There are 6 dominant species in the intestinal flora. Bacteriodetes and Firmicutes species constitute 90% and the rest is Actinobacteria, Fusobacteria, Proteobacteria and Verrucomicrobia species. In obesity cases, Bacteriodetes species decrease and Firmicutes species are found to be increased. In experiments with mice, when the microbiome of obese mice was transferred to sterile (germ-free) mice, sterile mice were found to be rapidly gaining weight. In 2004 Backhead and colleagues and in 2006, Turnbaugh and colleagues conducted similar studies and received almost the same results. They also showed a genetical inheritance. In 2006, Ley and colleagues published a very successful study about the importance of microbiota. They followed up 12 obese individuals for 1 year, applied a diet containing low carbohydrates and fat and examined the intestinal flora. They found that the increase in Bacteroidetes species and the weight loss were proportional to each other.
So how does this happen? How does the bacteria in the bowel wall affect our weight gain? We can explain this with several mechanisms:
1st Mechanism: There is an enzyme involved in regulation of eating: AMPK (AMP-active protein kinase) This enzyme is released from the hypothalamus. Disruption of microbiota has a repressive effect on AMPK activity, thus increasing the susceptibility to insulin resistance and obesity.
2nd Mechanism: It was described in a study by Schwiert and colleagues. When starch and fibers reach to the large intestine without digestion, they are digested by bacteria of the microbiota and short chain fatty acids (acetate, propionate and butyrate) occur. These fatty acids are used in the de novo synthesis of lipid and glucose, so 10% of daily energy is produced additionally and the possibility of weight gain increases. Schwiert and colleagues found that in obese subjects these fatty acids were 20% higher than in slim patients. The bacteria that produce short chain fatty acids are Firmicutes. The eating habit that leads to production of high-fat or starch-based sugars increases this bacterial colony, and every 20% increase means additional 150 calories.
3rd Mechanism: It suppresses the fat tissue factor (Fiaf) and consequently increases lipoprotein lipase activity, leading to increased adipose tissue.
4th Mechanism: In the procession of polysaccharides by an impaired intestinal microbiota, through the activation of sterol regulatory element binding proteins (SREBP-1c: regulates genes required to make fatty acids, SREBP-2: regulates genes of cholesterol metabolism) and carbohydrate regulatory element binding proteins (ChREBP), fat production in the liver increases.
Eating habits with high fat and simple carbohydrates decrease Bacteriodetes species and cause an increase of Firmicutes species, wherever diets containing plants, vegetables and high fiber have the opposite effect. In addition, a plant based diet balances the bile-resistant microorganisms while stimulating the digestion of carbohydrates and stimulating the genes necessary for the synthesis of amino acids.
Probiotics and Prebiotics in Obesity Treatment:
In a study conducted by Lee and colleagues in 2006, probiotics containing Lactobacillus Rhamnosus bacteria were given to obese mice for 8 weeks, followingly weight loss and decrease in adipose tissue were detected. In another study, Lactobacillus paracasei, Lactobacillus rhamnosus, and placebo were given to mice with similarities to human microbiota and the results were compared: hepatic lipid metabolism was positively changed compared to those given placebo, plasma lipoprotin levels decreased and glycolysis increased.
A study about the effect of prebiotic use on satiation and intestinal hormones has shown that 2 weeks of prebiotic treatment improves fermentation of intestinal microbials, decreases starvation and improves post-meal glucose response.
A New Approach to Obesity Therapy
With the strong scientific evidence of the importance of microbiota in obesity, it has been argued that microbiota of slim and healthy people can be used for therapeutic purposes. In a study by Eiseman and colleagues in 1958, feces of healthy individuals were transplanted to individuals with pseudomembranous enterocolitis and provided an improvement, which is then called fecal transplantation. Likewise, fecal transplantation from slim individuals to obese individuals showed decreased levels of triglycerides in obese individuals and improved insulin resistance. In 2012, a study by Vrieze and colleagues showed that butyrate producing bacteria level and insulin sensitivity increased in patients with metabolic syndrome who underwent intestinal microbiota transplantation from slim donors.