RATE-LIMITING STEPS IN FATTY ACID OXIDATION OF BROWN FAT MITOCHONDRIA

1981 ◽  
Vol 9 (2) ◽  
pp. 294P-294P
Author(s):  
D. Ryberg ◽  
K. Berg ◽  
H. J. Grav
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Brown Fat ◽  
Acid Oxidation ◽  
Rate Limiting ◽  
Brown Fat Mitochondria

Effect of adrenodemedullation on decline in muscle malonyl-CoA during exercise

1993 ◽  
Vol 74 (5) ◽  
pp. 2548-2551 ◽  
Author(s):  
W. W. Winder ◽  
R. W. Braiden ◽  
D. C. Cartmill ◽  
C. A. Hutber ◽  
J. P. Jones
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Malonyl Coa ◽  
Exercise Induced ◽  
Rate Limiting

Malonyl-CoA is an inhibitor of carnitine palmitoyltransferase, a rate-limiting enzyme of fatty acid oxidation. Previous studies have indicated that muscle malonyl-CoA declines in rats during treadmill running. This decrease may be important for allowing an increased rate of fatty acid oxidation during prolonged exercise. This study was designed to determine whether epinephrine is essential for inducing the decline in muscle malonyl-CoA during exercise. Male Sprague-Dawley rats underwent adrenodemedullation (ADM) or sham operation. After allowing 3 wk for recovery, rats were killed (pentobarbital anesthesia) at rest or after running at 21 m/min up a 15% grade for 60 min. Red quadriceps malonyl-CoA decreased from 2.6 +/- 0.3 to 0.8 +/- 0.07 nmol/g in sham-operated rats and from 2.2 +/- 0.3 to 0.8 +/- 0.1 nmol/g in ADM rats. White quadriceps malonyl-CoA decreased to similar levels during exercise in both sham-operated and ADM rats. A second experiment on 24-h fasted rats also showed no impairment in the exercise-induced decline in red quadriceps malonyl-CoA as a result of adrenodemedullation. The hormones of the adrenal medulla are therefore unessential for inducing the decline in malonyl-CoA during exercise.

scholarly journals CPT1B, a Metabolic Molecule, Is Also an Independent Risk Factor in CN-AML

2020 ◽  
Author(s):  
Qing Ling ◽  
Shihui Mao ◽  
Jiajia Pan ◽  
Wenwen Wei ◽  
Yu Qian ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Regulatory Network ◽  
Acid Oxidation ◽  
Fatty Acid Oxidation Rate ◽  
Potential Prognostic Factor ◽  
Prognostic Prediction ◽  
Rate Limiting ◽  
Different Levels

Abstract Background: In recent years, fatty acid oxidation has been considered as an important energy source for tumorigenesis and development. There are extensive studies on CPT1A, a kind of fatty acid oxidation rate-limiting enzyme. However, prognostic value and regulatory network of another subtype CPT1B in AML remains elusive. This submission aims to clarify the independent prognostic role of the metabolic molecule CPT1B in CN-AML from cilinical data and molecule levels including mRNA, miRNA and lncRNA. Method: First, we analysed the CPT1B expression in AML conhort via online database “GEPIA”. Following the assessments on differential mRNA, miRNA, lncRNA expression analysis on the paired CPT1B high and low expression groups, there were abnormal changes at different molecular levels. Moreover, we determine the preliminary predictions on the regulatory network of CPT1B in AML by constructing miRNA-mRNA and ceRNA networks. The study had yielded a series of molecules that potentially proved the prognostic prediction and metabolic function of CPT1B from the side. Finally, we analysed the CPT1B expression in our own conhort to make a verification. Result: Notably, there was a significantly high expression of CPT1B in AML patients than normal people and was associated with the poor outcome. Molecules from different levels verified our finding and revealed the possible regulatory mechanism of CPT1B in AML. Conclusion: CPT1B is a potential prognostic factor as well as a therapeutic target of AML.

Glucocorticoids promote mitochondrial fatty acid oxidation in the fetal heart

2019 ◽  
Author(s):  
Helena Urquijo ◽  
Emma N Panting ◽  
Roderick N Carter ◽  
Emma J Agnew ◽  
Caitlin S Wyrwoll ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fetal Heart ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid
Sign in / Sign up

Export Citation Format

Share Document