A breakthrough paper published in Nature in December 2006 reported that microbial populations in the gut are different between obese and lean people, and that when the obese people lost weight their microflora reverted back to that observed in a lean person, suggesting that obesity may have a microbial component.
At a recent scientific symposium organised by the Beneo Group, Dr. Kieran Touhy from the University of Reading noted that obese animals have significantly lower bifidobacteria levels than their lean counterparts, which suggests potential for prebiotic fibres since the growth of these bacteria is selectively promoted by inulin and fructooligosaccharides.
Dr. Nathalie Delzenne from the Catholic University of Louvain in Belgium and Dr. Robert Welch from the University of Ulster presented results from animal and human studies, respectively, which indicated the potential of prebiotic supplementation to regulated food intake.
The new study, involving scientists from Nestle, the Catholic University of Louvain, and the Institute of Molecular Medicine Rangueil in Toulouse, adds and expands this knowledge base, showing that direct modulation of the gut microflora could directly affect metabolism, as well as influencing the maintenance of whole body glucose equilibrium, independent of food intake or obesity.
Study details
The researchers tested the influence of gut microflora modification in genetically (ob/ob) and diet-induced (DIO) obese mice. The animals were given broad ranging antibiotics (norfloxacin and ampicillin, at a dose of 1g/L) for two weeks.
At the end of the study, a significant improvement in fasting glucose levels and oral glucose tolerance in both ob/ob and DIO mice was observed. Moreover, this was correlated with a reduction in the levels of triglycerides in the liver and an increase in levels of glycogen in the liver.
"Our results support the idea that modulating gut microbiota could be beneficial for improving glycemic control," wrote the authors.
"However, more work has to be done in order to prove that gut microbiota modulation is a safe and effective therapeutic strategy in treating or managing type 2 diabetes in humans," they concluded.
Source: FASEB Journal
Published online ahead of print, 7 March 2008, doi:10.1096/fj.07-102723
"Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice"
Authors: M. Membrez, F. Blancher, M. Jaquet, R. Bibiloni, P.D. Cani, R.G. Burcelin, I. Corthesy, K. Mace, C.J. Chou
The researchers tested the influence of gut microflora modification in genetically (ob/ob) and diet-induced (DIO) obese mice. The animals were given broad ranging antibiotics (norfloxacin and ampicillin, at a dose of 1g/L) for two weeks.
At the end of the study, a significant improvement in fasting glucose levels and oral glucose tolerance in both ob/ob and DIO mice was observed. Moreover, this was correlated with a reduction in the levels of triglycerides in the liver and an increase in levels of glycogen in the liver.
"Our results support the idea that modulating gut microbiota could be beneficial for improving glycemic control," wrote the authors.
I don't understand, Harry. is this study saying that giving these mice broad range antibiotics improved their gut microflora, and therefore had a positive effect on glucose levels?
I don't understand, Harry. is this study saying that giving these mice broad range antibiotics improved their gut microflora, and therefore had a positive effect on glucose levels?
ST,
My title, to this thread, wasn't very good.
The take-home message is best summarized in the first-part of my initial post:
Quote:
A breakthrough paper published in Nature in December 2006 reported that microbial populations in the gut are different between obese and lean people, and that when the obese people lost weight their microflora reverted back to that observed in a lean person, suggesting that obesity may have a microbial component.
At a recent scientific symposium organised by the Beneo Group, Dr. Kieran Touhy from the University of Reading noted that obese animals have significantly lower bifidobacteria levels than their lean counterparts, which suggests potential for prebiotic fibres since the growth of these bacteria is selectively promoted by inulin and fructooligosaccharides.
Dr. Nathalie Delzenne from the Catholic University of Louvain in Belgium and Dr. Robert Welch from the University of Ulster presented results from animal and human studies, respectively, which indicated the potential of prebiotic supplementation to regulated food intake.
The new study, involving scientists from Nestle, the Catholic University of Louvain, and the Institute of Molecular Medicine Rangueil in Toulouse, adds and expands this knowledge base, showing that direct modulation of the gut microflora could directly affect metabolism, as well as influencing the maintenance of whole body glucose equilibrium, independent of food intake or obesity.
So, to answer your question: Yes, the antibiotics did improve blood sugar management. But, the other theory is that there are other ways of modulating gut microflora (by using pre or probiotics, for instance).
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Harry, what I don't understand is I thought antibiotics wiped out the good bacteria in the gut (as well as the bad bacteria). hence the "broad spectrum" label.
when you take a blood clotting test, they will ask you if you've recently taken antibiotics. this is because if you have, you might not be clotting like you should. the reason is because the bacteria in your gut produces vitamin K, which affects clotting.
