Analysis of information sources in references of the Wikipedia article "Infectobesity" in English language version.
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.
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.
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.
