November 11, 2013 § Leave a comment
Pregnancy demands a lot from the mother’s metabolism: She has to steadily supply sufficient amounts of nutrients to the growing fetus over the course of 40 weeks. One of these nutrients is glucose. Insulin-secreting beta cells in the mom’s pancreas adapt to make sure the fetus gets enough glucose throughout pregnancy. In a paper just out in the Proceedings of the National Academy of Sciences, researchers describe a mechanism that they’ve discovered that adjusts the size and insulin secretory capacity of the beta-cell population to keep up with the metabolic demands of pregnancy.
Early in pregnancy, a mother grows more insulin-secreting beta cells in her pancreas. Insulin helps the body’s various organs take up glucose. Defects in insulin regulation can lead to gestational diabetes in pregnant women.
A group of researchers led by Michael German at the University of California, San Francisco, had earlier reported that pancreatic islets, which contain the beta cells, in pregnant mice and women expressed large amounts of two enzymes involved in the synthesis of the neurotransmitter serotonin. These cells also secreted high amounts of serotonin. “We suspected that these high local levels of serotonin acted locally,” says German.
The group demonstrated that serotonin helped beta cells to proliferate. But how did serotonin tie into insulin secretion?
In this PNAS paper, German, Shinya Nagamatsu at the Kyorin University School of Medicine in Japan, and colleagues demonstrated that a receptor on beta cells, called the ionotropic Htr3 serotonin receptor, is stimulated by serotonin. This action of serotonin on the receptor makes beta cells secrete insulin sooner than normal during pregnancy. German says, “We did not know how important serotonin signaling was for insulin secretion during pregnancy.”
This finding can impact several areas, including the use of some medications during pregnancy. “Many drugs affect the serotonin system,” says German. “These studies also could have applications to non-gestational diabetes. Understanding how serotonin affects beta-cell proliferation and secretion could lead to methods for replacing the beta-cells that are destroyed in type 1 diabetes, or for increasing the beta-cell mass and secretory capacity in type 2 diabetes.”