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  • Limiting access to food in mice increases levels of the hormone, ghrelin, which can also increase motivation to exercise, consistent with a study published within the Journal of Endocrinology. The study suggests that a surge in levels of appetite-promoting hormone, ghrelin, after a period of fasting prompted mice to initiate voluntary exercise. These novel findings indicate that better diet control, for instance limiting food intake to mealtimes or fasting intermittently, could help overweight people maintain a simpler exercise routine, reduce and avoid debilitating complications like diabetes and heart condition .

    Obesity may be a costly and growing, global health epidemic that needs simpler intervention strategies to avoid serious complications including heart condition and diabetes. Food restriction and regular exercise are the 2 main cost-effective strategies to stop and treat obesity; however the condition is usually related to a sedentary lifestyle and bad eating habits, like snacking and binge eating. Consequently, adhering to a daily exercise regime are often difficult thanks to an inability to exercise for a protracted period or a scarcity of motivation. Ghrelin, often mentioned because the ‘hunger hormone’, stimulates appetite through actions on the brain reward circuitry that increase motivation to eat. it’s also been reported to be essential for endurance exercise by increasing metabolism to satisfy the energy demands of prolonged exercise. Although previous studies have suggested a relationship between ghrelin and exercise, it’s not known whether ghrelin levels have an immediate effect on motivation to exercise.

    In this study, Dr Yuji Tajiri and colleagues from Kurume University School of drugs in Japan, investigated the connection between exercise and ghrelin levels in mice. Food intake and wheel-running activity were compared in mice given free access to food and people fed only twice each day for a limited time. Although both groups ate an identical amount of food, the restricted mice ran significantly more. Mice genetically altered to possess no ghrelin and on the restricted feeding diet ran but the mice given free access, however, this might be reversed by administering ghrelin. Furthermore, mice given free access to food and given ghrelin also ran significantly more. These findings suggest that ghrelin may play a crucial role within the motivation for both feeding and exercise, in response to restricted eating plans.

    Dr Tajiri comments, “Our findings suggest that hunger, which promotes ghrelin production, can also be involved in increasing motivation for voluntary exercise, when feeding is restricted . Therefore, maintaining a healthy eating routine, with regular mealtimes or fasting, could also encourage motivation for exercise in overweight people.”

    However, Dr Tajiri cautions. “These findings and former reports are supported animal studies; such a lot more work is required to verify that this ghrelin response is additionally present in people. If it are often established in clinical practice, it not only exposes new cost-effective diet and exercise strategies but can also indicate a replacement therapeutic application for ghrelin-mimicking drugs.”

    Dr Tajiri and his team now decide to perform more experiments to verify these findings in humans, to further characterise how ghrelin acts within the brain to supply motivation to eat or exercise and to explore any potential real-world, clinical benefits for the treatment and prevention of obesity.

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