Tremendous progress has been made in the field of ferroptosis since this regulated cell death process was first named in 2012. Ferroptosis is initiated upon redox imbalance and driven by excessive phospholipid peroxidation. Levels of multiple intracellular nutrients (iron, selenium, vitamin E and coenzyme Q10) are intimately related to the cellular antioxidant system and participate in the regulation of ferroptosis. Dietary intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) regulates ferroptosis by directly modifying the fatty acid composition in cell membranes. In addition, amino acids and glucose (energy stress) manipulate the ferroptosis pathway through the nutrient-sensitive kinases mechanistic target of rapamycin complex 1 (mTORC1) and AMP-activated protein kinase (AMPK). Understanding the molecular interaction between nutrient signals and ferroptosis sensors might help in the identification of the roles of ferroptosis in normal physiology and in the development of novel pharmacological targets for the treatment of ferroptosis-related diseases.

The influence of the source of dietary fat on postprandial thermogenesis and substrate oxidation rates, was examined in twelve postmenopausal women aged 57–73 years, with BMI 21·9–38·3 kg/m2. A single blind, randomised, paired comparison of two high-fat, isoenergetic, mixed test meals was conducted. The major source of fat was either cream (CREAM) or extra virgin olive oil (EVOO). RMR, diet-induced thermogenesis (DIT) and substrate oxidation rates over 5 h were measured by indirect calorimetry. There were no differences in body weight, RMR, fasting carbohydrate or fat oxidation rates between the two occasions. DIT (EVOO 97 (sd 46) v. CREAM 76 (sd 69) kJ/5 h and EVOO 5·2 (sd 2·5) v. CREAM 4·1 (sd 3·7)% energy) did not differ between the two test meals. The postprandial increase in carbohydrate oxidation rates, relative to their respective fasting values (ΔCOX), was significantly lower following the EVOO meal (EVOO 10·6 (sd 8·3) v. CREAM 17·5 (sd 10) g/5 h; paired t test, P=0·023), while postprandial fat oxidation rates (ΔFOX) were significantly higher (EVOO 0·0 (sd 4·4) v. CREAM -3·6 (sd 4·0) g/5 h; P=0·028). In the eight obese subjects, however, DIT was significantly higher following the EVOO meal (EVOO 5·1 (sd 2·0) v. CREAM 2·5 (sd 2·9) %; P=0·01). This was accompanied by a significantly lower ΔCOX (EVOO 10·9 (sd 9·9) v. CREAM 17·3 (sd 10·5) g/5 h; P=0·03) and significantly higher ΔFOX (EVOO 0·11 (sd 4·4) v. CREAM −4·1 (sd 4·5) g/5 h, P=0·034). The present study showed that olive oil significantly promoted postprandial fat oxidation and stimulated DIT in abdominally obese postmenopausal women.