This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
Anyone still laboring under the mistaken assumption that genes are the most important factor in determining destiny should take a look at research that is being reported in this week's Science about a particular strain of mice that have a genetic predisposition to develop type 1 diabetes. It turns out that a key element in whether or not they actually succumb to the condition has to do with the type of bacteria that live in their intestines. The results reveal a complex interplay between gut bacteria (part of the animal's microbiome), genes and, surprisingly, sex hormones.
Type 1 diabetes is the form of the disease in which the body's immune cells launch a self-destructive attack on the pancreas, obliterating the organ's ability to secrete insulin. (Such dysfunctional immune responses are the basis of autoimmune disorders in people as well as mice.) By transplanting specific gut bacteria from one group of mice to another (don't ask), the investigators, who hailed from Canada, the U.S., Germany, Denmark and Switzerland, were able to prevent some of the rodents from developing diabetes.
When the researchers took a closer look, they determined that the bacteria were able to change how genes in the recipient mice worked by increasing the animals' levels of testosterone. Bacteria from male mice transplanted into females raised their testosterone levels a bit and kept them from developing diabetes. This result may help to explain why some autoimmune disorders in people—such as multiple sclerosis and rheumatoid arthritis—are more common among women (who usually have comparatively low levels of testosterone) than men. Why the male mice happened to have bacteria that boosted testosterone levels is unknown at present. This strain of mice is a good model for diabetes in people because both species exhibit many of the same molecular and cellular characteristics as the condition progresses.
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Type 1 diabetes does not show a similar skewing between the sexes in people, however, perhaps because it usually develops before puberty. Apparently, there just isn't enough testosterone circulating in a boy's blood at that point to make much of a difference.
If the type of bacteria living in the gut plays as strong a role in triggering type 1 diabetes in people as it does in these mice, this new finding may help explain why the number of cases of type 1 diabetes has surged over the past several years. Perhaps something in our diet and our environment—which is where the bacteria in our microbiome ultimately come from—has changed so much that we no longer pick up friendly germs that can help us stave off this (and maybe even other) autoimmune disorders.
