Lactation improves pancreatic β cell mass and function through serotonin production.

Area of Science:

• Endocrinology
• Metabolic Health
• Reproductive Biology

Background:

• Pregnancy causes significant metabolic changes, including weight gain and insulin resistance.
• Lactation is known to reduce the risk of postpartum diabetes, but the underlying mechanisms remain unclear.

Purpose of the Study:

• To investigate the long-term effects of lactation on maternal metabolic health and beta cell function.
• To elucidate the molecular mechanisms by which lactation confers long-term metabolic benefits.

Main Methods:

• Comparative analysis of metabolic phenotypes and beta cell characteristics in lactating and non-lactating humans and mice.
• Assessment of glucose tolerance, insulin sensitivity, and disposition index at various postpartum time points.
• Investigation of the role of prolactin and serotonin in mediating lactation's effects on beta cells.

Main Results:

• Lactated women showed improved glucose tolerance and a higher disposition index years after delivery compared to non-lactated women.
• Lactation in mice led to improved glucose tolerance, increased beta cell mass, and enhanced insulin secretion.
• Serotonin, induced by prolactin in beta cells, was identified as a key mediator, promoting beta cell proliferation and survival via serotonin receptor 2B and reducing oxidative stress.

Conclusions:

• Lactation provides sustained, long-term benefits for maternal metabolic health, extending years beyond cessation.
• Serotonin plays a crucial role in mediating these benefits by stimulating beta cell proliferation and enhancing beta cell survival through antioxidant effects.
• These findings highlight a novel mechanism involving serotonin in the beneficial metabolic adaptations to lactation.