Links between gut bacteria and obesity

A new Johns Hopkins study of mice with the rodent equivalent of metabolic syndrome has added to evidence that the intestinal microbiome-a "garden" of bacterial, viral and fungal genes plays a substantial role in the development of obesity and insulin resistance in mammals, including humans.

Highlighting the potential to prevent obesity and diabetes by manipulating levels and ratios of gut bacteria, and modifying the chemical and biological pathways for metabolism-activating genes.

Metabolic syndrome, a cluster of conditions including obesity around the waist, high blood sugar and increased blood pressure, is a risk factor for heart disease, stroke and diabetes. While no precise cause for metabolic syndrome is known, previous studies of Toll-like receptor 4 (TLR4), a protein that receives chemical signals to activate inflammation, have suggested that TLR4 may be responsible in part for its development.

TLR4 signaling in different cells and their association with the bacterial environment could result in different effects on the development of metabolic syndrome. To determine whether TLR4 specifically in the intestinal epithelium (layer of cells that line the small and large intestines) would cause the development of metabolic syndrome, the research team ran a series of experiments on normal mice and mice genetically modified to lack TLR4 in their intestinal epithelium.

The researchers fed both groups of mice "standard chow," with 22 percent fat calories, for 21 weeks. Compared to normal mice, those lacking TLR4 showed a series of symptoms consistent with metabolic syndrome, such as significant weight gain, increased body and liver fat, and insulin resistance. The researchers then fed both groups of mice a high-fat diet comprised of 60 percent fat calories for 21 weeks to find out whether diet would affect the development of metabolic syndrome.

The genetically modified mice gained significantly more in weight and had greater body and liver fat than the normal mice. To confirm the role of TLR4 expression in the intestinal epithelium, the researchers genetically modified three more groups of mice: one group expressed TLR4 only in the intestinal epithelium, another group lacked TLR4 in all body cells and the third group lacked TLR4 only in white blood cells.

All groups ate standard chow, and all groups had similar body weight, body and liver fat, and glucose tolerance compared to normal mice. Compared with normal mice, belly and small intestine fat was higher in mice lacking TLR4 only in the intestinal epithelium. This, the researchers say, provides further evidence that deleting TLR4 specifically from the intestinal epithelium is required for developing metabolic syndrome.

To investigate the role the bacterial makeup of the gut had on the mice, they administered antibiotics to the normal and TLR4 intestinal epithelium-deficient mice. Antibiotics significantly reduced the amount of bacteria in the intestinal tract and prevented all symptoms of metabolic syndrome in the mice that lacked TLR4 in their intestinal epitheliums.

This shows that bacterial levels can be manipulated to prevent the development of metabolic syndrome. To further explore the role of intestinal epithelial TLR4 on the development of metabolic syndrome, the research team analyzed fecal samples from the TLR4 intestinal epithelium-deficient and normal mice.

The team found that specific clusters of bacteria that contribute to the development of metabolic syndrome were expressed differently in the deficient mice than in normal mice. They also determined that the bacteria expressed genes that made them "less hungry" and thus less able to digest the nutrients present in the mouse chow. This resulted in a greater abundance of food for the mouse to absorb, which contributed to obesity.

The researchers then analyzed the genes expressed in the lining of the intestinal mucosa-the site at which food absorption occurs in normal and TLR4 intestinal epithelium -deficient mice. Of note, the team determined that important genes in the perixisome proliferator-activated receptor (PPAR) metabolic pathway were significantly suppressed in the deficient mice.

Administering antibiotics prevented the differences in gene regulation between the two groups of mice, as did administering drugs to activate the PPAR signaling pathway. The bacterial sensor TLR4 regulates both host and bacterial genes that play unrecognized roles in energy metabolism leading to the development of metabolic syndrome in
mice.
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Gut bacteria could be good or bad

Bacteria that live in and on human body are emerging as an increasingly important player in health and wellness. Human co-existence with these organisms is complex, minor changes in this relationship can leads to adverse reaction on human health.

Researchers from the University of Rochester Medical Center found that impairing a rare group of cells in the small intestine allows gut bacteria to invade the organ and cause major inflammation. The study was conducted in mice, but has implications for the treatment of inflammatory bowel disease (IBD), a group of disorders characterized by chronic inflammation in the digestive track.

