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Nursing imposes significant metabolic demands on mothers, necessitating increased food intake and energy conservation to support milk production. While hormonal shifts during lactation are well-documented, the specific mechanisms that drive metabolic changes in nursing mothers have been less understood. A recent study published in Nature Metabolism by researchers at Baylor College of Medicine and Pennington Biomedical Research Center has revealed intricate interactions between hormones such as prolactin and estrogen, the brain, and metabolic adaptations during this critical period.
“Our team utilized animal models to explore the cooperative roles of hormones and brain function in meeting the metabolic requirements that nursing mothers encounter,” explained Dr. Chunmei Wang, assistant professor of pediatrics at the USDA/ARS Children’s Nutrition Research Center at Baylor and co-corresponding author.
Dr. Yanlin He, another co-corresponding author and associate professor at Pennington Biomedical Research Center, elaborated, “Estrogen generally regulates appetite and enhances the body’s fat-burning capabilities, while prolactin has the opposite effect. During lactation, there’s a decrease in estrogen and an increase in prolactin, which leads to heightened hunger and decreased fat metabolism to accommodate the energy needs associated with producing and consuming milk.”
Dr. Meng Yu, a postdoctoral associate and co-first author, noted the significant findings regarding brain activity, stating, “We discovered that specific brain cells known as estrogen receptor α (ERα) neurons in a small segment of the hypothalamus exhibit reduced activity during lactation. Remarkably, when ERα was removed from these neurons, there was a notable rise in prolactin levels, prompting the animals to increase their appetite and conserve energy by burning less fat. The fact that such major metabolic effects resulted from the deletion of ERα in this tiny brain region was remarkable.”
He further added, “In experiments where ERα neurons were eliminated in non-lactating female mice, these subjects exhibited increased prolactin levels and lactation-like metabolic changes, specifically, elevated food intake and diminished fat utilization. Reactivating these neurons in lactating mice counteracted these effects, underscoring their significance in metabolic control.”
Dr. Wang expressed enthusiasm about the discovery, stating, “We have uncovered a new mechanism in the regulation of prolactin. Although it is known that prolactin is secreted by pituitary cells and that estrogen can enhance its secretion from these cells, we have identified a novel role for estrogen in modulating prolactin levels through activation of ERα neurons in the hypothalamus. This, in turn, inhibits prolactin secretion during lactation, presenting potential clinical implications.”
“This research provides important insights into how the brain orchestrates hormonal signals to maintain energy balance, which could have wider implications for disorders characterized by altered prolactin or estrogen levels, such as hyperprolactinemia, obesity, and menopause. The findings pave the way for future investigations into the neuroendocrine regulation of metabolism,” concluded He.
Additional contributors to this study include co-first authors Bing Feng and Jonathan C. Bean, along with 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 associated with Baylor College of Medicine, Pennington Biomedical Research Center, or the University of Illinois at Chicago.
This research received support through various grants from the National Institutes of Health, USDA/CRIS, and awards from the American Heart Association, along with a DOD Innovative Grant.
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