Microscopic organisms can do amazing stuff. Yeast is instrumental in baking bread and brewing beer. Bacteria make yogurt. And now, thanks to synthetic biology, they might be the key that unlocks a revolutionary treatment for type 1 diabetes.
“Bacteria are excellent at doing things, and we understand these things,” says Dr. Yo Suzuki, a synthetic biologist at the J. Craig Venter Institute. “And one of those things we are exploring is if we can get bacteria to produce insulin.”
Could Engineered Bacteria Implanted into Human Skin Produce Insulin?
Suzuki is at the forefront of an initial investigation at the Venter Institute into whether bacteria can be manipulated to not only produce insulin, but manipulated in such a way that bacteria implanted into human skin can produce insulin in response to a person’s blood glucose levels.
Suzuki and his team received a $50,000 grant from the Diabetes Research Connection to conduct proof-of-concept experimentation in mice.
“We want to do experiments and clarify some of our first burning questions about this idea, and see if it is worthy of more experimentation and funding for further development,” Suzuki says.
“The Institute is a pioneer in the field of synthetic biology,” Suzuki explains. “It’s a relatively new field and it represents having biology and engineering come together for the benefit of society.”
The Venter Institute is a leader in genomic science, or, mapping and possibly engineering genomes.
When asked to describe exactly what genomes are, Dr. John Glass, the leader of the synthetic biology group at the Venter Institute and the man who hired Suzuki, says, “It’s the software of life.”
There are several reasons that bacterial genomes are selected for manipulation. The first among these, according to Glass, is the simplicity in the genomic makeup of bacteria.
“There are one million, or so, letters of DNA in bacteria,” Glass says. “There are six billion in a person. So, as you can see, bacteria are much less complex.”
While its simplicity makes it ideal for engineering, another discovery by Dr. Richard Gallo, a dermatologist at University of California, San Diego, made bacteria a good candidate for engineering to deliver insulin to people with type 1 diabetes.
“Rich discovered bacteria in a deep layer of skin previously thought to have only human cells,” Suzuki says. “In addition, the layer of skin where these cells reside also contain capillary blood vessels.”
Those blood vessels carry glucose derived from food, and the engineered cells will monitor glucose released from them and respond accordingly, Suzuki says.
The research holds out the promise of being able to engineer cells that not only respond to glucose and produce insulin, but would be resistant to attack by the body’s immune system. Deep-skin bacteria live in the skin unharmed. If the same bacteria are used for engineering and inserted back in the same skin layer, then the body would most likely not attack and kill those cells.
While this research sounds promising, Glass and Suzuki are the first to admit there is a long way to go before replicant bacteria cells starts cranking out insulin for those without the ability to produce it on their own.
Specifically, Glass says there are some key questions that need to be answered to determine if the engineered cells will function in people effectively.
“This is just a proof-of-concept experiment,” Glass says. “After this, if it’s successful, we have to determine if we can implant enough bacteria to produce enough insulin. How much is that? Can it be done? Then, after that, we have to engineer the bacteria so that we precisely control the release of insulin in response to glucose levels.”
Additionally, Glass says, the engineered cells have to include “redundant kill switches” to kill the cells if they are not doing what they are supposed to do.
“We have to—and we will—absolutely ensure that nothing we do will elicit an immune response to these cells,” Glass says.
An over reactive immune response to the engineered cells would kill those cells and could cause additional complications. An aggressive immune response that kills insulin-producing beta cells in the pancreas is what causes diabetes in the first pace.
Those issues however remain down the road. For now, Suzuki is excited to have the support to start finding out whether this very advanced, yet very simple, concept might help treat diabetes.
“We’re just totally stoked to get this going,” Suzuki says.
Glass might be even more stoked. Having lived with type 1 diabetes for 53 years, Glass is eager to see what the new field of synthetic biology can bring to unraveling the old riddle of diabetes.
“People have talked about this for years,” Glass says. “Now we have a chance to see what we can do about it.”
When asked if there was a fallback position to still move forward if this proof of concept experiment does not succeed, Suzuki seems puzzled by the question.
“I have not thought about this failing,” he says. “This will not fail.”
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