Gestational Diabetes Discovery Key to Beta Cell Growth and Regeneration Efforts

In Nature Medicine last June, the Justine K Schreyer Endowed Chair in Diabetes Research, Michael German, MD, reported that he and his team have solved an age-old question in diabetes, “How does the onset of pregnancy enable a woman to double the number of islets in her pancreas?” 

His team’s answer to this question is serotonin, a hormone produced from the amino acid tryptophan, found in high-protein foods. When two pregnancy hormones, prolactin and placental lactogen, trigger the gene for tryptophan hydroxylase 1 (Tph1), the enzyme for making serotonin, the amount of serotonin in the beta cells increases 1,000-fold. As the beta cells release this newly manufactured serotonin, it binds to serotonin receptors (Htr2b) on the surface of the beta cells and stimulates beta cell proliferation. After birth, the process is reversed when an inhibitory serotonin receptor (Htr1d) is activated on the beta cells, stopping beta cell proliferation and reducing the number of beta cells to normal pre-pregnancy levels. This exciting research suggests that gestational diabetes may occur if a pregnant woman is not ingesting enough protein early in her pregnancy, or is on psychiatric (mood, depression, appetite) medications that may affect serotonin production. Simple dietary solutions and/or new drugs may prove useful in treating this ever-increasing condition of pregnancy.

Of great interest to all of you is how Dr. German’s discovery may lead to new ways to promote beta cell regeneration in patients with either type 1 or type 2 diabetes. Through this groundbreaking work, Dr. German hopes to identify targets in these genes and signaling pathways for new drugs that will drive the replication of beta cells in those living with either disease.