Study finds the ability of cancer drugs to lower blood sugar levels
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In a study published in the journal Proceedings of the National Academy of Sciences (PNAS), University of Oklahoma researchers investigated a drug’s ability to prevent fat buildup in the liver. This condition often accompanies obesity and can lead to serious fatty liver disease.
The study expands on an earlier finding by Tiangang Li, Ph.D., and a team of researchers at OU Health Harold Hamm Diabetes Center. They discovered that a drug originally designed to fight cancerous tumors can also enhance insulin sensitivity and reduce blood sugar levels. This drug works by stopping the breakdown of a particular protein essential for all cells to react to insulin.
Cancer remains a significant global health challenge, with its prevalence steadily increasing over the years. According to the World Health Organization (WHO), cancer is one of the leading causes of morbidity and mortality worldwide, responsible for an estimated 10 million deaths annually.
In the study, researchers studied mice and removed a gene called Cul 3 from their livers. Normally, this gene is inhibited by the drug to stop the breakdown of a specific protein. By getting rid of the gene, they could see what happens when mice become obese from eating a lot of fatty foods.
The results showed that when the gene was removed, mice on a high-fat diet didn't store fat in their livers, even though they were overweight. Instead, the fat went into their bloodstream and ended up in other tissues like muscles, where it shouldn't be stored. This caused the muscles, which are the body's biggest organ, to respond poorly to insulin, leading to high blood sugar levels in the mice.
“By eliminating the gene, we aggressively prevented fat accumulation in the liver, but this worsened insulin resistance in the muscle, which tells us that fat metabolism in these organs is interconnected. These findings suggest that, in addition to lowering liver fat, the simultaneous reduction of obesity and improvement of insulin sensitivity are important for treating fatty liver disease. That’s because these improvements outside the liver are critical for preventing the fat that enters the liver from also building up in other tissues,” said Li.
“The research also illustrates why treating chronic conditions like Type 2 diabetes and fatty liver disease is never simple – an improvement in one area may trigger negative effects in another. Even so, the study was extremely helpful for understanding the process by which fatty liver disease occurs and what the drug is doing in the context of that disease,” said study co-author Jed Friedman, director of OU Health Harold Hamm Diabetes Center and a professor in the OU College of Medicine.
Reference: Gu, Lijie, Li, Tiangang, et al.; Cullin 3 RING E3 ligase inactivation causes NRF2-dependent NADH reductive stress, hepatic lipodystrophy, and systemic insulin resistance; 2024; Proceedings of the National Academy of Sciences; doi:10.1073/pnas.2320934121; https://www.pnas.org/doi/abs/10.1073/pnas.2320934121
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