Gluten and Weight Gain Study Part III: The Wrap Up

C/o Sott.net

C/o Sott.net

It is time for part 3 and to bring a close to the gluten free diet and weight gain paper. Part 1 and 2 discussed the results of the paper in regards to weight gain, adiposity, insulin resistance, glucose homeostasis, hormonal responses (i.e. leptin, resistin, and adiponectin, LPL, and HSL), along with nuclear receptor activity (PPAR).  To view my comments on these results see part 1 and part 2.  The last portion of the paper, and the topic of this post, is the role of gluten on inflammation and cell adhesion. Inflammation and cell adhesion are two main contributors to cardiovascular disease, more specifically, coronary artery disease. Here are two papers (1,2) that nicely describe this relationship and the mechanisms involved.  The authors of this study examined the effect of a gluten containing diet vs. a gluten free diet on markers of inflammation and cell adhesion in mice. The results of the study have some interesting implication in the role of gluten in inflammation and heart disease and I would like to examine them closely.

A

Figure A presents the data on the rolling and adhesion of leukocytes (white blood cells) in the mice. Without getting too technical, rolling and adhesion of leukocytes is hallmark in inflammation as it promotes repair in damaged tissue and the formation of plaque.  Here, the lower the number the less adhesion of leukocytes and the lower likelihood of CHD forming.  The results of the data indicate that GF mice have lower rolling measures (although NOT statistically significant) and lower leukocyte adhesion (this IS statistically significant).  From this it is logical to assume that a gluten free diet may have less deleterious health impacts when one gains weight, although we cannot be 100% certain whether this is due to the lower increase in weight gain and adiposity or directly due to the gluten itself. I would venture to guess both factors are at work in these results.

B

Figure B presents the data on the gene expression and adipose (fat) tissue concentration of MCP/CCL-2. MCP/CCL-2 is a cytokine (chemical messenger) that signals chemotactic activity for monocytes and basophils. Essentially, it attracts specific leukocytes to an area that is inflamed. Here we see no difference in gene expression between the two but we do see a significant lower concentration of this cytokine in the GF mice. This further supports the argument that we observe lower levels of chronic inflammation in the GF diet.

C

Figure C displays the results of the analysis of Macrophage-forming crown-like structures (CLS). CLS are often used to as biomarkers in inflammation.  These results corroborate the findings of A and C in that the GF diet had significantly lower measures of CLS.

DEF

Figures D-F  show the results of the three of the most well known biomarkers of inflammation, TNF-alpha, IL-6, and IL-10. GF mice show lower gene expression and tissue concentration of TNF-alpha along with lower tissue concentration of IL-6 and IL-10 than the gluten fed control mice.

The Wrap Up!

Now time to tie it all together and wrap it all up.  Essentially what we find in this study is that when there is weight gain, a GF diet yields less weight gain and less fat gain than a gluten containing diet. We also observe a better “fat-burning” environment in the GF diet alongside improved glucose control.  The last thing we see is lower inflammation and less cell adhesion in GF mice.

From my perspective, I think there are a few things going on to explain these results.  The first conclusion I would draw is that gluten containing diets result in greater systemic inflammation than a GF diet.  This leads to greater insulin resistance than a GF diet that produces decreased glucose control. Decreased glucose control alongside insulin resistance, changes the hormonal profile in the body, ultimately altering fat metabolism.  Alongside altered metabolism, the increased inflammation due to gluten also creates an environment that promotes leukocyte rolling and cellular adhesion.

We have covered the results and the implications of these findings quite thoroughly and I hope that it has been well articulated. There are a few issues with this paper that I do believe are worth noting.  The first is that we must remember this is a mouse model. Although mouse model’s are powerful tools and can tell us a great deal of information, their physiology is not identical to ours; therefore, we must be careful when extrapolating the results to humans. Additionally, I am not 100% familiar with the guy physiology of mice but they may display more or less gut permeability to gluten, and thus more or less inflammation in response to a certain dose of gluten.  Secondly, the mice on the gluten containing diet were fed a dose of 4.5% gluten by total diet.  This amount of gluten is quite high and it is highly unlikely that humans would eat a diet containing that much gluten (unless your main protein source is seitan). Lastly, these results are in the context of weight gain.  Therefore, the increased inflammation, hormonal/metabolic changes and leukocytes adhesion may not appear in an experiment comparing gluten to GF without excessive energy intake.

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