I went through this with my son. He was going to have an operation, and they always test the ability of the blood to clot before they perform surgery. It is to make sure the patient is not a "bleeder". They were surprised to find that my son (6 years old) failed the clotting test. I was horrified... they were talking about testing him for hemophilia.. and other problems.. but said first, let's wait a month.. test him again. so, I did my own research. I found this out about antibiotics, and I had had my son on antibiotics for an ear infection, but had stopped it before the test.
so, the next month, I gave my son probiotics every day. and he passed the next test.
My son also has a vein in his nose that must be fragile, because every once in a while he will get a nosebleed. It is a genetic thing. My husband had this problem, his father did. They both ended up having the vein cauterized, and that fixed the problem.
but I found that when my son would start getting nosebleeds, if I gave him probiotics, it seems to fix it for a while. and he still takes them (when he remembers to.. usually after he has a nosebleed )
so... I don't get how wiping out the bacteria in the stomach with an antibiotic improves glucose metabolism..
and, if it does, then how would taking probiotics do the same thing? I would think it would do the opposite..
Last edited by scorpiotiger; 05-10-2008 at 07:59 PM.
so... I don't get how wiping out the bacteria in the stomach with an antibiotic improves glucose metabolism..
and, if it does, then how would taking probiotics do the same thing? I would think it would do the opposite..
ST,
This is my understanding (or my understanding that is a misunderstanding ):
Generally speaking, it seems that leaner people have a smaller number or undesirable gut microflora (see the cut-and-paste section of my previous post). And, overweight folk generally have a greater quantity of undesirable microflora. When overweight folk lose weight ... their gut microfloral environment also appears to shift to that of a leaner person.
So, by taking antibiotics, overweight mice can reduce the number of undesirable bacteria and that appears to offer an advantage in regard to blood sugar management. Does this also affect the healthy microorganisms in their gut ... yes. But, the net result seems to tip the gut environment to a place where it improves glycemic control.
Probiotics and prebiotics can often achieve similiar results (as the antibiotics, but without the downsides) because they antagonize the harmful/undesirable microbes and selectively nourish and/or repopulate the beneficial critters.
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ok.. got it. they surmise that it is the undesireable bacteria that might be linked to obesity.. not the lack of good bacteria - and I realize that you are saying that the lack of good bacteria can result in the presence of bad bacteria.. but the study really doesn't address that.
I wonder if their next step would be to determine the specific type of bacteria that seems to negatively affect glucose?
Division of Gastroenterology and Hepatology, Mayo Clinic, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA. [email protected]
Obesity results from alterations in the body's regulation of energy intake, expenditure, and storage. Recent evidence, primarily from investigations in animal models, suggests that the gut microbiota affects nutrient acquisition and energy regulation. Its composition has also been shown to differ in lean vs obese animals and humans.
In this article, we review the published evidence supporting the potential role of the gut microbiota in the development of obesity and explore the role that modifying the gut microbiota may play in its future treatment.
Evidence suggests that the metabolic activities of the gut microbiota facilitate the extraction of calories from ingested dietary substances and help to store these calories in host adipose tissue for later use.
Furthermore, the gut bacterial flora of obese mice and humans include fewer Bacteroidetes and correspondingly more Firmicutes than that of their lean counterparts, suggesting that differences in caloric extraction of ingested food substances may be due to the composition of the gut microbiota. Bacterial lipopolysaccharide derived from the intestinal microbiota may act as a triggering factor linking inflammation to high-fat diet-induced metabolic syndrome.
Interactions among microorganisms in the gut appear to have an important role in host energy homeostasis, with hydrogen-oxidizing methanogens enhancing the metabolism of fermentative bacteria. Existing evidence warrants further investigation of the microbial ecology of the human gut and points to modification of the gut microbiota as one means to treat people who are over-weight or obese.
Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens, GA 30602, USA. [email protected]
BACKGROUND: Lactobacillus extracts and supernatants have been used as probiotics in human and veterinary medicine for their ability to enhance wound healing and immunity. Previous data from our laboratory demonstrated that Lactobacillus supernatant (LS) stimulated wound healing, angiogenesis and proliferation of embryonic cells after topical application. This current study shows that LS after its administration into the cerebral ventricles of male rats exerts systemic effects.
METHODS: The right lateral cerebral ventricle of young male rats was accessed through intracerebroventricular cannulation (ICV) under anesthesia and aseptic conditions. One group of control rats received saline solution, a second control group received 0.8 M lactic acid solution (to control for acidity of LS), and a third group received LS. The animals were sacrificed 12, 24, 48, 96 and 120 hours after the injection. Selected tissues were collected, fixed in 10% buffered formalin and used for immunohistochemistry and in situ hybridization. Other tissues were frozen and extracted for immunoblotting
RESULTS: LS-injected animals had a slight decrease in body weight when compared to their initial weight and to both control groups. Using immunohistochemistry and in situ hybridization leptin expression was studied in multiple brain sections and peripheral adipose tissue of control and LS-injected rats.
