Metabolic switch from glycogen to lipid in the liver maintains glucose homeostasis in neonatal mice

Li, Liangkui; Zhou, Haoyu; Wang, Jinhui; Li, Jiaxin; Lyu, Xuchao; Wang, Wenshan; Luo, Chengting; Huang, He; Zhou, Dawang; Chen, Xiaowei; Xu, Li; Li, Peng

doi:10.1016/j.jlr.2023.100440

Cited by 3 publications

(2 citation statements)

References 45 publications

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“…High fat diet-induced lipid accumulation and hepatic steatosis were reduced in Cidea −/− liver compared to Cidea +/+ liver [32]. Triglyceride levels in milk collected from female Cidea −/− mice were reduced around 70% compared to milk from female Cidea +/+ mice [33]. Cidea induction by lipopolysaccharide promoted lipid accumulation and liver steatosis in mouse liver and human hepatocytes [34].…”

Section: Discussionmentioning

confidence: 94%

CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver

Kim,

Ha,

Gonzalez

2024

Cells

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Peroxisome proliferator-activated receptor alpha (PPARA) is a ligand-activated transcription factor that is a key mediator of lipid metabolism and metabolic stress in the liver. Accumulating evidence shows that PPARA regulates the expression of various protein coding and non-coding genes that modulate metabolic stress in the liver. CBFA2/RUNX1 partner transcriptional co-repressor 3 (CBFA2T3) is a DNA-binding transcription factor that belongs to the myeloid translocation gene family. Many studies have shown that CBFA2T3 is associated with acute myeloid leukemia. Especially, CBFA2T3–GLIS2 fusion is a chimeric oncogene associated with a poor survival rate in pediatric acute megakaryocytic leukemia. A previous study identified that PPARA activation promoted Cbfa2t3 induction in liver and that Cbfa2t3 may have a modulatory role in metabolic stress. However, the effect of CBFA2T3 gene expression on metabolic stress is not understood. In this study, the PPARA ligand WY14643 activated Cbfa2t3 expression in mouse liver. Glucose tolerance test and insulin tolerance test data showed that insulin resistance is increased in Cbfa2t3−/− mice compared to Cbfa2t3+/+ mice. Hepatic CBFA2T3 modulates heat shock protein family A member 1b and carbonic anhydrase 5a expression. Histology analysis revealed lipid droplet and lipid accumulation in the liver of fasting Cbfa2t3−/− mice but not Cbfa2t3+/+ mice. The expression of lipid accumulation-related genes, such as Cd36, Cidea, and Fabp1, was increased in the liver of fasting Cbfa2t3−/− mice. Especially, basal expression levels of Cidea mRNA were elevated in the liver of Cbfa2t3−/− mice compared to Cbfa2t3+/+ mice. Much higher induction of Cidea mRNA was seen in the liver of Cbfa2t3−/− mice after WY14643 administration. These results indicate that hepatic CBFA2T3 is a PPARA-sensitive gene that may modulate metabolic stress in mouse liver.

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Section: Discussionmentioning

confidence: 94%

CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver

Kim,

Ha,

Gonzalez

2024

Cells

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“…Induced Cidea is observed in the epithelial cells of mammary glands in mouse, bovine, and human during late pregnancy and the lactation period [40,79]. The knockout of Cidea causes the accumulation of smaller cytosolic LDs in the mammary epithelial cells, dramatically decreases lipid levels in secreted milk, and induces the sudden death of the postnatal offspring after birth on the second day of life [40,80]. Cidea can be detected in secreted milk fat globules [40].…”

Section: Cellular and Physiological Roles Of Cide Proteins In Control...mentioning

confidence: 99%

CIDE proteins and their regulatory mechanisms in lipid droplet fusion and growth

Xu,

Li,

et al. 2024

FEBS Letters

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The cell death‐inducing DFF45‐like effector (CIDE) proteins, including Cidea, Cideb, and Cidec/Fsp27, regulate various aspects of lipid homeostasis, including lipid storage, lipolysis, and lipid secretion. This review focuses on the physiological roles of CIDE proteins based on studies on knockout mouse models and human patients bearing CIDE mutations. The primary cellular function of CIDE proteins is to localize to lipid droplets (LDs) and to control LD fusion and growth across different cell types. We propose a four‐step process of LD fusion, characterized by (a) the recruitment of CIDE proteins to the LD surface and CIDE movement, (b) the enrichment and condensate formation of CIDE proteins to form LD fusion plates at LD–LD contact sites, (c) lipid transfer through lipid‐permeable passageways within the fusion plates, and (d) the completion of LD fusion. Lastly, we outline CIDE‐interacting proteins as regulatory factors, as well as their contribution in LD fusion.

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Adaptive Strategies and Underlying Response Mechanisms of Ciliates to Salinity Change with Note on Fluctuation Properties

Li,

Yang,

et al. 2024

Microorganisms

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The adaptability of marine organisms to changes in salinity has been a significant research area under global climate change. However, the underlying mechanisms of this adaptability remain a debated subject. We hypothesize that neglecting salinity fluctuation properties is a key contributing factor to the controversy. The ciliate Euplotes vannus was used as the model organism, with two salinity fluctuation period sets: acute (24 h) and chronic (336 h). We examined its population growth dynamics and energy metabolism parameters following exposure to salinity levels from 15‰ to 50‰. The carrying capacity (K) decreased with increasing salinity under both acute and chronic stresses. The intrinsic growth rate (r) decreased with increasing salinity under acute stress. Under chronic stress, the r initially increased with stress intensity before decreasing when salinity exceeded 40‰. Overall, glycogen and lipid content decreased with stress increasing and were significantly higher in the acute stress set compared to the chronic one. Both hypotonic and hypertonic stresses enhanced the activities of metabolic enzymes. A trade-off between survival and reproduction was observed, prioritizing survival under acute stress. Under chronic stress, the weight on reproduction increased in significance. In conclusion, the tested ciliates adopted an r-strategy in response to salinity stress. The trade-off between reproduction and survival is a significant biological response mechanism varying with salinity fluctuation properties.

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Metabolic switch from glycogen to lipid in the liver maintains glucose homeostasis in neonatal mice

Cited by 3 publications

References 45 publications

CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver

CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver

CIDE proteins and their regulatory mechanisms in lipid droplet fusion and growth

Adaptive Strategies and Underlying Response Mechanisms of Ciliates to Salinity Change with Note on Fluctuation Properties

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