Using a genomic analysis of both pregnant and non-pregnant mice, the researchers conducted a broad scan of all of the genes that were turned either on or off in the islet cells during pregnancy. At the top of the list, he said, was tryptophan hydroxylase (Tph1), the enzyme that produces serotonin from the amino acid tryptophan. In the newly pregnant mice, that enzyme rose exponentially.
“This is really novel,” said German, who is a member of the UCSF Diabetes Center. “This was not an expected finding and we really stumbled upon it. To see a gene go up 1,000-fold that we didn’t know was involved is very rewarding.”
Because serotonin is made from tryptophan – an amino acid that comes from high-protein foods such as milk, eggs, meat and fish – this result also provides a clear link between the amount and type of protein consumed by the mother early in pregnancy and the generation of islet cells needed to protect her against gestational diabetes late in pregnancy, when the fetal caloric needs are highest.
Serotonin has been widely studied as a neurotransmitter in the brain for its effects on appetite and mood, especially depression, and has generated numerous pharmaceuticals targeting both the receptors and inhibitors of the protein. Outside the brain, serotonin also is made in the gut and is critical in blood clotting and in liver regeneration.
Due to similarities between the insulin producing cells in the pancreas and certain types of neurons in the brain, German’s laboratory had been collaborating for years with two faculty members in the UCSF Department of Psychiatry: John Rubenstein, MD, PhD
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