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Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice
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Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice
Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice
Abstract
OBJECTIVE—Diabetes and obesity are characterized by a low-grade inflammation whose molecular origin is unknown. We previously determined, first, that metabolic endotoxemia controls the inflammatory tone, body weight gain, and diabetes, and second, that high-fat feeding modulates gut microbiota and the plasma concentration of lipopolysaccharide (LPS), i.e., metabolic endotoxemia. Therefore, it remained to demonstrate whether changes in gut microbiota control the occurrence of metabolic diseases.
RESEARCH DESIGN AND METHODS—We changed gut microbiota by means of antibiotic treatment to demonstrate, first, that changes in gut microbiota could be responsible for the control of metabolic endotoxemia, the low-grade inflammation, obesity, and type 2 diabetes and, second, to provide some mechanisms responsible for such effect.
RESULTS—We found that changes of gut microbiota induced by an antibiotic treatment reduced metabolic endotoxemia and the cecal content of LPS in both high-fat–fed and ob/ob mice. This effect was correlated with reduced glucose intolerance, body weight gain, fat mass development, lower inflammation, oxidative stress, and macrophage infiltration marker mRNA expression in visceral adipose tissue. Importantly, high-fat feeding strongly increased intestinal permeability and reduced the expression of genes coding for proteins of the tight junctions. Furthermore, the absence of CD14 in ob/ob CD14−/− mutant mice mimicked the metabolic and inflammatory effects of antibiotics.
CONCLUSIONS—This new finding demonstrates that changes in gut microbiota controls metabolic endotoxemia, inflammation, and associated disorders by a mechanism that could increase intestinal permeability. It would thus be useful to develop strategies for changing gut microbiota to control, intestinal permeability, metabolic endotoxemia, and associated disorders.
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a<r- Admin
- Posts : 819
Join date : 2011-05-12
Age : 33
Re: Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice
great. so basically we are putting our intestinal normal flora out of whack and feeding the bad bacteria with sugar, carbs fats etc(modern diet) which then produce endotoxins responsible for metabolic syndrome, type II diabetes etc (typical unhealthy disease)
and the only way to stop this and put it back in balance (apart from just a paleo or similar diet) is to take anti-biotics?
great. pity except for severe chest infections and the like, they are only good short term, not to mention they help create MRSA and resistant strains. And all this time i thought the anti biotics put the normal flora out of whack. just more evidence our diets r fuked up i guess.
and the only way to stop this and put it back in balance (apart from just a paleo or similar diet) is to take anti-biotics?
great. pity except for severe chest infections and the like, they are only good short term, not to mention they help create MRSA and resistant strains. And all this time i thought the anti biotics put the normal flora out of whack. just more evidence our diets r fuked up i guess.
rofl- Posts : 857
Join date : 2009-11-21
Re: Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice
Just some rambling thoughts here:
I wonder how much intestinal permeability and endotoxemia are involved in the pathogenesis of autoimmunity.
http://www.scientificamerican.com/article.cfm?id=celiac-disease-insights
Interesting article, he thinks that increased intestinal permeability exposes the immune system to antigens that can trigger autoimmunity. The link between celiac disease (gut inflammation and increased intestinal permeability) and type I diabetes and autoimmune hypothyroidism seems to be there. Gluten withdrawal has been shown to reduce hypothyroidism in celiac patients. The author started up a company producing a drug that reduces intestinal permeability with the aim of treating autoimmune diseases, just FYI.
---
Another interesting point is that interferon therapy for hepatitis C can induce autoimmune hypothyroidism.
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It's probably not accurate to say that antibiotics can put the gut flora back into balance. Antibiotics can change the gut flora, sometimes in a good way.
---
http://www.wired.com/wiredscience/2011/08/killing-beneficial-bacteria/
Another article, talking about a possible connection between antibiotics and asthma, obesity, etc.
Here's the referenced Nature article:
http://www.nature.com/nature/journal/v476/n7361/full/476393a.html
And an article referenced by the Nature article:
Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation
I wonder how much intestinal permeability and endotoxemia are involved in the pathogenesis of autoimmunity.
http://www.scientificamerican.com/article.cfm?id=celiac-disease-insights
Interesting article, he thinks that increased intestinal permeability exposes the immune system to antigens that can trigger autoimmunity. The link between celiac disease (gut inflammation and increased intestinal permeability) and type I diabetes and autoimmune hypothyroidism seems to be there. Gluten withdrawal has been shown to reduce hypothyroidism in celiac patients. The author started up a company producing a drug that reduces intestinal permeability with the aim of treating autoimmune diseases, just FYI.
---
Another interesting point is that interferon therapy for hepatitis C can induce autoimmune hypothyroidism.
---
It's probably not accurate to say that antibiotics can put the gut flora back into balance. Antibiotics can change the gut flora, sometimes in a good way.
---
http://www.wired.com/wiredscience/2011/08/killing-beneficial-bacteria/
Another article, talking about a possible connection between antibiotics and asthma, obesity, etc.
Here's the referenced Nature article:
http://www.nature.com/nature/journal/v476/n7361/full/476393a.html
And an article referenced by the Nature article:
Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation
We examined the distal gut microbiota of three individuals over 10 mo that spanned two courses of the antibiotic ciprofloxacin
In all subjects, the composition of the gut microbiota stabilized by the end of the experiment but was altered from its initial state. As with other ecosystems, the human distal gut microbiome at baseline is a dynamic regimen with a stable average state. Antibiotic perturbation may cause a shift to an alternative stable state, the full consequences of which remain unknown.
crincrin- Posts : 358
Join date : 2010-04-15
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