scholarly journals Aurintricarboxylic acid is a potent inhibitor of phosphofructokinase

1989 ◽  
Vol 259 (3) ◽  
pp. 925-927 ◽  
Author(s):  
S A McCune ◽  
L G Foe ◽  
R G Kemp ◽  
R R Jurin
Keyword(s):  
Protein Synthesis ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Potent Inhibitor ◽  
Rat Hepatocytes ◽  
Acid Synthesis ◽  
Rabbit Liver ◽  
Irreversible Binding ◽  
Aurintricarboxylic Acid ◽  
Inhibitory Site

Aurintricarboxylic acid (ATA) was found to be a very potent inhibitor of purified rabbit liver phosphofructokinase (PFK), giving 50% inhibition at 0.2 microM. The inhibition was in a manner consistent with interaction at the citrate-inhibitory site of the enzyme. The data suggest that inhibition of PFK by ATA was not due to denaturation of the enzyme or the irreversible binding of inhibitor, since the inhibition could be reversed by addition of allosteric activators of PFK, i.e. fructose 2,6-bisphosphate or AMP. Two other tricarboxylic acids, agaric acid and (-)-hydroxycitrate, were found to inhibit PFK. ATA at much higher concentrations (500 microM) was shown to inhibit fatty acid synthesis from endogenous glycogen in rat hepatocytes; however, protein synthesis was not altered.

scholarly journals The effects of orthovanadate on fatty acid synthesis in isolated rat hepatocytes

1982 ◽  
Vol 202 (3) ◽  
pp. 791-794 ◽  
Author(s):  
L Agius ◽  
W J Vaartjes
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Rat Hepatocytes ◽  
Acid Synthesis ◽  
Insulin Stimulation ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat ◽  
Stimulation Of

Extracellular Ca2+ stimulated fatty acid synthesis in isolated rat hepatocytes. Orthovanadate (0.2-2.0 mM), an inhibitor of Ca2+-dependent ATPases, stimulated fatty acid synthesis in both the presence and the absence of extracellular Ca2+. Insulin stimulated fatty acid synthesis only in the presence of extracellular Ca2+. The contribution of extracellular Ca2+ to insulin stimulation of fatty acid synthesis is discussed.

scholarly journals BHLHE40, a third transcription factor required for insulin induction of SREBP-1c mRNA in rodent liver

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jing Tian ◽  
Jiaxi Wu ◽  
Xiang Chen ◽  
Tong Guo ◽  
Zhijian J Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Gene Knockout ◽  
Rat Hepatocytes ◽  
Acid Synthesis ◽  
Gene Encoding ◽  
Fasted Rats

In obesity, elevated insulin causes fatty liver by activating the gene encoding SREBP-1c, a transcription factor that enhances fatty acid synthesis. Two transcription factors, LXRα and C/EBPβ, are necessary but not sufficient for insulin induction of hepatic SREBP-1c mRNA. Here, we show that a third transcription factor, BHLHE40, is required. Immunoprecipitation revealed that BHLHE40 binds to C/EBPβ and LXRα in livers of rats that had fasted and then refed. Hepatic BHLHE40 mRNA rises rapidly when fasted rats are refed and when rat hepatocytes are incubated with insulin. Preventing this rise by gene knockout in mice or siRNAs in hepatocytes reduces the insulin-induced rise in SREBP-1c mRNA. Although BHLHE40 is necessary for insulin induction of SREBP-1c, it is not sufficient as demonstrated by failure of lentiviral BHLHE40 overexpression to increase hepatocyte SREBP-1c mRNA in the absence of insulin. Thus, an additional event is required for insulin to increase SREBP-1c mRNA.

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