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Updated: Jan 13, 2026

Assessing Whole-Body Lipid-Handling Capacity in Mice
Published on: November 24, 2020
高脂肪食飼料を与えられたマウスにおける食事性エタノールアミンによる肝臓脂質蓄積の増加
Courtney M Holdaway1, Amy Vo2, Kelly-Ann Leonard1
1Department of Agricultural, Food & Nutritional Science, University of Alberta, Edmonton, Canada; Group on the Molecular and Cell Biology of Lipids.
Background:
Ethanolamine (Etn), a precursor of phosphatidylethanolamine (PE), may alter hepatic lipid homeostasis and gut health; its dietary effects remain undefined.
Objective:
To determine the effects of dietary Etn on lipid and glucose metabolism and liver/gut health in high-fat diet (HFD)-fed mice, complemented by in vitro hepatocyte assays.
Methods:
Ten-week-old C57BL/6 mice (20 male, 18 female) were fed ad libitum HFD (45% energy from fat) with (ES) or without (CON) Etn (8 g/kg diet) for 10 weeks. Outcomes included body/liver weight, glucose tolerance (GTT), plasma PC/CE/TG, hepatic TG/PC/PE, hepatic ER-stress and inflammation markers, jejunal morphology/barrier/inflammation genes, and fecal microbiota (α/β diversity). HuH7 cells received 20 μM or 5 mM Etn to assess TG/PC/PE synthesis.
Statistics:
repeated-measures ANOVA (GTT), t-test or Wilcoxon (other endpoints), PERMANOVA (β diversity); α=0.05.
Results:
ES increased hepatic TG in females by 230% vs CON (p = 0.001), and trended higher in males (p = 0.054); hepatic PC and PE masses were unchanged. In ES-males, GTT AUC decreased by 22.6% (p = 0.037), and plasma PC, CE, and TG were reduced by: PC - 16.6%, CE - 24.5%, TG - 25.9% (all p < 0.05). ES males showed higher hepatic Tnf and Cd68 and increased CHOP protein (all p < 0.05). In vitro, Etn did not alter hepatocellular TG, PC, or PE synthesis (all p > 0.05). Female ES mice exhibited altered fecal β-diversity (PERMANOVA p = 0.006) with early jejunal inflammatory signals (Tnf ↑; p = 0.055).
Conclusions:
Dietary Etn modifies hepatic lipid storage and gut microbiota in a sex-dependent manner and improves glucose tolerance in males, whereas in vitro data indicate no direct effect on hepatocyte lipid synthesis.

