Callan Young

Introduction. Obesity is known as being caused by an imbalance between energy consumption and expenditure. Many scientists, researchers and physicians note that obesity is also linked to genetics, environmental factors, gender, age and socioeconomic status, among others. Recently, research has proved that the human microbiome also provides a major contribution to the development of obesity.1 90% of the gut microbiota consists of either one of the 2 phyla of bacteria: Bacteriodetes, Firmicutes or Actinobacteria.2 These pathogens that reside in our gut are responsible for nutrient metabolism and gut barrier protection in the gastrointestinal tract. The gut microbiota contribution is not well understood; however, studies have shown the composition can influence host metabolism by means of insulin sensitivity and short-chain fatty acid receptor signaling.3,4 When comparing obese and lean mice, the ratio of Bacteriodetes and Firmicutes bacteria is considerably different. The consensus among researchers regarding human microbiota composition is simply that the ratio of Bacteriodetes and Firmicutes is out of balance in obese individuals.1 Modification of the microbiota composition by probiotic administration or fecal microbiota transplant may, therefore, serve as a therapeutic solution for obese individuals. Methods. Review analysis of studies utilizing RNA isolation and fecal microbiota quantification with real-time quantitative PCR (RT-PCR), insulin sensitivity detection through a hyperinsulinemic euglycemic clamp, and GPR43 detection by in situ hybridization.3,4 Results. Insulin sensitivity increased in obese individuals with metabolic syndrome six weeks following infusion of microbiota from lean donors.4 Levels of butyrate-producing intestinal microbiota increased as well. Short chain fatty acid (SCFA) receptor GPR43 utilizing SCFAs produced by intestinal microbiota is abundantly expressed in white adipose tissue. GPR43 is expressed higher in lean mice and was found to suppresses insulin signaling in adipose tissue and promote energy expenditure.3 Conclusion. Studies confirm intestinal microbiota possesses a role in host metabolism and can influence the development of obesity and insulin resistance.1-5 By means of metabolism of nutrients in the intestine, these microbes produce end products that are important energy sources for the host. These end products can alter metabolic homeostasis through insulin signaling and GPR43 signaling in adipose tissue, leading to an obese or lean state.3 Gut microbiota transfer procedures may serve to combat insulin resistance and obesity.4,6,7

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