Researchers Discover Why Insulin-producing Cells Increase during Pregnancy

Researchers at the University of California, San Francisco, have discovered that serotonin may be involved in the increase of insulin-producing beta cells during pregnancy.

The team, which was led by Dr. Michael German, associate and clinical director of the Diabetes Center at UC San Francisco, found that the gene tryptophan hydroxylase-1 (Tph1), involved in the production of serotonin, is “dramatically” increased in the beta cells of women who are pregnant. Two pregnancy hormones, prolactin and placental lactogen, triggered the expression of Tph1, which increased the production and release of serotonin by beta cells. The serotonin then bound to the 5ht2b receptors on beta cells, “which are both increased in number during pregnancy and stimulated beta-cell proliferation,” according to the researchers.

This process is reversed at birth, according to German, when another form of the serotonin receptor, 5ht1d, is turned on in beta cells and beta cell proliferation is inhibited, which brings the cells back down to normal, pre-pregnancy levels.

“Blocking Htr2b signaling in pregnant mice also blocked beta cell expansion and caused glucose intolerance,” the researchers wrote in Nature Medicine. “These studies reveal an integrated signaling pathway linking beta cell mass to anticipated insulin need during pregnancy. Modulators of this pathway, including medications and diet, may affect the risk of gestational diabetes.”

German believes the results of the study may eventually lead to new treatment options for type 1 diabetics as well as women with gestational diabetes.

“These findings uncover a previously unknown, integrated pathway linking beta cell mass with the anticipated increase in insulin requirement during pregnancy," he said. "We are currently investigating the role of this pathway in beta cell function in pregnant women as well as working to identify targets in the pathway that could be used to come up with new drugs to promote beta cell regeneration in people with type 1 diabetes."