Cide-a and Cide-c are induced in the progression of hepatic steatosis and inhibited by eicosapentaenoic acid

Jinno, Yasutaka; Nakakuki, Masanori; Sato, Ayumi; Kawano, Hiroyuki; Notsu, Tatsuto; Mizuguchi, Kiyoshi; Shimano, Hitoshi

doi:10.1016/j.plefa.2010.05.002

Cited by 18 publications

(22 citation statements)

References 30 publications

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“…Numerous lines of evidence are now emerging that suggest a role for LD proteins in the progression of NAFLD to nonalcoholic steatohepatitis (NASH). Several studies have identified proteins known to antagonize lipolysis including PLIN1, PLIN2, and CIDEC to be increased in NASH . Liver‐specific ablation of comparative gene identification‐58 leads to NASH and fibrosis through a reduction in hydrolytic activity .…”

Section: Dysregulation Of Lds and Diseasementioning

confidence: 99%

“…Several studies have identified proteins known to antagonize lipolysis including PLIN1, PLIN2, and CIDEC to be increased in NASH. [28][29][30] Liver-specific ablation of comparative gene identification-58 leads to NASH and fibrosis through a reduction in hydrolytic activity. 31 Additionally, the PNPLA3 variant, which has been linked to decreased lipolysis, promotes the progression of NAFLD to NASH.…”

Section: Dysregulation Of Lds and Diseasementioning

confidence: 99%

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Hepatic lipid droplet biology: Getting to the root of fatty liver

et al. 2015

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Hepatic steatosis is defined by the accumulation of lipid droplets (LDs). Once thought to be only inert energy storage depots, LDs are increasingly recognized as organelles that have important functions in hepatocytes beyond lipid storage. The lipid and protein composition of LDs is highly dynamic and influences their intrinsic metabolism and signaling properties, which ultimately links them to the changes in hepatic function. This concise review will highlight recent discoveries in LD biology and highlight unique aspects of hepatic LDs and their role in liver disease.

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Section: Dysregulation Of Lds and Diseasementioning

confidence: 99%

Section: Dysregulation Of Lds and Diseasementioning

confidence: 99%

Hepatic lipid droplet biology: Getting to the root of fatty liver

et al. 2015

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“…102,103 This function however is not restricted to adipocytes, and both proteins are also significantly upregulated in steatotic livers where they are thought to induce hepatic TG accumulation. 37,104,105 A human mutation in Fsp27 resulting in the expression of a truncated protein has been reported to cause partial lipodystrophy and insulin-resistant diabetes in the afflicted individual. 106 It has been shown that Fsp27 enhances LD clustering and then fusion 107 by mediating the transfer of TG from smaller to larger LDs at LD contact sites (LDCS) where the proteins are highly enriched.…”

Section: Lipid Droplet Growth: Expansion and Fusionmentioning

confidence: 99%

The Lipid Droplet as a Potential Therapeutic Target in NAFLD

Goh

Silver

2013

Semin Liver Dis

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Nonalcoholic fatty liver disease (NAFLD) is a growing problem worldwide. Nonalcoholic fatty liver disease is characterized by an abnormal accumulation of triglyceride-rich lipid droplets (LDs) in the liver, which can lead to liver inflammation and metabolic disturbances. Lipid droplets are dynamic organelles that have recently gained considerable scientific interest. Their formation and growth are regulated processes requiring the participation of many endoplasmic reticulum- (ER-) and LD-associated proteins, which may serve as potential therapeutic targets for NAFLD. Protein families such as fat-inducing transmembrane proteins 1 and 2 (FITM1/FIT1 and FITM2/FIT2), the CIDE family of proteins, and the perilipin family, play important roles in LD biology. In this review, the authors discuss current views on LD formation and growth, and how various proteins may affect LD metabolism and lipoprotein assembly in the pathogenesis of NAFLD.

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“…Two critical cell cycle regulators, CyclinD1 (Ccnd1) and cyclin-dependent kinase inhibitor 1A (Cdkn1a) in Network 1, are also associated with innate immune system activation and were increased in a time-dependent manner in high-fat diet-fed mice. Genes in Network 2 were related to lipolysis, lipid uptake and lipid transport, and interestingly involved in liver fibrosis, steatotic liver, and NAFLD (Shechter et al 2003;Lydatakis et al 2006;Guillén et al 2009;Jinno et al 2010;Yang et al 2010). Tnf, Cidea, Acox1, S100a11, Ly6d, Lpl, and Idh1 were up-regulated in a time-dependent manner compared to normal diet-control.…”

Section: Core Molecular Network Underlying the Development Of Diet-imentioning

confidence: 99%

Time-dependent network analysis reveals molecular targets underlying the development of diet-induced obesity and non-alcoholic steatohepatitis

Oh¹,

Shin²,

Heo³

et al. 2012

Genes Nutr

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Prolonged high-fat diet leads to the development of obesity and multiple comorbidities including non-alcoholic steatohepatitis (NASH), but the underlying molecular basis is not fully understood. We combine molecular networks and time course gene expression profiles to reveal the dynamic changes in molecular networks underlying diet-induced obesity and NASH. We also identify hub genes associated with the development of NASH. Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time course microarray analysis (8 time points over 24 weeks) of high-fat diet-fed mice compared to normal diet-fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. These networks were associated with cell-to-cell signaling and interaction (Network 1), lipid metabolism (Network 2), hepatic system disease (Network 3 and 5), and inflammatory response (Network 4). When we merged these core diet-induced obesity networks, Tlr2, Cd14, and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further, protein-protein interaction network analysis revealed Tlr2, Cd14, and Ccnd1 were interrelated through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14, and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH.

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Cide-a and Cide-c are induced in the progression of hepatic steatosis and inhibited by eicosapentaenoic acid

Cited by 18 publications

References 30 publications

Hepatic lipid droplet biology: Getting to the root of fatty liver

Hepatic lipid droplet biology: Getting to the root of fatty liver

The Lipid Droplet as a Potential Therapeutic Target in NAFLD

Time-dependent network analysis reveals molecular targets underlying the development of diet-induced obesity and non-alcoholic steatohepatitis

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