoupler, into the nanoshells and coated them with a lipid bilayer for long-term removal of ROS in the liver tissue of type 2 diabetes models.

The treatment successfully reversed oxidative stress, insulin resistance, and impaired glucose consumption in vitro. In addition, in diabetic mouse models, induced by a high-fat diet and streptozotocin significantly improved hepatic steatosis and antioxidant capacity.

Intravenous administration of the treatment also showed therapeutic effects on hyperlipidemia, insulin resistance, hyperglycemia, and diabetic nephropathy, providing a promising approach for type 2 diabetes treatment by reversing hepatic insulin resistance through long-term ROS scavenging.

While more research is needed to validate these findings and determine their applicability to human subjects, the Nanjing University study opens up new possibilities for tackling type 2 diabetes at its core.

With continued advancements in medical research, there is hope for improved treatments and outcomes for individuals affected by this prevalent condition.