Keeping guts in good shape requires the cooperation of multiple intestinal cells with the bacteria that live around them. Though small in number, intestinal cells called Paneth cells play an important role; they make antimicrobial compounds that keep bacteria in check and help form the lining of the small intestine, a physical barrier between the organ and the resident bacteria.

Previous research shows that changes or mutations in Paneth cells are associated with increased inflammation, including in individuals with Crohn's disease, a type of IBD. But, scientists were unsure how Paneth cells opened the door to inflammatory damage.

Researchers led by Felix O. Yarovinsky, M.D. found the answer in a process called autophagy, which helps cells remove unwanted cellular material or debris. His team turned off autophagy in Paneth cells in mice and then exposed them to a stressor-a parasite called Toxoplasma gondii. Without autophagy, the barrier between the small intestine and the gut bacteria broke down; bacteria invaded the organ and caused severe infection and inflammation.

Paneth cells are like the guardians of the intestine and autophagy is like their armor, when their  armor were removed, the Paneth cells couldn't control the intestinal bacteria and it went wild, causing severe disease. The study suggests that normal autophagy in Paneth cells is required to regulate bacteria in the gut, keeping it at bay and preventing the gut bacteria from invading host tissue.

Paneth cells make up just 2 percent of the cells in the intestine, and the fact that restricting autophagy in these cells led to big problems was an unexpected result. Gut bacteria play a role in the development of IBD, which includes Crohn's disease and ulcerative colitis. But how bacteria in the gut are controlled in these conditions remains elusive. This study and others point to Paneth cells as key regulators of the interactions between host and gut bacteria, and further research could inform the design of future therapies.
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Aging leads to an imbalance in gut bacteria

According to a new study in PLOS Pathogens, different changes to the microbial community of the stomach may be the reason why conditions are associated with different risk levels and types of gastric tumor. Autoimmune disease or infection with Helicobacter pylori bacteria can damage the stomach and reduce gastric acid secretion.

Despite their similar effects, each of these conditions is associated with higher risk of a different type of gastric tumor. Meanwhile, widely used medications known as proton pump inhibitors PPIs also reduce gastric acid secretion, but they do not increase cancer risk. Elderly people tend to have different gut bacteria profiles from younger people.

This new research suggests that this change in balance is linked to inflammaging, which is related to most late-onset diseases and disorders. Inflammaging is a catch-all term for the tendency of elderly people to have generalized inflammation. It is thought to be related to evolved changes that the immune system undergoes as a person gets older.

It isn’t clear whether aging causes inflammation or inflammation causes aging, but the two go hand-in-hand, and susceptibility to many diseases goes along with both of them. Researchers took samples from older mice – whose gut bacteria composition, like humans’, changes with age – and introduced them to the bodies of younger mice. After the procedure, the younger mice developed chronic inflammation, like the inflammaging that would normally have struck them later in life.

They also transplanted gut bacteria from one group of younger mice to another group of mice of around the same ages to see if the immune response was just to the introduction of foreign bacteria. The mice with transplanted gut bacteria from older ones developed inflammaging.

The differences in the responses suggested to the researchers that aging leads to an imbalance in gut bacteria, such that there are more ‘bad’ bacteria than good in the microbiome. The proliferation of the bad bacteria leaves the gut lining more permeable to toxins that can contaminate the bloodstream and lead to disorders like inflammatory bowel disease, obesity, diabetes, anxiety, autism and cancer.
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Gut bacteria may change after severe injury

After a severe traumatic injury, the composition of a patient's intestinal bacteria changes and this could affects patient's prognosis. The gut microbiome experiences a depletion in the presence of some bacteria and an increase in the presence of others came from a small investigation, involving critically injured adults.

Stool samples were collected from each person three times: when they were admitted to the hospital, and then 24 and 72 hours later. The samples were compared with those from 10 other patients who had not sustained traumatic injury.

Samples taken at the time of admission were similar in both groups. But within 24 hours, differences started to show, the investigators found. By 72 hours, three types of bacteria were depleted in the traumatic injury group, relative to the non-injury group, and the levels of two other types of bacteria had risen.

