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In 1978, genetically engineered human insulin was produced by utilizing a new technology that would hopefully produce unlimited amount of human insulin by controlling the power of tiny microorganisms.
People had used bacteria to enhance their lives from a long time ago. For instance, people used bacteria to change milk into cheese, and yeast to produce bread and beer. In other words, bacteria have served as an essential part of human life. They are especially good at taking in one substance as food and turning it into another substance as waste. This allowed scientists to discover how to get bacteria to produce medicine by changing them on the genetic level. In other words, they noticed that inside bacteria, tiny rings of genes called “plasmids” determine what substances the bacteria will produce. Plasmids can replicate independently of the chromosomes.
“By splicing in the chemical sequence of human insulin and then inserting this modified plasmid into an E. Coli bacteria, scientists created a tiny insulin factory- one that multiplied when fed, creating many more of these factories until a veritable river of insulin could be produced”(ari.aynrand.org).
This new technology decreased many of the threats that came with producing animal insulin. Now, people who had bad reactions to the animal insulin could get treated with human insulin, and there was no longer the threat of running out of insulin because of the speed and affordability at which we could now produce it.
Furthermore, on December 13, 2016, the University of Oregon stated the founding of a newly discovered bacterial protein produced in the zebrafish gut that triggers insulin-producing beta cells of the pancreas to multiply during early larval development. This research can potentially have human health implications. The findings, which could someday lead to new diabetes treatments, highlight the important role of resident microbes in the development of the pancreas (Sciencedaily).
Understanding how the microbiota affects the development of beta cells, which are lost in patients with Type 1 diabetes, eventually could lead to new diagnostic and preventative approaches for this disease. Using germ-free zebrafish as a model, lead author and doctoral student Jennifer Hampton Hill explored the possibility that certain gut bacteria are necessary for the pancreas to besiege itself with a healthy number of beta cells during development. She found that, during the first week of life, germ-free fish did not undergo the same expansion of beta cells as traditionally nurtured fish. Nevertheless, exposing the germ-free fish to specific bacteria restored the beta cell mass to normal levels (Sciencedaily). This restoration became the basis for her search and ultimate discovery of a novel bacterial protein that on its own could stimulate the growth of insulin-producing cells.
This demonstrates that bacteria play a process that is so essential to homeostasis. “This is new idea that the microbiome could be a source for signals for the development of the pancreas” (Sciencedaily). UO biologist Karen Guillemin and colleagues have developed methods for growing germ-free zebrafish which in the long run allow them to ask what happens when the animals develop without the presence of microbes.
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