TLR/NF-kB is a reporter gene mice that help in sequencing and recognizing the areas of inflammation. Additionally, the timeframe of inflammation was observed to introduce the connection of high diet and insulin resistance. The results of this experiment showed that in conventionally raised specific pathogen free mice high fat diet induced increase in the body weight unlike germ-free mice. Moreover, fecal slurries analysis provided activation of NF-κBEGFP in GF NF-κBEGFP mice. Thus, high fat diet does interact to promote inflammation which eventually causes weight gain and insulin resistance. (Ding, et al, 2010)
Several tests were made to obtain this result. These methods were body weight and composition observation, sample collection, fasting plasma glucose and insulin measurements, RNA extraction and real-time PCR, and enhanced GFE imaging. Each test was done to test and analyze the body fat composition and inflammation. For …show more content…
The connections made in Ding,et al ,(2010) reinforced a clear understanding of each possible cause of inflammation and the connection of inflammation with high fat diet. Unlike Armougom, et al (2009), the reason of GF mice’s less body fat was stated which provided a clear understanding of the metabolism of less body fat. This information helped in building an explicit comprehension of the research biological mechanism. Ding, et al, (2010) provided beneficial information about the role of lipoprotein, adipose factor, gut bacteria in the body. Additionally, more reliable and constructed approach to prove and connect the hypothesis was provided. For example, they mentioned different researches that indicated high level of fat diet is associated with lower bacteroidetes and increase intestinal permeability. Thus, increased intestinal permeability can lead to modifications of the intestinal microbiota causing inflammation in CONV
Several tests were made to obtain this result. These methods were body weight and composition observation, sample collection, fasting plasma glucose and insulin measurements, RNA extraction and real-time PCR, and enhanced GFE imaging. Each test was done to test and analyze the body fat composition and inflammation. For …show more content…
The connections made in Ding,et al ,(2010) reinforced a clear understanding of each possible cause of inflammation and the connection of inflammation with high fat diet. Unlike Armougom, et al (2009), the reason of GF mice’s less body fat was stated which provided a clear understanding of the metabolism of less body fat. This information helped in building an explicit comprehension of the research biological mechanism. Ding, et al, (2010) provided beneficial information about the role of lipoprotein, adipose factor, gut bacteria in the body. Additionally, more reliable and constructed approach to prove and connect the hypothesis was provided. For example, they mentioned different researches that indicated high level of fat diet is associated with lower bacteroidetes and increase intestinal permeability. Thus, increased intestinal permeability can lead to modifications of the intestinal microbiota causing inflammation in CONV