The bugs that make you fat, irritate your bowel.
Obesity is not just a matter of thermodynamics; energy in minus energy out equals energy stored, both sides of the equation may be modified by bacteria. As George Bray, leading light in obesity research, once quipped, ‘Obesity is not rocket science; it’s much more complicated!’ Eating a high fat diet increases the abundance of the phylum Firmacutes in the bowel and obese individuals have a higher ratio of Firmacutes compared with bacteroides than people who are not obese1. This shift in microbiota not only increases the salvage of nutrient in the colon but reduces the release of the gut hormone GLP2, making the gut more permeable to organisms coated with pro-inflammatory lipopolysaccharide2. These invade the blood stream and gain access to the fat cells, setting up a mild inflammatory reaction that causes more fat storage and unhinges appetite from regulation by fat stores.
But there’s more. Bacteria in the colon occupy several different niches, rather like the plants that grow in the forest and scientists have speculated that the fastidious organisms live in the mucus layer adjacent to the colonic epithelium may have a particular function. Akkermannsia muciniphilia comprises about 5% of the colonic microbiome but it occupies this essential niche. As it’s name reveals, this seemingly inauspicious little bug stimulates the production of mucus on which it feeds. This action helps to maintain the mucosal barrier and reduces the permeability of the gut3. Populations of Akkermannsia are depleted in obese individuals, probably because of diets rich in fat, though antibiotics would also play a key role. So obese people produce less mucus, rendering the gut more permeable to more pro-inflammatory bacteria2,4. Obese and overweight individuals with high levels of Akkermannsia are more healthy and respond better to weight loss regimes.
Eating disorders are common in patients with IBS. IBS diarrhoea is often associated with binge eating and weight gain5, as opposed to constipation which is frequently coupled with anorexia – nothing in, nothing out! Microbial depletion, increased gut permeability and increased activity of the gut immune system are all features of IBS-diarrhoea2. Like the fat cells in obese individuals, the gut wall in patients with IBS-D is mildly inflamed. Patients with IBS-D demonstrated an increase in Firmacutes and also a reduction in Akkermannsia in IBS2,6. This would not only allow other organisms to gain access to gut wall, but also food allergens (see my previous post on the links between food allergy and food intolerance).
Companies would be developing smart probiotics containing Akkermannsia right now were not this organism so fastidious and difficult to culture.
References.
- D’Aversa F, Tortora A, Ianiro, P et al, Gut Microbiota and Metabolic Syndrome. Internaal and Emergency Medicine. DOI:10.1007/s11739-013-0916-z
- Bischoff SC, Barbara G, Buurman W. 2014. Intestimal Permeability, a new target for disease prevention and therapy. BMC Gastroenterology 14. 189.
- Dao MC; Everard A, Aron-Wisnewsky J;(2015). “Akkermansia muciniphila and improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology”. Gut. doi:10.1136/
- Caesar R Tremaroli V Kovatcheva-Datchar P; Cani Bäckhed F (2015). “Crosstalk between Gut Microbiota and Dietary Lipids Aggravates WAT Inflammation through TLR Signaling”. Cell Metabolism. doi:10.1016/j.cmet.2015.07.026.
- Talley NJ, Quan C, Jones MP, Horowitz, M (2004). Association of upper and lower gastrointestinal tract symptoms with BMI in an Australian cohort. Neurogastroenterology and Motility 4. 413-419.
- Jeffery, I. B. et al. 2012. An irritable bowel syndrome subtype defined by species-specific alterations in faecal microbiota. Gut 61, 997–1006 .
The Sensitive Gut 