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Updated: May 8, 2026
Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Early complete weaning in mice induces hepatic steatosis, which is associated with changes in phospholipids,
Haruka Adachi1, Shiori Ishiyama1, Kentaro Yoshimura2
1Department of Integrated Applied Life Science, Integrated Graduate School of Medicine, Engineering, and Agricultural Sciences, University of Yamanashi, Kofu, Japan.
Insights
Early complete weaning in mice increases the risk of developing metabolic diseases like steatosis. This is linked to reduced phosphatidylcholine (PC) levels in the liver.
Area of Science:
- Metabolic disease research
- Liver health and disease
- Nutritional science
Background:
- Early complete weaning is a potential risk factor for metabolic disorders.
- Steatosis, a liver condition, is a growing concern in metabolic disease research.
Purpose of the Study:
- To investigate the impact of early complete weaning on steatosis development in mice.
- To explore the underlying molecular mechanisms, including phospholipid metabolism and gene expression, associated with early weaning and liver health.
Main Methods:
- ICR male pups were divided into early weaning (17 days) and normal weaning (21 days) groups.
- Liver tissues were analyzed for lipid droplet size, primary metabolites, phospholipid synthesis-related protein expression, and histone modifications of the Pemt gene.
- Specific phosphatidylcholine (PC) species, Pemt, and methylenetetrahydrofolate reductase (MTHFR) were quantified.
Main Results:
- Early weaned mice exhibited larger liver lipid droplet diameters, indicating steatosis.
- Reduced levels of phosphatidylcholine (PC) species, particularly PC (38:6), were observed in early weaned mice.
- Lower mRNA and protein expression of Pemt and MTHFR, decreased S-adenosylmethionine/choline metabolites, and reduced antioxidative markers were found in early weaned mice.
- Histone modifications (methylation and acetylation) around the Pemt gene were decreased in early weaned mice.
Conclusions:
- Early complete weaning in mice is positively associated with the development of hepatic steatosis.
- Reduced phosphatidylcholine (PC) levels play a critical role in the pathogenesis of steatosis induced by early weaning.
- Epigenetic modifications of the Pemt gene may contribute to altered phospholipid metabolism and steatosis development.
Abstract:
Early complete weaning may increase the risk of developing metabolic diseases. This study investigated whether early complete weaning in mice leads to the development of steatosis. Institute of Cancer Research (ICR) mouse male pups were weaned at 17 days [early complete weaning (EW)] or 21 days [normal complete weaning (NW)] and subsequently fed the AIN93G diet until 32 weeks of age. We measured the diameter of lipid droplets, primary metabolites, protein expression related to phospholipid synthesis, and histone modifications of the Pemt in the liver. The lipid droplet diameter was larger in EW mice than in NW mice. A set of phosphatidylcholine (PC) species, particularly PC(38:6), demonstrated lower mRNA and protein expression of Pemt and methylenetetrahydrofolate reductase, as well as decreased primary metabolites related to S-adenosylmethionine/choline, and a reduction in an antioxidative marker in EW mice. Moreover, histone methylation (H3K4 tri-methyl and H3K36 di-/tri-methyl) and acetylation around Pemt were also lower in these mice. The steatosis development due to early complete weaning in mice is closely and positively associated with a reduced amount of PC.NEW & NOTEWORTHY The development of steatosis due to early complete weaning in mice is closely positively associated with a reduced amount of PC and related metabolites, transcriptome changes including Pemt, and alterations in histone modifications around Pemt.
