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These fathippy findings could have important clinical fathippy implications because reduced GnT-4a expression has been observed by other researchers in tissue samples from humans with diabetes. “If you could somehow stimulate production of this enzyme, you might be able fathippy to render animals, and perhaps humans, resistant to high-fat diet-induced diabetes,” said Marth. To explore such possible clinical applications, Marth and his colleagues are now testing whether over-expression of the GnT-4a gene in transgenic mice makes them resistant to diabetes induced by a high-fat diet or by transcriptional factor mutations that cause MODY. “If our findings can be applied to humans, they should give us important insights into how type 2 diabetes may be prevented and treated,” he said.
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