<div class="FTQUOTE"><begin quote><em>Originally posted by: <strong>saveferris2009</strong></em> Are these the types of articles you were looking for, Havoc? I always enjoy your POV so let me know your thoughts <img alt="" /></end quote>
Yes. With the exception of the last study you cited, it seems that increased PFt's had to do more with increase in BMI, which we know has a linear correlation with lung function, and not necessarily bacterial conlonization. These articles are also older and I was unable to search for any refutations (I'm still out of town on business). The research I have found is recent and suggests that BSG does not have any impact on the amout of glucose in airway surface liquid, which is what you would need to support a hypothesis that increased BSG feeds colonies of bacteria in the lungs. Here is the link the the study (it's long)
<a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016166">http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016166</a>
For those that may not want tpo read the whole thing, here is an excerpt:
<span>In this study, we describe a novel mechanism that allows human airway epithelia to generate a transepithelial glucose concentration gradient. Moreover, this gradient results in an ASL that contains a low glucose concentration. Our studies suggest that this low concentration of glucose plays an important role in limiting the growth of bacteria and maintaining the sterility on the surface of human airway epithelia and leads us to speculate that the concentration of other carbon sources in ASL may also be low.
Glucose is exclusively supplied to the airways from circulating blood, reaching the basolateral side of epithelial cells, where uptake of glucose can occur. Glucose can reach the ASL through both the paracellular and transcellular pathways at a specific rate, but the epithelial cells have the capacity to absorb it through the apical membrane at an equal or higher rate (<a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016166#pone-0016166-g003">Figure 3D</a>).
What is the driving force that allows epithelial absorption of glucose from both the apical and basolateral compartments? Our data supports interesting conclusions. Intracellular glucose, under normal conditions, is constantly phosphorylated by hexokinase in an ATP-dependent reaction, creating flux into a chemical “fourth compartment”. This would maintain an intracellular non-phosphorylated glucose concentration that is lower than that of blood, and a glucose concentration gradient that can be the driving force for basolateral uptake. Any glucose reaching the ASL would therefore be absorbed at a rate that would keep it at concentration equilibrium with intracellular non-phosphorylated glucose (<a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016166#pone-0016166-g006">Figure 6, A</a>). Data supporting this idea come from studies performed in isolated lung cells grown in suspension, in which the intracellular concentration of glucose was found to be[41].
