A recent paper provides the groundwork to establish a way for exercise to diminish appetite. Or, more likely, for sedentary behavior to increase appetite.
It is well known that exercise burns calories. Personally, I think that’s overrated: Strength building raises your metabolic demand, and THAT burns calories. But that is not the main topic at hand. New research indicates that exercise also increases the sensitivity of neurons that are related to the control of the feeling of satiation. Therefore, you feel full rather than hungry sooner and/or more often.
In rodents. So far.
The research team made obese rodents exercise was found to increase the amount of IL-6 and IL-10 protein levels in the hypothalamus, which in turn changed the threshold for the feedback system that ultimately releases insulin and leptin, which are the magic juices that seem to affect hunger and related system. Indeed, leptin has been seen for some time as a key to understanding weight control, has been implicated in various concepts like the “set point” and is linked to numerous rather complex systems. What may be happening here is that insulin and leptin levels act one way in the sedentary person and a slightly different way in the active person.
I’m going the gym.
Oh, wait, OK, I’ll finish this blog post first.
Here’s what the authors say about the study:
The hypothalamus is a brain region that gathers information on the body’s nutritional status and governs the release of multiple metabolic signaling molecules such as insulin and leptin to maintain homeostasis. Overeating and obesity are associated with insulin and leptin resistance in the hypothalamus, and recent studies provide an intriguing link between inflammation and dysfunction of hypothalamic insulin and leptin signaling through activation of IKKβ, a key player in immune response, and endoplasmic reticulum (ER) stress. This means that strategies to reduce the aberrant activation of inflammatory signaling in the hypothalamus are of great interest to improve the central insulin and leptin action and prevent or treat related metabolic diseases. Using a combination of pharmacological, genetic, and physiological approaches, our study indicates that physical activity reorganizes the set point of nutritional balance through anti-inflammatory signaling mediated by interleukin (IL)-6 and IL-10 in the hypothalamus of rodents. Hence, IL-6 and IL-10 are important physiological contributors to the central insulin and leptin action mediated by exercise, linking it to hypothalamic ER stress and inflammation.
And, if you want to know a LOT more about this process, click here to download a PDF primer on Exercise and Hypothalamic ER Stress.
You can read the paper, published in PLoS Biology, here.
Ropelle, E., Flores, M., Cintra, D., Rocha, G., Pauli, J., Morari, J., de Souza, C., Moraes, J., Prada, P., Guadagnini, D., Marin, R., Oliveira, A., Augusto, T., Carvalho, H., Velloso, L., Saad, M., & Carvalheira, J. (2010). IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition PLoS Biology, 8 (8) DOI: 10.1371/journal.pbio.1000465