Infectobesity

The term "infectobesity" refers to the hypothesis that obesity in humans can be caused by pathogenic organisms, and the emerging field of medical research that studies the relationship between pathogens and weight gain. The term was coined in 2001 by Dr. Nikhil V. Dhurandhar, at the Pennington Biomedical Research Center.

Bacteria

The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.[1]

A possible mechanistic explanation linking gut flora to obesity involves short chain fatty acids. Humans are unable to digest complex polysaccharides and rely on gut microbiota to ferment these polysaccharides into short chain fatty acids. In contrast to polysaccharides, humans can use short chain fatty acids as a source of energy.[2] In addition, research in rodents has indicated that the abundance of short chain fatty acids in the gut can affect the blood levels of gut hormones such as GLP-1, GLP-2 and peptide YY. These changes in gut hormone levels have shown to affect glucose tolerance, insulin signaling, intestinal barrier function and have led to weight gain in rodents. Dietary diversity is associated in humans and animals with a more healthy gut microbiota, and thus may be necessary for effective long-term health improvement strategies, but is often overlooked in animal studies.[3] Furthermore, administration of antibiotics to rodents alters gut microbiota composition and ensuing changes in gut hormone levels are also detected. These results may provide the mechanistic explanation for the claim that antibiotics can lead to obesity in humans. Yet, whether these findings can be replicated in human studies remains to be seen.[4]

Viruses

An association between viruses and obesity has been found in humans, as well as a number of different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.[5] A fat virus is the popular name for the notion that some forms of obesity in humans and animals have a viral source.

See also

References
  1. DiBaise JK, Zhang H, Crowell MD, Krajmalnik-Brown R, Decker GA, Rittmann BE (April 2008). "Gut microbiota and its possible relationship with obesity". Mayo Clinic Proceedings. 83 (4): 460–9. doi:10.4065/83.4.460. PMID 18380992.
  2. Diamant, M.; Blaak, E. E.; Vos, W. M. (2010). "Do nutrient-gut-microbiota interactions play a role in human obesity, insulin resistance and type 2 diabetes?". Obesity Reviews. 12 (4): 272–281. doi:10.1111/j.1467-789X.2010.00797.x. PMID 20804522. S2CID 38615798.
  3. Heiman, ML; Greenway, FL (May 2016). "A healthy gastrointestinal microbiome is dependent on dietary diversity". Molecular Metabolism (Review). 5 (5): 317–320. doi:10.1016/j.molmet.2016.02.005. PMC 4837298. PMID 27110483. Stable, diverse and healthy GI microbial ecosystems are an important component to consider when using diet to perturb physiological systems in animal models of disease, and it is an aspect often overlooked. A common model to study obesity and insulin resistance is one in which the diet is switched from a basic chow diet to a "Western" or "high fat" diet with a predominance of fat and sugar. Conclusions are typically based on the shift to the calorie dense diet. However, chow diets are classically more diverse. They contain macronutrients from many sources such as whole wheat, dehulled soybean meal, ground corn, animal fat and condensed whey (for example, Purina 5015 Mouse Diet). A common diet used to induce obesity in a mouse is much less diverse such as Research Diets D12492 that contains casein as the source of protein, cornstarch and sucrose as the carbohydrate, and lard as the fat source. The loss of dietary biodiversity may be an important component for the development of obesity that is associated with a narrowing of GI microbiome diversity. Clues to solve another medical mystery are derived from secondary bile acids that are a result of GI microbiota processing. Bariatric procedures such as Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG) are associated with considerable improvements in co-morbidities of obesity rapidly after the procedure and prior to significant weight loss. Outcomes from RYGB and VSG appear to be related to bile acid signaling through the farnesoid X receptor (FXR) – to regulate physiological systems and also to increase gut permeability by reducing the mucosal barrier. It is now clear that bile acid diversity is dependent on the gut microbial diversity. Expanding dietary fat diversity (for example, saturated-, monounsaturated and polyunsaturated fatty acids) can shift microbiome diversity and thus regulate the bile acid diversity. Additional research into expanding gut microbial richness by dietary diversity is likely to expand concepts in healthy nutrition, stimulate discovery of new diagnostics, and open up novel therapeutic possibilities. In the future, an adult seeking treatment for obesity may be surveyed about dietary preferences and present a stool specimen. Weight loss therapy may begin with a specific dietary plan to widen that person's GI microbiome richness as a prelude to obesity treatments to maintain a weight loss over a long period, as is the case for preadolescent children with obesity and obesity surgery. Indeed, short-term personalized dietary interventions based on a personalized GI microbiome, can improve postprandial glucose regulation in prediabetics and T2D. Already a GI microbiome modulator (GIMM) has been developed and tested to treat prediabetes, which opens new avenues for drug discovery.
  4. Mikkelsen, Kristian H.; Allin, Kristine H.; Knop, Filip K. (2016). "Effect of antibiotics on gut microbiota, glucose metabolism and body weight regulation: a review of the literature". Diabetes, Obesity and Metabolism. 18 (5): 444–453. doi:10.1111/dom.12637. PMID 26818734. S2CID 44953511.
  5. Falagas ME, Kompoti M (July 2006). "Obesity and infection". Lancet Infect Dis. 6 (7): 438–46. doi:10.1016/S1473-3099(06)70523-0. PMID 16790384.
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