scholarly journals Role of Malic Enzyme during Fatty Acid Synthesis in the Oleaginous Fungus Mortierella alpina

2014 ◽  
Vol 80 (9) ◽  
pp. 2672-2678 ◽  
Author(s):  
G. Hao ◽  
H. Chen ◽  
L. Wang ◽  
Z. Gu ◽  
Y. Song ◽  
...  
1967 ◽  
Vol 242 (18) ◽  
pp. 4013-4022 ◽  
Author(s):  
Arthur F. Whereat ◽  
Franklin E. Hull ◽  
Margaret W. Orishimo ◽  
Joseph L. Rabinowitz

2015 ◽  
Vol 125 (3) ◽  
pp. 407-422 ◽  
Author(s):  
Nastassia Shtaida ◽  
Inna Khozin-Goldberg ◽  
Sammy Boussiba

2017 ◽  
Vol 150 ◽  
pp. 310-322 ◽  
Author(s):  
Jessica Brandi ◽  
Ilaria Dando ◽  
Elisa Dalla Pozza ◽  
Giulia Biondani ◽  
Rosalind Jenkins ◽  
...  

1980 ◽  
Vol 43 (3) ◽  
pp. 571-579 ◽  
Author(s):  
G. R. Herzberg ◽  
N. Janmohamed

The effect of varying dietary levels of maize oil and tripalmitin (0–250 g fat/kg) on hepatic lipogenesis and the levels of hepatic fatty acid synthetase (FAS), glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G6PD), malic enzyme (EC 1.1.1.38, 1.1.1.39, 1.1.1.40; ME) and glucokinase (EC 2.7.1.2; GK) was examined in meal-fed mice.2. Meal-fed mice compared to mice fed ad lib. show enhanced hepatic lipogenesis as demonstrated by an increased rate of in vivo fatty acid synthesis and increased levels of FAS, ME and G6PD. The level of GK in meal-fed mice was unchanged by meal feeding.3. Maize oil more effectively reduced in vivo hepatic lipogenesis than tripalmitin in meal-fed mice.4. Maize oil more effectively reduced the hepatic levels of FAS, G6PD, ME and GK than tripalmitin in meal-fed mice.5. The increased inhibition by maize oil is observed at all levels of fat in the diet investigated and has been shown not to be due to decreased carbohydrate intake nor to differences between the absorption of maize oil and tripalmitin.


1965 ◽  
Vol 44 (5) ◽  
pp. 840-848 ◽  
Author(s):  
Rubin Bressler ◽  
Richard I. Katz

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1419 ◽  
Author(s):  
Moris Sangineto ◽  
Rosanna Villani ◽  
Francesco Cavallone ◽  
Antonino Romano ◽  
Domenico Loizzi ◽  
...  

Metabolic reprogramming is critically involved in the development and progression of cancer. In particular, lipid metabolism has been investigated as a source of energy, micro-environmental adaptation, and cell signalling in neoplastic cells. However, the specific role of lipid metabolism dysregulation in hepatocellular carcinoma (HCC) has not been widely described yet. Alterations in fatty acid synthesis, β-oxidation, and cellular lipidic composition contribute to initiation and progression of HCC. The aim of this review is to elucidate the mechanisms by which lipid metabolism is involved in hepatocarcinogenesis and tumour adaptation to different conditions, focusing on the transcriptional aberrations with new insights in lipidomics and lipid zonation. This will help detect new putative therapeutic approaches in the second most frequent cause of cancer-related death.


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