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Abstract Cancer cells reprogramme their metabolism to support unrestrained proliferation and survival in nutrient-poor conditions

Preclinical studies in rodent models have evaluated outcomes such as fat oxidation, body-weight change patterns, and metabolic markers tied to fat breakdown and storage

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Oxidative stress may promote myocardial injury either due to direct myocardial damage through lipid peroxidation and protein changes or through the induction of apoptosis in cardiomyocytes that are exposed to ischemiareperfusion [6, 7]

Phospho-protein kinase B (phospho-AKT) (Cat #9271), phospho-ribosomal protein S6 (phopho-RPS6K1) (Cat# #2215), and Glycerinaldehyde-3-phosphate-Dehydrogenase (GAPDH) (Cat #4691) were purchased from Cell Signaling Technologies (Danvers, MA, USA)