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In this issue, we deal with three compounds. One is a hormone involved in fat metabolism, while another is a mineral whose status may be altered by exercise. The final is a fat that might be digested and metabolised more efficiently than our common dietary fat sources.
Leptin is a hormone secreted primarily by adipocytes from the white adipose tissue in direct proportion to the amount of body fat present. Leptin plays a crucial role in the regulation of appetite, body fat mass, basal metabolic rate and gonadal function.1 Congenital deficiency of leptin is rare, but causes morbid obesity which is normalised following leptin treatment. Circulating leptin levels change acutely in accordance with energy balance; leptin levels increase with food ingestion and reduce with prolonged exercise and fasting. When there is a severe acute negative energy balance, serum leptin levels dramatically reduce by 60–80%, despite small changes in total fat mass. Preventing this reduction in leptin levels could attenuate hunger in dieting athletes, facilitating the adjustment of body mass to specific targets. Nevertheless, there is no account of leptin misuse by athletes for this purpose.
Leptin receptors are densely expressed in the cerebellum, even more so than in the hypothalamus where leptin is supposed to exert its main action. Leptin-related changes owing to physical activity levels may promote structural changes in the cerebellum, which is strongly implicated in motor control and learning. Leptin receptors are also expressed in human skeletal muscle,2 3 and more abundantly in women than men.3 Here, the main action of leptin is believed to be the stimulation of fatty acid oxidation via several pathways.4 Interestingly, these pathways are also activated 30 min after sprint exercise5 and, like sprint exercise, leptin induces PGC1α expression and mitochondrial biogenesis. It is known that exercise …
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