Just got my Medscape email and there's a very interesting article on gut permeability and many health problems (I was looking for Celiac disease info myself) including its
role in obesity and fatty liver disease. Here's a direct quote and I will post the link to the whole article although you will probably have to join Medscape to read it.
Role of Intestinal Permeability and Probiotics in Obesity and Fatty Liver Disease. The new concepts on the pathophysiology of obesity and associated metabolic diseases such as NAFLD and NASH, type 2 diabetes mellitus or cardiovascular diseases, stating that such pathologies are related to the intestinal barrier and the intestinal microbiota, derived predominantly from mouse studies. It could be clearly shown that metabolic diseases are linked to increased intestinal permeability and translocation of bacteria or bacterial products like endotoxin from the intestine to the liver and to other tissues.[96,144,213,214] Moreover, it became clear that the microbiota of obese[215,216] and diabetic[217] individuals differs from that of the healthy, lean population. In the meantime, evidence is growing suggesting that these alterations are of functional relevance.
The altered microbiota in obesity and metabolic diseases contributes to an enhanced harvest of energy from nutrients. In particular, energy harvest from food carbohydrates depends on the microbiota, because specific bacteria found to be increased in obese individuals provide enzymes not expressed by host cells and allowing the digestion of otherwise more or less indigestible carbohydrates.[218–220] In type 2 diabetes, the microbiota looses its capacity to generate SCFA from prebiotics,[217] which might be a genuine defect or an adaptation to low fiber intake, which has been revealed by several epidemiologic studies.[221,222]
The altered intestinal barrier and the subsequent translocation of small amounts of bacteria or bacterial products is now regarded as one important mechanism causing the low-grade inflammation characteristic for metabolic diseases possibly linked to the subsequent infiltration of organs such as liver, muscle and heart muscle with fat.[223–226] Western style diet rich in fat and sugars alters the intestinal barrier in a way resulting in enhanced permeability and elevated endotoxin levels in the portal vein.[104,150,227]
The result of such alterations is enhanced infiltration of tissues with bacteria and bacterial products and subsequent tissue inflammation and fat accumulation, which can be observed first in the liver and later on in other tissues such as muscle or heart muscle.[150,219,228] Also in peripheral blood and in adipose tissue bacteria or bacterial products can be observed following feeding with energy-rich Western style diet, an observation that might enable to define new bacterial biomarkers of intestinal barrier dysfunction in metabolic diseases.[89,214] However, the two alterations, barrier dysfunction and microbiota alteration, are not necessarily linked, but can occur independently.[229] These findings provide a new concept on the pathophysiology of obesity and metabolic diseases that might offer new therapeutic strategies both at the level of diets and of drugs (Figure 7).
Considering these mechanisms it is tempting to speculate that probiotics and prebiotics might have beneficial effects in chronic metabolic disorders. First data derived from experimental studies in mice or from preliminary, human pilot studies indeed point in this direction. For example, possible effects of probiotic bacteria or particular diets on the gut barrier can be studied using organ culture models[230] or feeding models.[13,231] In humans, overfeeding alters the bacterial composition of the commensal microbiota in healthy individuals in a way that results in increased energy harvest from food.[232] The composition of the commensal microbiota might allow the prediction of weight gain in human individuals at risk like pregnant women.[233] In addition, administration of selected prebiotics or probiotics can improve metabolic alterations in animal models of metabolic liver disease[103,127] and in obese human individuals.[234,235] Such data suggest that new therapeutic concepts could be developed in the future to support treatment or prevention of obesity and associated diseases.
Link:
http://www.medscape.com/viewarticle/837168
Liana
(the numbers in the text are links to the actual studies referenced)