The Regulation of Fat Metabolism during Aerobic Exercise

Since the lipid profile is altered by physical activity, the study of lipid metabolism is a remarkable element in understanding if and how physical activity affects the health of both professional athletes and sedentary subjects. Although not fully defined, it has become clear that resistance exercise uses fat as an energy source. The fatty acid oxidation rate is the result of the following processes: (a) triglycerides lipolysis, most abundant in fat adipocytes and intramuscular triacylglycerol (IMTG) stores, (b) fatty acid transport from blood plasma to muscle sarcoplasm, (c) availability and hydrolysis rate of intramuscular triglycerides, and (d) transport of fatty acids through the mitochondrial membrane. In this review, we report some studies concerning the relationship between exercise and the aforementioned processes also in light of hormonal controls and molecular regulations within fat and skeletal muscle cells.

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

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.