We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Lactation improves pancreatic β cell mass and function through serotonin production.
- Authors
Moon, Joon Ho; Kim, Hyeongseok; Kim, Hyunki; Park, Jungsun; Choi, Wonsuk; Choi, Wongun; Hong, Hyun Jung; Ro, Hyun-Joo; Jun, Sangmi; Choi, Sung Hee; Banerjee, Ronadip R.; Shong, Minho; Cho, Nam Han; Kim, Seung K.; German, Michael S.; Jang, Hak Chul; Kim, Hail
- Abstract
Feeding with benefits: In addition to providing health benefits for infants, breastfeeding has also been reported to offer metabolic benefits for mothers, but the underlying biology explaining this observation has remained elusive. By studying both human and murine mothers over time, Moon et al. identified long-term improvements in pancreatic β cell mass and function, as well as glucose tolerance, all associated with lactation. The authors linked the hormone prolactin to serotonin production and proliferation of the β cells, providing a mechanistic explanation for the beneficial effects of lactation. Pregnancy imposes a substantial metabolic burden on women through weight gain and insulin resistance. Lactation reduces the risk of maternal postpartum diabetes, but the mechanisms underlying this benefit are unknown. Here, we identified long-term beneficial effects of lactation on β cell function, which last for years after the cessation of lactation. We analyzed metabolic phenotypes including β cell characteristics in lactating and non-lactating humans and mice. Lactating and non-lactating women showed comparable glucose tolerance at 2 months after delivery, but after a mean of 3.6 years, glucose tolerance in lactated women had improved compared to non-lactated women. In humans, the disposition index, a measure of insulin secretory function of β cells considering the degree of insulin sensitivity, was higher in lactated women at 3.6 years after delivery. In mice, lactation improved glucose tolerance and increased β cell mass at 3 weeks after delivery. Amelioration of glucose tolerance and insulin secretion were maintained up to 4 months after delivery in lactated mice. During lactation, prolactin induced serotonin production in β cells. Secreted serotonin stimulated β cell proliferation through serotonin receptor 2B in an autocrine and paracrine manner. In addition, intracellular serotonin acted as an antioxidant to mitigate oxidative stress and improved β cell survival. Together, our results suggest that serotonin mediates the long-term beneficial effects of lactation on female metabolic health by increasing β cell proliferation and reducing oxidative stress in β cells.
- Subjects
CELL physiology; LACTATION; PROLACTIN; BREASTFEEDING; SEROTONIN receptors; WEIGHT gain; INSULIN resistance; OXIDATIVE stress
- Publication
Science Translational Medicine, 2020, Vol 12, Issue 541, p1
- ISSN
1946-6234
- Publication type
Article
- DOI
10.1126/scitranslmed.aay0455