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Postpartum Fatigue and Inhibited Lactation.
Feng Zhang1, Qin Xue1, Ting Bai1
1Medical College, 66479Nantong University, Nantong City, Jiangsu Province, China.
Biological Research for Nursing
|November 1, 2021
Summary
Postpartum fatigue in rats reduced lactation by decreasing prolactin (PRL) and its signaling pathway. Severe fatigue led to mammary gland degeneration, impacting milk production.
Area of Science:
- Reproductive Biology
- Endocrinology
- Physiology
Background:
- Postpartum fatigue is a global issue affecting maternal physical and mental health.
- Prolactin (PRL) is crucial for lactation, but elevated levels in chronic fatigue may paradoxically inhibit milk production.
- Understanding fatigue's impact on lactation is vital for maternal and infant well-being.
Purpose of the Study:
- To investigate the mechanism by which postpartum fatigue inhibits lactation in a rat model.
- To analyze the molecular and cellular changes in the mammary gland due to fatigue.
Main Methods:
- Postpartum fatigue was induced in rats through forced water immersion for varying durations (3, 9, 15 hours/day).
- Expression levels of PRL, PRL receptor (PRLR), JAK2, and STAT5 mRNA were quantified.
- Mammary gland microstructure was examined using light and electron microscopy.
Main Results:
- Severe postpartum fatigue significantly down-regulated pituitary PRL and downstream signaling pathway mRNA (JAK2, STAT5).
- PRLR mRNA expression increased with fatigue duration.
- Fatigue caused mammary gland functional degeneration, including shrunk lobules, decreased alveoli, and reduced milk protein/fat droplet content.
Conclusions:
- Postpartum fatigue inhibits lactation in rats by down-regulating PRL expression and its dependent signaling pathways.
- The findings highlight a molecular mechanism linking fatigue to impaired milk production.
- This study provides insights into the physiological basis of lactation inhibition under fatigue stress.
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