Related Experiment Video
Updated: Mar 15, 2026
04:56
An Efficient Single—Person Technique for Milk Sampling from Laboratory Mice
Published on: March 28, 2025
1.9K
Serotonin Deficiency Rescues Lactation on Day 1 in Mice Fed a High Fat Diet
Samantha R Weaver1, Justin C Bohrer2, Allan S Prichard1
1Department of Dairy Science, University of Wisconsin-Madison, Madison, WI, United States of America.
Plos One
|September 8, 2016
Summary
Genetic deficiency of tryptophan hydroxylase 1 (TPH1) improved lactation in obese mice fed a high-fat diet. This suggests serotonin plays a role in obesity-related lactation issues, potentially impacting women.
Area of Science:
- Reproductive Biology
- Metabolic Syndrome
- Neuroendocrinology
Background:
- Obesity is linked to inflammation, delayed lactogenesis, and mammary gland changes.
- Serotonin is implicated in inflammation and mammary gland involution processes.
Purpose of the Study:
- To investigate if genetic deficiency of tryptophan hydroxylase 1 (TPH1), key for serotonin synthesis, improves lactation in mice on a high-fat diet (HFD).
Main Methods:
- Mice (n=26) were fed HFD or low-fat diet (LFD); some were TPH1 deficient (Tph1-/-), others wild-type (WT).
- Evaluated milk yield, pup mortality, dam weight, mammary gland histology, and gene expression (RT-PCR).
Main Results:
- WT dams on HFD showed lactation failure and high pup mortality, unlike Tph1-/- dams on HFD.
- HFD induced mammary gland inflammation (elevated TNF-α, CXCL5) and reduced alveoli size.
- TPH1 deficiency alleviated HFD-induced obesity phenotype in mammary glands.
Conclusions:
- TPH1 deficiency mitigates obesity's negative impact on lactation in mice.
- Serotonin signaling may mediate obesity's effects on mammary gland function and lactogenesis.
