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

Probably the latter, but health officials seem interested in the developing data.

From CTV:

… in a report released Friday, health officials detailed the cases of 10 Michigan patients who were very sick from swine flu in late May and early June and ended up at a specialized hospital in Ann Arbor. Three of them died.

Nine of the 10 were either obese or extremely obese. Only three of the 10 had other health problems. Two of the three that died had no other health conditions.

This hardly settles the question of whether obesity is its own risk factor for swine flu. It’s possible the patients had undiagnosed heart problems or other unidentified conditions.

The report is called Intensive-Care Patients With Severe Novel Influenza A (H1N1) Virus Infection — Michigan, June 2009 and is published in MMWR, the CDC’s rapid turnaround publication for disease. The report warns:

This report describes the clinical findings of a limited series of patients with novel influenza A (H1N1) virus infection and refractory ARDS …. This patient group represents the most severely ill subset of persons with novel influenza A (H1N1) virus infection and is notable for the predominance of males, the high prevalence of obesity (especially extreme obesity), and the frequency of clinically significant pulmonary emboli and MODS. All required advanced mechanical ventilator support, reflecting severe pulmonary damage. The pulmonary compromise described in this report suggests that severe pulmonary damage occurred as a result of primary viral pneumonia. Although data are not available, this damage also might be attributable to secondary host immune responses (e.g., through cytokine dysregulation triggered by high viral replication). However, bacterial coinfection in the lung not identified by blood culture or bronchoalveolar lavage cannot be excluded.

…

The high prevalence of obesity in this case series is striking. Whether obesity is an independent risk factor for severe complications of novel influenza A (H1N1) virus infection is unknown. Obesity has not been identified previously as a risk factor for severe complications of seasonal influenza. ….

Further characterization of severe cases of novel influenza A (H1N1) virus infection in the United States and worldwide is needed to determine the frequency of the findings from this limited case-series.

You can read the report here.

Clearly this is very preliminary and I suspect that this will not develop. In other words, I suspect that existing poor health related to the cardiopulmonary system is a serious risk factor with any flu. But we shall see.