scholarly journals Abnormal histopathology, fat percent and hepatic apolipoprotein A I and apolipoprotein B100 mRNA expression in fatty liver hemorrhagic syndrome and their improvement by soybean lecithin

2017 ◽  
Vol 96 (10) ◽  
pp. 3559-3563 ◽  
Author(s):  
Yalu Song ◽  
Jiming Ruan ◽  
Junrong Luo ◽  
Tiancheng Wang ◽  
Fei Yang ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Mrna Expression ◽  
Soybean Lecithin ◽  
Apolipoprotein A ◽  
Apolipoprotein B100 ◽  
Hepatic Apolipoprotein

Su1036 Hepatic Apolipoprotein A-IV Gene Expression Is Increased in Non-Alcoholic Fatty Liver Disease and Is Modulated by Gender and Inflammation

2015 ◽  
Vol 148 (4) ◽  
pp. S-1045
Author(s):  
Nathan J. Shores ◽  
Melissa A. Verhague ◽  
Janet K. Sawyer ◽  
Adolfo Z. Fernandez ◽  
Lawrence L. Rudel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Apolipoprotein A ◽  
Hepatic Apolipoprotein ◽  
Alcoholic Fatty Liver Disease

Lp(a): der akzeptierte unabhängige Risikofaktor

2019 ◽  
Vol 23 (09) ◽  
pp. 388-391
Author(s):  
Volker Schettler
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Apolipoprotein B100

Lipoprotein(a) (Lp(a)) besteht aus einem LDL-Partikel, an dem über das Apolipoprotein B100 des Partikels eine Disulfidbrücke zu einem Apolipoprotein(a) besteht ( Abb. 1 ). Obwohl Lp(a) bereits 1963 von Berg et al. erstmals als „lipoprotein associated antigen“ entdeckt 1 und schon früh ein Zusammenhang mit kardiovaskulären Ereignissen diskutiert wurde 2, konnten diese Annahmen der klinischen Eigenschaften erst deutlich später im Rahmen von epidemiologischen Evaluationen bestätigt werden 3, 4. Ab einer Lp(a)-Konzentration von über 30 mg/dl (> 75 nmol/l) besteht ein nahezu linearer Zusammenhang zwischen dem Anstieg der Lp(a)-Konzentration und kardiovaskulären Ereignissen wie Myokardinfarkt und das Risiko für eine Aortenklappenstenose 3, 4.

Effects of dietary fat saturation on plasma lipoprotein(a) and hepatic apolipoprotein(a) mRNA concentrations in cynomolgus monkeys

1994 ◽  
Vol 106 (1) ◽  
pp. 109-118 ◽  
Author(s):  
Margaret E. Brousseau ◽  
Jose M. Ordovas ◽  
Robert J. Nicolosi ◽  
Ernst J. Schaefer
Keyword(s):  
Dietary Fat ◽  
Plasma Lipoprotein ◽  
Fat Saturation ◽  
Cynomolgus Monkeys ◽  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Hepatic Apolipoprotein

scholarly journals Increase of E3 ubiquitin ligase NEDD4 expression leads to degradation of its target proteins PTEN/IGF1R during the formation of goose fatty liver

2020 ◽  
Vol 98 (9) ◽  
Author(s):  
Chunchi Yan ◽  
Minmeng Zhao ◽  
Shuo Li ◽  
Tongjun Liu ◽  
Cheng Xu ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Mrna Expression ◽  
Messenger Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Normal Liver ◽  
Protective Mechanism ◽  
Nonalcoholic Fatty Liver ◽  
Target Proteins ◽  
Protein Levels ◽  
Gene 4

Abstract Goose fatty liver may have a unique protective mechanism as it does not show a pathological injury even in the case of severe steatosis. Although neural precursor cell-expressed developmentally downregulated gene 4 (NEDD4) participates in repair and regeneration of injured liver through its target proteins, its role in nonalcoholic fatty liver disease remains unknown. Using quantitative polymerase chain reaction (PCR) and immunoblot analyses, here, we found that the messenger RNA (mRNA) and protein expressions of NEDD4 were induced in goose fatty liver compared with normal liver. The mRNA expression of the gene of phosphate and tension homology deleted on chromosome ten (PTEN) and insulin-like growth factor 1 receptor (IGF1R) was also induced in goose fatty liver; however, their protein expression was or tended to be suppressed. Moreover, the co-immunoprecipitation analysis indicated that there was a physical association between NEDD4 and PTEN in goose liver, which was consistent with the ubiquitination of PTEN in goose fatty liver. Furthermore, NEDD4 overexpression in goose primary hepatocytes suppressed the PTEN and IGF1R protein levels without a significant effect on their mRNA expression. In conclusion, the increased expression of NEDD4 leads to the degradation of PTEN and IGF1R proteins through ubiquitination in goose fatty liver, suggesting that NEDD4 may protect goose fatty liver from severe steatosis-associated injury via its target proteins during the development of goose fatty liver.

scholarly journals Endocannabinoid Receptors Gene Expression in Morbidly Obese Women with Nonalcoholic Fatty Liver Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Teresa Auguet ◽  
Alba Berlanga ◽  
Esther Guiu-Jurado ◽  
Ximena Terra ◽  
Salomé Martinez ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Mrna Expression ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Morbidly Obese ◽  
Receptor Subtypes ◽  
Obese Women ◽  
Nonalcoholic Fatty Liver

Background. Recent reports suggest a role for the endocannabinoid system in the pathology of nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the relationship between liver expression of cannabinoid (CB) receptor subtypes, CB1 and CB2, in morbidly obese (MO) women with different histological stages of NAFLD.Methods. We analysed hepatic CB1 and CB2 mRNA expression, and the expression of genes involved in lipid metabolism in 72 MO women, subclassified by liver histology into MO with normal liver (NL,n=16), simple steatosis (SS,n=28), and nonalcoholic steatohepatitis (NASH,n=28) by enzyme-linked immunosorbent assay and RT-PCR.Results. We found that CB1 mRNA expression was significantly higher in NASH compared with SS and correlated negatively with PPARα. Regarding CB2, CB2 mRNA expression correlated positively with ACC1, PPARγ, IL6, TNFα, resistin, and adiponectin.Conclusions. The increased expression of CB1 in NASH and the negative correlation with PPARαsuggest a deleterious role of CB1 in NAFLD. Regarding CB2, its positive correlation with the anti-inflammatory molecule adiponectin and, paradoxically, with inflammatory genes suggests that this receptor has a dual role. Taken together, our results suggest that endocannabinoid receptors might be involved in the pathogenesis of NAFLD, a finding which justifies further study.

scholarly journals Complex effects of inhibiting hepatic apolipoprotein B100 synthesis in humans

2016 ◽  
Vol 8 (323) ◽  
pp. 323ra12-323ra12 ◽  
Author(s):  
Gissette Reyes-Soffer ◽  
Byoung Moon ◽  
Antonio Hernandez-Ono ◽  
Marija Dionizovik-Dimanovski ◽  
Jhonsua Jimenez ◽  
...  
Keyword(s):  
Apolipoprotein B100 ◽  
Hepatic Apolipoprotein
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