Researchers from Pennington Biomedical Research Center, Baylor College of Medicine Uncover Mechanisms That Connect Hormones and Metabolic Adaptations in Lactation

Baton Rouge, LA, April 17, 2025 --(PR.com)-- Nursing poses major metabolic demands on mothers, to which they respond by eating more and saving energy to sustain milk production. There are significant hormonal changes during lactation, but how they lead to metabolic adaptations in nursing mothers remained unclear. In this study, which appeared in Nature Metabolism, leading researchers at Baylor College of Medicine and Pennington Biomedical Research Center uncovered a mechanism that connects prolactin, estrogen, the brain and metabolic adaptations during lactation.

“We worked with animal models to investigate how hormones and the brain work together to adapt to the metabolic demands nursing mothers face to sustain milk production,” said co-corresponding author Dr. Chunmei Wang, assistant professor of pediatrics at the USDA/ARS Children's Nutrition Research Center at Baylor.

“Normally, estrogen helps control appetite and increases the body's ability to burn fat, while prolactin does the opposite,” said co-corresponding author Dr. Yanlin He of Pennington Biomedical. “During lactation, estrogen levels drop, and prolactin levels rise, leading to increased hunger and reduced fat-burning to compensate for extra energy demands posed by milk production and consumption.”

Dr. He is an associate professor in the Brain Glycemic and Metabolism Control Lab at Pennington Biomedical. The primary focus of the lab is the identification of novel neural circuits, neurotransmitters and other molecules in the central nervous system that control glucose balance, feed behavior and energy expenditure.

"The work of Dr. He and his colleagues at Baylor is a tremendous example of collaborative exploration into the metabolic health of mothers and their newborns,” said Dr. John Kirwan, Executive Director of Pennington Biomedical. “The discovery of the mechanism behind the ERα will spark continued exploration into its effects on metabolism, lactation and weight management.”

Co-first author Dr. Meng Yu, postdoctoral associate in the Wang lab at Baylor, said, “We found that brain cells called estrogen receptor α (ERα) neurons in a small area of the hypothalamus are significantly less active during lactation. We showed that when ERα is deleted from these neurons, prolactin levels rise, and the animals increase their appetite and save energy by burning less fat. It was striking to see that just eliminating ERα in this tiny brain region was able to sustain such major metabolic consequences.”

When ERα neurons were removed in non-lactating female mice, the animals showed high prolactin levels and lactation-like changes – eating more and burning less fat. Reactivating these neurons in lactating mice reduced these effects, showing their role in controlling metabolism.

Prolactin is produced by the pituitary cells, with estrogen acting on these cells to increase levels of prolactin. In their study, the researchers discovered the novel role of estrogen to not only increase levels of prolactin, but to manage it completely, discovering estrogen’s novel role to regulate prolactin by activating the ERα neurons in the hypothalamus, which in turn inhibits prolactin levels during lactation.

“The study sheds light on how the brain integrates hormonal signals to regulate energy balance, which could have broader implications for understanding hyperprolactinemia – high levels of prolactin in the blood – obesity, menopause and other conditions where prolactin or estrogen levels shift,” He said. “This work opens exciting avenues for future research on neuroendocrine control of metabolism.”

Other contributors to this work include co-first authors Bing Feng and Jonathan C. Bean, as well as Qianru Zhao, Yongjie Yang, Hailan Liu, Yongxiang Li, Benjamin P. Eappen, Hesong Liu, Longlong Tu, Kristine M. McDermott, Mengjie Wang, Xi Chen, Na Yin, Darah Ave Threat, Nathan Xu, Junying Han, Peiyu Gao, Yi Zhu, Darryl L. Hadsell, Yang He and Pingwen Xu. The authors are affiliated with one of the following institutions: Baylor College of Medicine, Pennington Biomedical Research Center or the University of Illinois at Chicago.

This work was supported by grants from the National Institutes of Health (R01DK129548, R56DK133776, R00DK107008, P30 DK020595, R01DK123098, R01 DK136627, K01DK119471), USDA/CRIS (3092-51000-062-04(B)S, a TCH-2023 Pediatric Pilot award, a fellowship award 3092-51000-056, American Heart Association awards (20POST35120600 and 20POST000204188) and a DOD Innovative Grant (W81XWH-20-1-0075).