You may have heard of the bacteria called Helicobacter pylori. They are responsible for many of our gastric woes, such as ulcers and some types of cancers. That being the case, you may think it’s a good thing that the microbes are being eradicated in developed nations. Not so fast. H. pylori actually has a mixed record where human health is concerned. Yes, it does cause ulcers, but on the other hand, there is some evidence that H. pylori colonization protects against asthma and allergies. Even more intriguingly, the bacteria may also protect against obesity.
Electron micrograph of H. pylori possessing multiple flagella
H. pylori secrete chemicals that in turn affect the production of a variety of hormones manufactured by the gut epithelial cells. For example, when the bacteria are present, ghrelin plasma levels go way down. Once H. pylori are eradicated, ghrelin levels rise. And what does ghrelin do? Stimulate the appetite. H. pylori are also associated with higher concentrations of the hormone leptin, which is responsible for the feelings of satiety. So, is it a coincidence that developed nations have both a low incidence of H. pylori infection and a high incidence of obesity? Josep Bassaganya-Riera of Virginia Tech and his colleagues don’t think so.
The researchers used a couple of mouse models for their studies. One strain of mouse was deficient in leptin receptors and the other were normal mice that were fed a high-fat diet. Either way, the mice were expected to quickly become obese during the course of the experiments. However, H. pylori infection had a number of effects on them.
Mice that were fed the high fat diet had four times more leptin after being infected with H. pylori. Remember, this is a hormone that tells us it’s time to stop eating. Fasting blood glucose levels were significantly lower in infected mice of both types and returned to normal more quickly following a glucose challenge. In addition, infected mice had less white adipose tissue, a.k.a. fat. Finally, H. pylori carriers has less insulin resistance than their uninfected cohorts. This suggests that H. pylori may play a role in helping its hosts maintain a healthy weight.
Bassaganya-Riera, J., Dominguez-Bello, M., Kronsteiner, B., Carbo, A., Lu, P., Viladomiu, M., Pedragosa, M., Zhang, X., Sobral, B., Mane, S., Mohapatra, S., Horne, W., Guri, A., Groeschl, M., Lopez-Velasco, G., & Hontecillas, R. (2012). Helicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanism PLoS ONE, 7 (11) DOI: 10.1371/journal.pone.0050069.