Strong cytoplasmic stain was observed by both techniques in neurons of the cerebral cortex, thalamus, hypothalamus, hippocampus and, to lesser degree, in the cells of the choroid plexus in the LS-injected rats. Control animals demonstrated much less intense staining in neurons located in the same regions using immunohistochemistry and almost no staining with in situ hybridization technique. Adipose tissue exhibited slight presence of leptin in LS-treated animals.
In contrast no immunohistochemical staining for GM-CSF and TNFalpha was observed in brains from control and treated rats. Western blotting showed mild increase in leptin and leptin receptors in intestines and retroperitoneal adipose tissues of LS-injected rats.
CONCLUSION: This study demonstrates that direct administration of LS into rat CNS leads to a decrease in body weight of rats and an increase in the expression of leptin in specific areas of the brain and retroperitoneal adipose tissue.
I don't get the 2nd study. I wonder why they injected it into the brain of the rats? why not feed it to them?
I wonder what the results would have been if they had fed the rats the LS? The other thing is that how is this affecting gut flora, if it is injected into the brain?
(Harry is thinking.. why is she asking ME all these questions.. I didn't design the study )
That's a good question, ST. I'll see if I can find an answer to it.
Harry, I really didn't expect you to find the answer. but sometimes I wonder why they do the things they do in some of these clinical trials.
one thing I always look for is "how was the substance being tested applied? transdermal - to the skin, intravenously (usually a shot), or fed -through the digestive system?"
for each route, there are different barriers that the substance has to get through for the effect to be seen in the body. so, I would think the test would correlate to whatever goal they have in mind. shot, skin application, supplement, etc.
I don't know the answer to scorpiotiger's question, but "Blood-brain Barrier" came to mind when I read it. Some - many- drugs, foods, etc, cannot pass through to the brain from the blood stream so it needs a different route. Maybe so in this case?
Harry, I really didn't expect you to find the answer. but sometimes I wonder why they do the things they do in some of these clinical trials.
ST,
I understood where you were coming from but, since I noticed that the main author's e-mail address was posted in the abstract, I thought I'd try to get an answer from him anyhow.
I sent him an e-mail yesterday morning. So far, no response. I'll post any reply I get.
And, I share your interest/amazement at the unusual choices often made by researchers - when designing studies. I think some scientists have a sense of humor after all.
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SAN DIEGO (Reuters Health) - In a study conducted at Stanford University, obese patients who took probiotics after undergoing gastric bypass surgery lost more weight than patients who had the surgery but did not take the supplements.
These findings were presented Tuesday during Digestive Disease Week 2008 by Dr. John M. Morton, during a session on the management of patients with obesity.
"We have better treatments for crack cocaine addiction than we do for obesity," Dr. Morton asserted, "but there has been a real revolution with bariatric (obesity) surgery. It provides strikingly durable weight loss...As a result, blood pressures will normalize...We have seen diabetes cure rates of 82 percent, and this can occur within weeks of surgery."
According to the World Health Organization: "probiotics are live microorganisms which, when administered in adequate amounts, confer a health benefit." Most probiotics are bacteria similar to the type normally found the people's guts, the "good" bacteria, which helps maintain a balance in the digestive tract and may confer natural protection against disease. The most common probiotics taken as supplements are Lactobacillus and Bifidobacterium.
The trial involved 44 patients who underwent gastric bypass surgery and were randomly assigned to receive either 2.4 billion lactobacilli daily or no probiotic therapy for the next 6 months. Quality of life, hydrogen (H2) breath tests, vitamin B12 levels and weight were measured before surgery and at 3 and 6 months afterward.
At six months, the probiotic group had lower H2 breath tests, lower fasting insulin, lipoprotein A and triglyceride levels, and higher HDL cholesterol levels compared with the placebo group, although the differences were not statistically significant.
There was, however, a significantly greater improvement in quality of life in patients taking probiotics compared with those taking placebo.
"What was surprising was that probiotic patients lost more weight after surgery," Morton told Reuters Health. The study group lost 70 percent of their excess weight after 6 months compared with a loss of 66 percent of excess weight in controls.
He added, "This suggests that the cause of the weight increase may be bacterial...and may help explain the observation that fat people have fat friends...Some of it may be environmental and related to social factors, but it may also be related to high bacteria levels in some way."