Rapid alterations in intestinal microbiota represent a critical and unrecognized phenomenon that may influence clinical course and outcomes after severe trauma. The intestinal bacterial composition could in some way be critical to patient outcomes after a traumatic injury. This could create the way towards interventions, such as administering probiotic regimens that might improve patient outcomes after injury.
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Links between microbiomes and autoimmune disorders

Bacteria in human body have all kinds of positive effects on our health, the bacteria in the gut have many beneficial functions. They help in digestion, prevent infection by pathogens and strengthen immune system to fight diseases.

A new function of a protein in the gut microbiome reveals potential impacts for those who suffer from inflammatory bowel disease IBD. A protein expressed by gut bacteria called Bacteroides works to prevent IBD by rapidly recruiting white blood cells to kill a cell of the immune system that is responsible for orchestrating IBD.

However, there is a flipside to the protein's call for help. In some people, the white blood cells overreact to the presence of the IBD bacteria. This is what causes problems like IBD, it's not the bacteria itself, but the immune system's severe reaction triggered by the protein.

These same overstimulated white blood cells are also the cells that cause other autoimmune disorders like diabetes, this discovery demonstrates the effect the gut microbiome has on the immune system and unearths a novel mechanism through which changes in the gut microbiome can increase the risk of autoimmune disorders.
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Prevotella bacteria levels prevents weight loss

Having low levels of Prevotella bacteria in stools prevents weight loss, regardless of whether you are consuming fruits and vegetables or junk foods. Prevotella is associated with plant-based diets- rich in fruit, vegetables, leafy greens, seeds, nuts, beans and lentils with little or no animal products.

However change in bacteria will not be effective immediately, Prevotella may aid weight loss by influencing fat storage and how people respond to hunger hormones. Eating more fruits, vegetables, fibres and whole grains may be effective for weight loss in some people but not every body will benefit from this.

 Researchers analysed some people with an increased waist circumference over six months, some of the participants ate a diet rich in whole grains and fibre, the rest consumed red meat and confectionery.

The results reveal that eating foods rich  in fibre causes weight loss, participants with high levels of the strain of Prevotella bacteria lost more weight. Those with lower amounts of Prevotella did not lose weight after eating high amounts of whole grains and fibre.

Prevotella is associated with plant-based diets made up of fruits, nuts vegetables, whole grain, pulses and seeds, with little or no animal products.
It can take a long time of adopting a particular diet before gut bacteria levels adapt to the change. Regular physical activity can work for those that have less Prevotella bacteria.
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Links between gut bacteria and autism

According to the latest research, gut bacteria could cause spectrum disorder. Pathogens in the stomach alter the brain's development and may increase risk of suffering from the spectrum disorder.

Links between the brain, gut and stress hormone cortisol can influence how messages are passed in the body, which may cause autistic symptoms.

Changes in neurometabolites in childhood can have dangerous effects on brain development. Collection of bacteria, fungi, and viruses living in humans gut may be responsible for the disorder.

Autism may be corrected by changing of diet, taking probiotics and adopting a gluten-free lifestyle which may improve social behaviour and ability to express emotions in autistic people.

Leaky gut releases toxins and even undigested food enter the bloodstream and travel to the brain, which may cause autism symptoms. Probiotics can change this by enhancing the gut's lining.
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Use synbiotics for gut health

Probiotics are live bacteria that are good for digestive system. Probiotics are said to keep gut and digestion healthy by replacing the bad bacteria with good one.

Synbiotics combined a probiotic bacterial strain with prebiotics, which actually feed and increase the good bacteria in the gut.

Probiotics can not survive for a long periods of time, heat and stomach acid can kill them, making them ineffective before digestion.

 Synbiotics are the best way to ensure a maximum benefit from the ingested probiotics. It is the combination of probiotics and prebiotics to feed the human microbiome. Synbiotics could have beneficial effects on obesity and diabetes.

Research has linked our gut health to a range of conditions like obesity, depression, multiple sclerosis and rheumatoid arthritis. Probiotics may prevent and treat fatty liver disease and keep it from advancing to liver cancer.

 Pre-and pro-biotics work together to provide a combined benefit, while the probiotic settles in and pushes out the bad bacteria, the prebiotic feeds the growth of positive strains.

A healthy, balanced microbiome breaks down foods, protects human from infection, trains immune system and produces vitamins K and B12. It also controls mood, anxiety and appetite.
Imbalances in the gut are linked to a range of conditions.

