The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulation in nonalcoholic fatty liver disease

Guzmán, Carla; Benet, Marta; Pisonero-Vaquero, Sandra; Moya, Marta; García‐Mediavilla, María Victoria; Martínez‐Chantar, María Luz; González‐Gallego, Javier; Castell, José V.; Sánchez-Campos, Sonia; Jover, Ramiro

doi:10.1016/j.bbalip.2012.12.014

Cited by 82 publications

(63 citation statements)

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“…Various FABPs have been investigated for clinical use in detecting early tissue damage. When there is ongoing damage, FABP is measurable in serum [7][8][9][10][11][12][13][14][15][16]. The designation of each of the proteins in this family has been taken from the tissue where it was originally isolated, and key members of this group of proteins include liver fatty acid-binding protein (L-FABP), intestinal FABP, heart FABP and epidermal FABP [17].…”

Section: Introductionmentioning

confidence: 99%

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Akbal

Koçak

Akyürek

et al. 2014

Wien Klin Wochenschr

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Section: Introductionmentioning

confidence: 99%

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Akbal

Koçak

Akyürek

et al. 2014

Wien Klin Wochenschr

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“…4A). Previous studies from our laboratory have demonstrated that FABP1 gene was regulated predominantly by liver-enriched transcription factors HNF3␤ and C/EBP␣ (21), and a functional PPAR␣-responsive element was recently reported to play an important role in FABP1 gene regulation (30). The putative binding sites of HNF3␤, C/EBP␣, and PPAR␣ on the FABP1 promoter were shown in Fig.…”

Section: Hbv Infection Upregulates Fabp1 Expressionmentioning

confidence: 99%

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

Peng

Zhu

et al. 2016

J Virol

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Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined. mRNA and protein levels of FABP1 were measured by quantitative RT-PCR (qPCR) and Western blotting. HBx-mediated FABP1 regulation was evaluated by luciferase assay, coimmunoprecipitation, and chromatin immunoprecipitation. Hepatic lipid accumulation was measured by using Oil-Red-O staining and the triglyceride level. It was found that expression of FABP1 was increased in HBV-producing hepatoma cells, the sera of HBV-infected patients, and the sera and liver tissues of HBV-transgenic mice. IMPORTANCEAccumulating evidence from epidemiological and experimental studies has indicated that chronic HBV infection is associated with hepatic steatosis. However, the molecular mechanism underlying HBV-induced pathogenesis of hepatic steatosis still remains to be elucidated. In this study, we found that expression of liver fatty acid binding protein (FABP1) was dramatically increased in the sera of HBV-infected patients and in both sera and liver tissues of HBV-transgenic mice. Forced expression of HBx led to FABP1 upregulation, whereas knockdown of FABP1 remarkably diminished lipid accumulation in both in vitro and in vivo models. It is possible that HBx promotes hepatic lipid accumulation through upregulating FABP1 in the development of HBV-induced nonalcoholic fatty liver disease. Therefore, inhibition of FABP1 might have therapeutic value in steatosis-associated chronic HBV infection. H epatitis B virus (HBV) infection is a serious health problemworldwide, causing acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (1). Emerging evidence from epidemiological and experimental studies suggests that chronic HBV infection, as well as HCV infection, is associated with hepatic steatosis (2, 3). The frequency of hepatic steatosis in subjects with a chronic HBV infection ranges from 27 to 51% (4). Furthermore, HBV X protein (HBx) is known to cause hepatic lipid deposition by inhibiting the secretion of apolipoprotein B (5). A previous report showed that the increased HBx expression can cause lipid accumulation in hepatocytes, likely mediated by sterol regulatory element binding protein 1 and peroxisome proliferator-activated receptor ␥ (PPAR␥) (4). The molecular mechanism by which HBV induces the pathogenesis of hepatic steatosis remains elusive. Using fluorescent two-dimensional difference gel electrophoresis and matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis, we found that the protein level of liver fatty acid binding protein (L-FABP ...

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“…Up-regulation of LXR activated SREBP1c, and FAS is involved in fat synthesis (Enjoji et al 2012). Furthermore, NAFLD is related to over-expression of C/EBPa and aP2, which stimulate adipocyte differentiation (Guzman et al 2013;Pan et al 2015). In addition, hepatic lipolysis is controlled by several genes, including peroxisome proliferator-activated receptor a (PPARa) and mitochondrial uncoupling protein 2 (UCP2), in response to lipid metabolic process and NAFLD progression (Peng et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

2015

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Obesity is associated with chronic diseases such as fatty liver, type 2 diabetes, cardiovascular disease, and severe metabolic syndrome. Obesity causes metabolic impairment including excessive lipid accumulation and fibrosis in the hepatic tissue as well as the increase in oxidative stress. In order to investigate the effect of mulberry leaf (Morus alba L.) extract (MLE) on obesity-induced oxidative stress, lipogenesis, and fibrosis in liver, MLE has been gavaged for 12 weeks in high-fat diet (HFD)-induced obese mice. MLE treatment significantly ameliorated LXRa-mediated lipogenesis and hepatic fibrosis markers such as a-smooth muscle actin, while MLE up-regulated lipolysis-associated markers such as lipoprotein lipase in the HFD-fed mice. Moreover, MLE normalized the activities of antioxidant enzymes including heme oxygenase-1 and glutathione peroxidase in accordance with protein levels of 4-hydroxynonenal in the HFDfed mice. MLE has beneficial effects on obesity-related fatty liver disease by regulation of hepatic lipid metabolism, fibrosis, and antioxidant defense system. MLE supplementation might be a potential therapeutic approach for obesity-related disease including non-alcoholic fatty liver disease.

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The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulation in nonalcoholic fatty liver disease

Cited by 82 publications

References 65 publications

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

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