High blood glucose levels may enhance the immune system’s ability to fight certain types of cancer. This is the conclusion reached by researchers who studied the effects of hyperglycemia on T cells — immune cells that recognize and destroy infected and potentially dangerous cells in the body. In experiments involving mice, high blood sugar slowed tumor growth, while an analysis of human blood samples revealed similar changes in immune cells. The findings were published in The Journal of Immunology.
Previous studies have identified an association between type 1 diabetes and a reduced risk of developing certain types of cancer, but the reasons behind this relationship remained unclear. To investigate the possible mechanism, researchers compared tumor growth in mice with high blood glucose levels, animals with diabetes that received insulin, and mice with normal blood sugar levels.
Tumors grew more slowly in animals with hyperglycemia that did not receive insulin to lower their blood glucose levels. Their T cells were also more numerous and more effective at suppressing tumor growth. When insulin was administered to diabetic mice, the enhanced antitumor activity of their T cells decreased.
Further analysis showed that high blood sugar altered T-cell function, including the activity of a specific intracellular signaling pathway. These changes may have sustained a stronger inflammatory response in immune cells and enhanced their ability to suppress tumors.
The researchers also examined immune cells in blood samples from people with hyperglycemia. They found increased activity in the same signaling pathway identified in the mouse experiments. This similarity suggests that the mechanism may also be relevant to humans, although it does not yet prove that hyperglycemia provides people with the same level of antitumor protection.
“Our findings open up new avenues for research in cancer immunotherapy. We can investigate the changes observed in T cells from patients with type 1 diabetes and try to reproduce them using new treatment approaches,” said the study’s senior author, Anamika Bose, an associate professor at the National Institute of Pharmaceutical Education and Research in India.
The researchers hope that understanding the identified signaling mechanism will help them develop immunotherapies that enhance the ability of T cells to recognize and suppress tumors without inducing hyperglycemia. However, further research will be needed before such an approach can be used to treat patients.
Chronically elevated blood sugar levels are dangerous to health and should not be considered a means of preventing or treating cancer. The study identifies a potential mechanism for future therapies, not a benefit of uncontrolled hyperglycemia.
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