The researchers discovered these cells during the course of a different study, one that looked at how the immune system reacts to obesity and what complications may arise from this response. Through this they found NK cells, which normally target malignant cells.
However, the researchers noted how the NK cells of obese mice were markedly different from the NK cells of normal-weight mice. Specifically, these NK cells expressed a few myeloid lineage genes, the most striking of which was the colony-stimulating factor 1 receptor (Csf1r). Also known as the macrophage colony-stimulating factor receptor (M-CSFR), this gene is known for its role in activating the immune system and promoting insulin resistance, the forerunner of diabetes.
By extracting blood samples from obese patients, the researchers found these variations of NK cells were found in humans as well. Based on their findings, study co-author and physician scientist at the Max-Planck-Institute for Metabolism Research Sebastian Theurich has recommended dieting as a way to ward off diabetes. “If our obese patients went on a strict diet, losing up to 30 kilograms, the number of altered killer cells also decreased, as well as the level of systemic inflammation and the risk for diabetes,” elaborated Theurich.
In addition to dieting, genetic modification was cited as another possible method of decreasing the likelihood of diabetes. Mice who were fed on a fat-enriched diet managed to avoid gaining weight and developing insulin resistance when the researchers modified the NK cells. These modifications prevented the NK cell sub-population from properly developing, which in turn allowed the fatty-food mice to remain the same weight as the mice from a control group.
“This sub-population of killer cells could provide an effective point of attack for new therapeutic approaches if we succeeded to selectively switch them off,” said Theurich.
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