Obesity and the gut microbiome have both been the focus of recent studies. The term "gut flora" refers to the collection of microorganisms—mostly bacteria—that inhabit the human digestive tract. Fascinatingly, bacteria make up about half of our daily fecal output and have been estimated to number in the tens of trillions in the human gut.
There is growing evidence that intestinal flora may have a special role in the development of metabolic diseases such as obesity and type 2 diabetes. This understanding of intestinal flora has continuously increased over time, which has led to the accumulation of this data. At the level of the phylum, the abundance of flora belonging to the Firmicutes is increased in individuals who are obese, whereas the quantity of flora belonging to the Bacteroidetes is decreased. There is growing evidence that some bacteria, such as those belonging to the family Lachnospiraceae and the phylum Firmicutes, may have a role in the development of obesity and type 2 diabetes.
However, little is known about the mechanisms by which intestinal flora contributes to diseases such as obesity and type 2 diabetes.
Recently, Prof. Hiroshi Ohno's team from the RIKEN Center for Integrative Medical Sciences in Japan published important research in Cell Metabolism. The results showed that the abundance of Fusimonas intestine (FI), a symbiotic bacterium of the Trichoderma family, was significantly increased in the intestine of both obese and hyperglycemic humans and mice, and that FI promotes high-fat diet (HFD)-induced obesity and insulin resistance by producing long-chain fatty acids.
Trichophyton spp. FI, a symbiotic bacteria, was discovered to be highly higher in the feces of both obese and type 2 diabetes people and mice when researchers initially sought to extract the dominating bacteria in the intestines of obese and diabetic animal models (db/db mice). 70.6% of the diabetes research participants had FI colonization of their stools, but only 38.2% of the healthy controls did. Furthermore, fasting hyperglycemia and body mass index were favorably linked with FI abundance.
The next step is to examine FI's potential impact on metabolic disorders including obesity. Mice that had been colonized with FI were fed an HFD. In order to create a mouse model of FI with E. coli, the researchers developed a double colonization mouse model, as FI cannot be colonized in germ-free animals alone. Colonized FI mice exhibited greater increases in body weight and adiposity in response to the HFD compared to their uncolonized counterparts. Colonized FI mice showed a moderate rise in blood glucose levels during the insulin tolerance test (ITT) and the oral glucose tolerance test (OGTT).
In other words, mice with FI are more likely to gain weight and fat while happily enjoying the "calorie bomb" and are more likely to have problems with glucose metabolism.
Adipose tissue from FI-fixed mice also showed markedly elevated expression of the inflammatory markers Tnfa, LPS-binding protein (Lbp), and the leptin-encoding gene (Lep). Inflammation caused by the HFD diet appears to be made worse by FI, according to these findings.
Subsequently, the researchers used a random forest model to distinguish lipid metabolites that were characteristically altered in FI+HFD mice. The results showed that methyl transoleate and palmitate were the most distinguishing metabolites in FI+HFD mice. And methyl transoleate is a strongly associated risk factor for cardiovascular disease.
Scientists inoculated germ-free mice with E. coli in which the FadR gene, which controls fatty acid production, was overexpressed. Overexpression of FadR in Escherichia coli led to an increase in methyl transoleate production and an obesity-related phenotype. Similar changes in the related metabolic profile were seen when db/db mice were directly fed methyl transoleate.
resource: https://www.creative-biolabs.com/drug-discovery/therapeutics/rodent-diab...
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