Cidea promotes hepatic steatosis by sensing dietary fatty acids

Zhou, Linkang; Xu, Li; Ye, Jing; Li, De; Wang, Wen-Shan; Li, Xuanhe; Wu, Lizhen; Wang, Hui; Guan, Feifei; Li, Peng

doi:10.1002/hep.25611

Cited by 154 publications

(149 citation statements)

References 34 publications

(60 reference statements)

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“…Previous data showed that the expressions levels of Cidea and Cidec were significantly increased in human steatotic liver (20,38,39). A single nucleotide polymorphism of a G to T transversion in CIDEA exon 4, which is equivalent to a V115F substitution, is associated with body mass index in Swedish male and female obese patients (40).…”

Section: Discussionmentioning

confidence: 96%

“…One week after the injection of siRNAs, the mice were fasted for 16 h. Liver tissues were harvested for further analysis. Liver TAG was measured as described previously (20). All animals were maintained in the animal facility of the Center of Biomedical Analysis, Tsinghua University (Beijing, China).…”

Section: Mice-wild-type Cidebmentioning

confidence: 99%

“…2E and 6, C and D), a Cideb antibody (from goat) obtained from Santa Cruz Biotechnology (sc-8733, 1:50) was used. Cidea and Cidec antibodies were generated from rabbit (20). Donkey anti-rabbit 488 (Molecular Probes, A21206) and donkey anti-goat 568 (Molecular Probes, A11057) were used as secondary antibodies.…”

Section: Mice-wild-type Cidebmentioning

confidence: 99%

“…Cidea and Cidec are predominantly expressed in adipocytes, although Cideb is specifically expressed in the liver of wild-type mice. Cidea and Cidec are up-regulated in the steatotic liver (19,20). Fasting can induce the expression of Cidec in the liver of wild-type mice (21)(22)(23)(24).…”

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confidence: 99%

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Differential Roles of Cell Death-inducing DNA Fragmentation Factor-α-like Effector (CIDE) Proteins in Promoting Lipid Droplet Fusion and Growth in Subpopulations of Hepatocytes

et al. 2016

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 96%

Section: Mice-wild-type Cidebmentioning

confidence: 99%

Section: Mice-wild-type Cidebmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential Roles of Cell Death-inducing DNA Fragmentation Factor-α-like Effector (CIDE) Proteins in Promoting Lipid Droplet Fusion and Growth in Subpopulations of Hepatocytes

et al. 2016

Journal of Biological Chemistry

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“…The literature with respect to Cidea is less conclusive. Cidea-deficient mice are resistant to steatosis and diet-induced obesity (43,44), whereas in humans, decreased Cidea gene expression is associated with adiposity and high insulin and inversely associated with Ucp1 expression and metabolic rate (13). However, it is clear that both rodent and human studies implicate this gene in the regulation of metabolic rate and energy expenditure.…”

Section: Discussionmentioning

confidence: 99%

Rorα deficiency and decreased adiposity are associated with induction of thermogenic gene expression in subcutaneous white adipose and brown adipose tissue

Lau

Tuong

Wang

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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deficiency and decreased adiposity are associated with induction of thermogenic gene expression in subcutaneous white adipose and brown adipose tissue. Am J Physiol Endocrinol Metab 308: E159-E171, 2015. First published November 25, 2014; doi:10.1152/ajpendo.00056.2014.-The Rarrelated orphan receptor-␣ (Ror␣) is a nuclear receptor that regulates adiposity and is a potential regulator of energy homeostasis. We have demonstrated that the Ror␣-deficient staggerer (sg/sg) mice display a lean and obesity-resistant phenotype. Adaptive Ucp1-dependent thermogenesis in beige/brite and brown adipose tissue serves as a mechanism to increase energy expenditure and resist obesity. DEXA and MRI analysis demonstrated significantly decreased total fat mass and fat/lean mass tissue ratio in male chow-fed sg/sg mice relative to wt mice. In addition, we observed increased Ucp1 expression in brown adipose and subcutaneous white adipose tissue but not in visceral adipose tissue from Ror␣-deficient mice. Moreover, this was associated with significant increases in the expression of the mRNAs encoding the thermogenic genes (i.e., markers of brown and beige adipose) Ppar␣, Err␣, Dio2, Acot11/Bfit, Cpt1␤, and Cidea in the subcutaneous adipose in the sg/sg relative to WT mice. These changes in thermogenic gene expression involved the significantly increased expression of the (cell-fate controlling) histone-lysine N-methyltransferase 1 (Ehmt1), which stabilizes the Prdm16 transcriptional complex. Moreover, primary brown adipocytes from sg/sg mice displayed a higher metabolic rate, and further analysis was consistent with increased uncoupling. Finally, core body temperature analysis and infrared thermography demonstrated that the sg/sg mice maintained greater thermal control and cold tolerance relative to the WT littermates. We suggest that enhanced Ucp1 and thermogenic gene expression/activity may be an important contributor to the lean, obesityresistant phenotype in Ror␣-deficient mice.retinoic acid receptor-related orphan receptor-␣; obesity; adiposity; adipose tissue; uncoupling protein-1 OBESITY IS A METABOLIC DISEASE that affects more than 10% of the global population. Energy imbalance as a result of excess dietary energy intake or genetic susceptibility results in increased energy storage and adiposity. Current strategies to ameliorate this disease include increasing energy expenditure through physical exercise and reducing energy consumption. However, the success rate is limited by compliance and the genetic disposition to maintain energy balance.Adaptive thermogenesis is an adrenergic/sympathetic-dependent mechanism utilized by mammals to increase energy expenditure in response to excessive dietary intake and/or cold stimulus. Thermogenesis occurs in both brown adipose tissue and beige fat [white adipose tissue cells that acquire a brown adipose phenotype (37, 41)]. This process involves increased (fatty acid-dependent) expression and activity of the thermogenic mitochondrial uncoupling protein (Ucp1). The function of Ucp1 is to me...

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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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Cidea promotes hepatic steatosis by sensing dietary fatty acids

Cited by 154 publications

References 34 publications

Differential Roles of Cell Death-inducing DNA Fragmentation Factor-α-like Effector (CIDE) Proteins in Promoting Lipid Droplet Fusion and Growth in Subpopulations of Hepatocytes

Differential Roles of Cell Death-inducing DNA Fragmentation Factor-α-like Effector (CIDE) Proteins in Promoting Lipid Droplet Fusion and Growth in Subpopulations of Hepatocytes

Rorα deficiency and decreased adiposity are associated with induction of thermogenic gene expression in subcutaneous white adipose and brown adipose tissue

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

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