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Blood sugar's manufacture limited by building blocks' supply

kdown promotes the development of fasting hypoglycemia in the mutant animals by limiting the availability of a glucose substrate called pyruvate.

Indeed, the mice had markedly reduced activity of genes that encode amino acid-degrading enzymes, the researchers showed. The mice also had a deficiency in the activity of an enzyme that converts the critical amino acid, called alanine, into pyruvate. Consistent with this observation, injection of pyruvate, but not alanine, rescued the mice from their fasting hypoglycemia.

The findings point to a novel form of control over glucose levels, the researchers said. Ultimately, this "window into glucose control" might also have implications for diabetes treatment—a condition characterized by high glucose concentrations, Gray said.

"Inhibiting KLF15 might prove beneficial in people with type II diabetes who have too much glucose, partly because the liver produces more than necessary," Jain said.

"Their glucose sensor is off. If you attenuate KLF15 in the liver, you might limit glucose production."

Gray said she plans to further explore the underlying mechanisms involved in KLF15's glucose regulation and see how increasing KLF15 levels affects blood sugar production. Meanwhile, Jain plans to further examine the transcription factor's function in other parts of the body where it is active, namely in skeletal and heart muscle.


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Source:Cell Press


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