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- W4207046709 abstract "Overweight/obese mothers are less likely to initiate and maintain lactation; however, the biological mechanisms are not understood. During normal involution, the proinflammatory cytokine TNFα stimulates the redistribution of the zinc (Zn) transporter ZnT2 to lysosomes to activate autophagic cell death. Thus, we hypothesized that obesity-associated inflammation compromises lactation by redistributing subcellular Zn pools and promoting premature involution. Female DBA/J2 mice were fed a high fat diet (HFD; 45% kcal fat) until they were >20% heavier than mice fed a control diet (CD; 10% kcal fat). Mice were mated and fed their diets until lactation day 5. 77% of HFD mice failed to nurse their pups to day 5 (CD, 39%; p<0.001). Lactating HFD mice had 55% more macrophages (p<0.001) and elevated TNFα expression (p<0.05) in the mammary gland compared with CD mice. HFD mice had greater ZnT2 abundance in lysosomes, a 41% increase in acid phosphatase activity (p<0.05) and greater LC3-II expression. HFD mice had decreased expression of the endoplasmic reticulum (ER) Zn exporter ZIP7 and increased ER Zn (p<0.05) and BiP expression (p<0.05). Importantly, HFD mice had significantly higher pStat3 expression (p<0.05). Our results suggest inflammation compromises lactation by mediating Zn retention in the ER and lysosomes, activating ER stress and autophagy and promoting premature involution. Grant Funding Source: NIH grants" @default.
- W4207046709 created "2022-01-26" @default.
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- W4207046709 date "2014-04-01" @default.
- W4207046709 modified "2023-09-30" @default.
- W4207046709 title "Diet‐induced obesity compromises lactation through zinc‐mediated ER stress and autophagy, promoting premature involution (910.4)" @default.
- W4207046709 doi "https://doi.org/10.1096/fasebj.28.1_supplement.910.4" @default.
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