Gastritis Clinical Trial
Official title:
The Metabolic Contribution of the Human Microbiota to Resting Energy Expenditure
The purpose of our study is to evaluate the metabolic contribution of the human microbiota to resting energy expenditure
There are now >500 million adult humans in the world who are overweight [body mass index
(BMI) of 25.0-29.9 kg/m2] and 250 million who are obese (BMI 30 kg/m2). This growing
epidemic threatens both industrialized and developing countries and has been accompanied by
worldwide increases in obesity-related disorders, including type II diabetes, hypertension,
cardiovascular pathology, and nonalcoholic fatty liver disease. In the United States, 64% of
adults are overweight or obese, prompting the Surgeon General to designate this condition as
the most important public health challenge of our time.
The worldwide obesity epidemic is stimulating efforts to identify host and environmental
factors that affect energy balance. The Human gut contains an immense number of
microorganisms, collectively known as the microbiota. This community consists of at least
1013 citizens, is dominated by anaerobic bacteria, and includes 500-1,000 species whose
collective genomes are estimated to contain 100 times more genes than our own human genome.
The microbiota can be viewed as a metabolic "organ" exquisitely tuned to our physiology that
performs functions that we have not had to evolve on our own. These functions include the
ability to process otherwise indigestible components of our diet, such as plant
polysaccharides, and therefore may have an impact on our energy balance.
Comparisons of the distal gut microbiota of genetically obese mice and their lean
littermates, as well as those of obese and lean human volunteers have revealed that obesity
is associated with changes in the relative abundance of two dominant bacterial divisions,
the Bacteroidetes and the Firmicutes. Turnbaugh et al demonstrated through metagenomic and
biochemical analyses that these changes affect the metabolic potential of the mouse gut
microbiota. Furthermore, this trait is transmissible: colonization of germ-free mice with an
'obese microbiota' results in a significantly greater increase in total body fat than
colonization with a 'lean microbiota'. These results identify the gut microbiota as an
additional contributing factor to the pathophysiology of obesity. It has been suggested,
therefore, that the obese microbiome has an increased capacity to harvest energy from the
diet.
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Observational Model: Defined Population, Time Perspective: Cross-Sectional
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