The composition of human gut microbiota is determined by genes but it can also be influenced by lifestyle factors such as diet, alcohol intake, exercise, and medications.
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Artificial sweeteners cause different health problems

Artificial sweeteners are sugar substitutes, these are food additives that taste like sugar. Common artificial sweeteners are stevia, aspartame, sucralose, neotame, acesulfame potassium, saccharin and advantame.

 It has negative effects on metabolism, gut bacteria and appetite. Consumption of artificial sweeteners is associated with weight gain, obesity, diabetes, high blood pressure, kidney damage and heart disease. It increases the risk of metabolic disorder and cancer.

Artificial sweeteners are used to prepare these : toothpaste, mouthwash, chewing gum, alcoholic beverages, liquid medicine, salad dressing, frozen desserts, frozen yogurt, candies and processed snacks.

Artificial sweeteners can be replaced with healthy natural foods like raw honey, dates, coconut sugar, maple syrup, banana puree and natural fruits jam.
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Western diet may cause liver inflammation

Liver inflammation occurs when the organ becomes larger than normal. Diet, gender, and different antibiotic treatments can alter the gut microbiota as well as bile acid profile and have different effects on liver inflammation.

Farnesold x receptor FxR, is a member of the family of nuclear hormone receptors. Broad-spectrum antibiotics, which eliminated most gut bacteria, affected hepatic inflammation differently in FXR-deficient mice, the diet provided will determine the how it affects gut bacteria.

 In control diet-fed mice, a cocktail of ampicillin, neomycin and vancomycin blocked hepatic neutrophil and lymphocyte infiltration. The cocktail of antibiotics Abx was not able to eliminate hepatic inflammation in Western diet-fed Farnesold x receptor knock out FXR KO mice.

Other investigation showed that many inflammatory genes had higher expression levels in Western diet than control diet-fed FXR KO mice after antibiotics treatment.

Analyzing the composition of the gut microbiota, researchers discovered that that Proteobacteria and Bacteroidetes persisted after the broad-spectrum antibiotic treatment in the Western diet-fed FXR KO mice.

Adverse effects of Western diet on the liver may be explained by the persistence of pro-inflammatory Proteobacteria and the reduction of anti-inflammatory Firmicutes in the gut.
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High fat diet reduces symptoms of Crohn's disease

High fat diet changes gut bacteria, reduces inflammation and symptoms of Crohn's disease. Crohn's disease is a type of inflammatory bowel syndrome that causes intestinal swelling, cramping and diarrhea.

 Diet of plant-based fats, reduced bacterial diversity in mice with Crohn's-like disease. Researchers fed mice with different fat diet, mice fed fatty diets had up to thirty percent fewer kinds of gut bacteria as those fed a normal diet.

 Crohn's patient can reduce their gut inflammation by adding good fat to their diet in moderation to prevent inflammation bowel syndrome.

All the good fats may have different results in different patients. Patients can start by trying different fat diet to discover the one that is good for their gut bacteria.

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Vigorous exercise increases health risks

Vigorous exercise for a long period of time can change the composition of gut bacteria.

The research looked at soldiers taking part in an intensive training programme and found that pro-longed exercise caused the protective barrier in their guts to become permeable and triggered leaky gut syndrome.

Gut health and overall health are linked, intense physiological stress could raise the risks of many types of illnesses.

 Poor gut health is linked to conditions ranging from irritable bowel syndrome, diabetes, high blood pressure, depression, obesity, childhood asthma, colitis and colon cancer.

The study is the first to investigate the response of gut microbiome - the term for the population of microbes in the intestine - during military training.

It looked at a group of 73 Norwegian Army soldiers taking part in a military-style cross country skiing training programme.

The group skied 31 miles (51 km) while carrying 99-pound (45 kg) packs, across four days. Before and after the training
exercise, researchers collected blood and stool samples from the soldiers.

It was found that the microbiome and metabolites - the substance formed in or necessary for metabolism - in the soldiers' blood and stool altered 'significantly' by the end of the aggressive training period.

Furthermore, sucralose excretion in their urine samples rose considerably, indicating an increase in intestinal permeability (IP).

Scientists know that healthy intestines have a semi-permeable barrier, which acts as a defense to keep bacteria and other harmful substances out, while allowing healthy nutrients into the bloodstream.