Animal gastrointestinal tract contains a complex community of microbes, whose composition ultimately reflects the co-evolution of microorganisms with their animal host. The gut microbial community of humans and animals has received significant attention from researchers because of its association with health and disease. The application of metagenomics technology enables researchers to study not only the microbial composition but also the function of microbes in the gastrointestinal tract. In this paper, combined with our own findings, we summarized advances in studying gastrointestinal tract microorganism with metagenomics and the bioinformatics technology.
Animals ; Gastrointestinal Tract ; microbiology ; Humans ; Hyperglycemia ; etiology ; Inflammatory Bowel Diseases ; etiology ; Metagenome ; physiology ; Metagenomics ; methods ; Obesity ; etiology

Advances in sequencing technology and the development of metagenomics have opened up new ways to investigate the microorganisms inhabiting the human gut. The intestinal microbiota confer protection against pathogens, contribute to the maturation of the immune system, and regulate host metabolism. The composition of gut microbiota in early life is influenced by mode of birth, diet, and antibiotics. Decreased biodiversity and alterations in the composition of the intestinal microbiota have been observed in many diseases including obesity, neonatal necrotizing enterocolitis, inflammatory bowel disease, and recurrent Clostridium difficile infection. Therapeutic options for the diseases linked to imbalance in the microbiota include modifying the gut microbiota through diet, probiotics, and fecal transplants.
Animals ; Anti-Bacterial Agents/therapeutic use ; Clostridium difficile/isolation & purification/pathogenicity ; Enterocolitis, Pseudomembranous/drug therapy/microbiology/pathology ; Fatty Liver/etiology/microbiology ; Humans ; Inflammatory Bowel Diseases/etiology/microbiology ; Intestines/*microbiology ; *Microbiota ; Obesity/etiology/microbiology

Human gut microbiota plays a key role in the development of obesity. Intestinal flora can regulate energy absorption and nutrition metabolism, increasing the energy harvesting from diet. Alteration of gut flora produces excessive lipopolysaccharide, which, when absorbed into the blood, can induce inflammatory reactions and promote the high-fat diet-associated obesity and metabolic syndrome. Intestinal flora increase visceral fat deposition by lowering the expression of Fiaf in intestinal mucosa. Different immune status also affects the intestinal flora.The gut microbiota is hypothesized to be an environmental factor that contributes to obesity; by interacting with factors such as host and diet, it adjusts the energy metabolism. Antibiotics or probiotics may alter the composition of intestinal microflora and improve the metabolic syndrome, and thus provides new treatment options.
Animals ; Diet, High-Fat ; Gastrointestinal Tract ; microbiology ; Humans ; Inflammation ; etiology ; Mice ; Obesity ; microbiology ; therapy ; Probiotics ; therapeutic use

In recent years, more and more studies have noted the close association between gut microbiota and the development and progression of obesity. Gut microbiota may act on obesity by increasing energy intake, affecting the secretion of intestinal hormones, inducing chronic systemic inflammation, and producing insulin resistance. This article reviews the association between childhood obesity and gut microbiota, as well as possible mechanisms, in an attempt to provide a reference for the etiology, prevention and treatment of childhood obesity.
Animals ; Energy Metabolism ; Gastrointestinal Microbiome ; Glucagon-Like Peptide 2 ; physiology ; Humans ; Insulin Resistance ; Obesity ; etiology ; microbiology ; prevention & control

Despite a higher incidence and less favorable outcome of malignant tumors in obese patients, much less recognized is the link between obesity and cancer. The mechanism of the association of obesity with carcinogenesis remains incompletely understood. Postulated mechanisms include insulin resistance, insulin-like growth factor signaling, chronic inflammation, immunomodulation, hyperglycemia-induced oxidative stress, and changes of intestinal microbiome. Insulin resistance leads to direct mitogenic and antiapoptotic signaling by insulin and the insulin-like growth factor axis. Obesity can be considered to be a state of chronic low-grade inflammation. In obesity, numerous proinflammatory cytokines are released from adipose tissue which may involve in carcinogenesis. Hyperglycemia in susceptible cells results in the overproduction of superoxide and this process is the key to initiating all damaging pathways related to diabetes. This hyperglycemia-induced oxidative stress could be one possible link among obesity, diabetes, and cancer development. The role of obesity-related changes in the intestinal microbiome in gastrointestinal carcinogenesis deserves further attention.
Adipokines/metabolism/physiology ; Gastrointestinal Neoplasms/*etiology/microbiology ; Humans ; Inflammation/etiology ; Insulin/metabolism/physiology ; Leptin/metabolism/physiology ; Obesity/*complications/immunology/metabolism ; Oxidative Stress ; Somatomedins/metabolism/physiology

Bacteria ; genetics ; isolation & purification ; Bacterial Physiological Phenomena ; Bacteroidetes ; genetics ; isolation & purification ; Body Mass Index ; Body Weight ; Child ; Energy Metabolism ; Humans ; Infant ; Intestines ; metabolism ; microbiology ; Lactobacillus ; Obesity ; etiology ; metabolism ; prevention & control ; Probiotics ; therapeutic use ; Risk Factors