scholarly journals Abrogation of hepatic ATP-citrate lyase protects against fatty liver and ameliorates hyperglycemia in leptin receptor-deficient mice

Hepatology ◽  
2008 ◽  
Vol 49 (4) ◽  
pp. 1166-1175 ◽  
Author(s):  
Qiong Wang ◽  
Lei Jiang ◽  
Jue Wang ◽  
Shoufeng Li ◽  
Yue Yu ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Leptin Receptor ◽  
Atp Citrate Lyase ◽  
Citrate Lyase ◽  
Deficient Mice

scholarly journals A biochemical explanation for the fatty liver and kidney syndrome of broilers: its alleviation by the short-term use of dietary fat

1977 ◽  
Vol 38 (3) ◽  
pp. 319-328 ◽  
Author(s):  
D. Balnave ◽  
R. B. Cumming ◽  
T. M. Sutherland
Keyword(s):  
Fatty Liver ◽  
Broiler Chickens ◽  
Specific Activity ◽  
Liver Lipid ◽  
Liver Weight ◽  
Atp Citrate Lyase ◽  
Commercial Diet ◽  
Meat Meal ◽  
Citrate Lyase ◽  
Liver And Kidney

1. Fatty liver and kidney syndrome (FLKS) was induced in young broiler chickens by giving them a diet composed principally of wheat and meat meal.2. FLKS resulted in reduced growth and increased liver weight; fasting for 18 h increased mortality, liver lipid and the specific activity of hepatic ATP-citrate lyase compared with birds fed on a commercial diet. The specific activities of hepatic fructose-l,6-diphosphate-l-phosphohydrolase and pyruvate carboxylase were reduced in birds suffering from FLKS and fasted for 18 h.3. Feeding of the FLKS-inducing diet supplemented with 150 g animal tallow/kg for 54 h considerably reduced mortality while restoring liver composition and enzyme activities towards those observed in birds fed a commercial diet. Investigations indicated that the glycerol component of the fat was not responsible for the observed responses.4. The present results suggest that in FLKS insufficiencies of biotin are induced in specific enzyme systems, but the syndrome may be alleviated without the use of supplementary biotin.5. The evidence indicates that, when stressed, birds affected by FLKS die from the hypoglycaemia occurring as a result of a reduced capacity for gluconeogenesis.

scholarly journals Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Yunchen Luo ◽  
Zhijian Zhang ◽  
Liping Xiang ◽  
Bing Zhou ◽  
Xuejiao Wang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Leptin Receptor ◽  
Alcoholic Fatty Liver ◽  
High Fructose Diet ◽  
High Fructose ◽  
Deficient Mice ◽  
Alcoholic Fatty Liver Disease

Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. However, the relationship between m6A methylation modifications and NAFLD remains poorly understood. In the present study, through methylated RNA immunoprecipitation sequencing and RNA transcriptome sequencing in high fructose diet-induced NAFLD mice, we found that hypermethylation-encoding genes were mainly enriched in lipid metabolism processes. We identified 266 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and m6A modification level. Among them, 193 genes displayed increased expression and m6A modification, indicating that m6A RNA modifications tend to be positively correlated with NAFLD. We further compared the high fructose diet-induced NAFLD mouse model with leptin receptor-deficient mice and found that DEGs enriched in the lipid metabolism pathway were up-regulated in both groups. In contrast, DEGs associated with the immune inflammatory response were up-regulated in the high fructose diet group, but down-regulated in leptin receptor-deficient mice. Taken together, our results demonstrate that m6A methylation modifications may play an important role in the development of NAFLD.

scholarly journals Enhanced acetylation of ATP-citrate lyase promotes the progression of nonalcoholic fatty liver disease

2019 ◽  
Vol 294 (31) ◽  
pp. 11805-11816 ◽  
Author(s):  
Liang Guo ◽  
Ying-Ying Guo ◽  
Bai-Yu Li ◽  
Wan-Qiu Peng ◽  
Xin-Xia Chang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Atp Citrate Lyase ◽  
Nonalcoholic Fatty Liver ◽  
Citrate Lyase

Cloning and Expression Analysis of ATP-Citrate Lyase Genes from Sugarcane

2013 ◽  
Vol 38 (11) ◽  
pp. 2024-2033 ◽  
Author(s):  
Chang-Ning LI ◽  
Qian NONG ◽  
Qin-Liang TAN ◽  
SRIVASTAVA Manoj Kumar ◽  
Li-Tao YANG ◽  
...  
Keyword(s):  
Expression Analysis ◽  
Cloning And Expression ◽  
Atp Citrate Lyase ◽  
Citrate Lyase

Acetyl-CoA is produced by the citrate synthase homology module of ATP-citrate lyase

2021 ◽  
Author(s):  
Kenneth Verstraete ◽  
Koen H. G. Verschueren ◽  
Ann Dansercoer ◽  
Savvas N. Savvides
Keyword(s):  
Citrate Synthase ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Citrate Lyase ◽  
Homology Module

scholarly journals IGF1-mediated HOXA13 overexpression promotes colorectal cancer metastasis through upregulating ACLY and IGF1R

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Chenyang Qiao ◽  
Wenjie Huang ◽  
Jie Chen ◽  
Weibo Feng ◽  
Tongyue Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Growth Factor ◽  
Cancer Metastasis ◽  
Combined Treatment ◽  
Insulin Like Growth Factor ◽  
Atp Citrate Lyase ◽  
Citrate Lyase ◽  
Elevated Expression ◽  
Igf1r Inhibitor ◽  
Colorectal Cancer Metastasis

AbstractMetastasis is the major reason for the high mortality of colorectal cancer (CRC) patients and its molecular mechanism remains unclear. Here, we report a novel role of Homeobox A13 (HOXA13), a member of the Homeobox (HOX) family, in promoting CRC metastasis. The elevated expression of HOXA13 was positively correlated with distant metastasis, higher AJCC stage, and poor prognosis in two independent CRC cohorts. Overexpression of HOXA13 promoted CRC metastasis whereas downregulation of HOXA13 suppressed CRC metastasis. Mechanistically, HOXA13 facilitated CRC metastasis by transactivating ATP-citrate lyase (ACLY) and insulin-like growth factor 1 receptor (IGF1R). Knockdown of ACLY and IGFIR inhibited HOXA13-medicated CRC metastasis, whereas ectopic overexpression of ACLY and IGFIR rescued the decreased CRC metastasis induced by HOXA13 knockdown. Furthermore, Insulin-like growth factor 1 (IGF1), the ligand of IGF1R, upregulated HOXA13 expression through the PI3K/AKT/HIF1α pathway. Knockdown of HOXA13 decreased IGF1-mediated CRC metastasis. In addition, the combined treatment of ACLY inhibitor ETC-1002 and IGF1R inhibitor Linsitinib dramatically suppressed HOXA13-mediated CRC metastasis. In conclusion, HOXA13 is a prognostic biomarker in CRC patients. Targeting the IGF1-HOXA13-IGF1R positive feedback loop may provide a potential therapeutic strategy for the treatment of HOXA13-driven CRC metastasis.

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