Metabolic syndrome is one of the leading causes in causing many diseases such as type II diabetes and obesity. It is a combination of symptoms leading to high risk factors such as
- High blood pressure
- Large Waist Line
- High Blood Sugar
- Unhealthy cholesterol (More LDL than HDL)
- High abdominal or visceral fat
Other external factors that could contribute to these risk factors are smoking, drug abuse or overexposing nutritional needs. Most importantly, these risk factors lead to metabolic and cardiovascular diseases such as coronary heart disease, hypercholesterolaemia, Type II diabetes and stroke. The microbiota has been seen to be responsible in increasing these factors when there is a large physiological shift that disrupts homeostatic microbiota function.
The microbiome has been described to being the centre in controlling metabolic processes, which has redefined some of our understanding towards metabolic diseases. Animal studies with rats, where specific microbes were induced can influence host biology to drive weight loss or gain, which suggests that gut microbiota might be the cause of obesity issues. For example,Suez et.al (2014) (original paper) displayed that experimental mice fed with saccharin water (artificial sweetener) had a higher glucose intolerance compared to control mice with normal glucose water. Fecal samples were taken from these mice and under metagenomic sequencing, it showed that gut microbiota caused a change in glycan fermentation, which increased the synthesis of short-chain free fatty acids and hence it has been hypothesised that these fatty acids can be precursors or signalling molecules to enhance lipolysis. Due to the changes in these metabolic pathways this can induce obesity. Moreover, another recent study by DiBaise, Frank & Mathur (2012) displayed that gut microbiota may be influencing biochemical pathways that induce low grade inflammation, which is clearly seen in obesity patients through the exposure of bacteria lipopolysaccharide derived from intestinal microbiota. Specific bacteria include bacteroidetes and firmicutes corresponded to the increase of fatty acid oxidation which was seen when saccharin was given. Artificial sweeteners have been seen to trigger higher gene expression for enzymes that import, metabolise and produce end products for indigestible polysaccharides which have been suggested to increase free fatty acid formation. These experiments have seen to provide insight to a human subject as well which poses the questioning of the role artificial sweeteners in maintaining weight. Furthermore, diet composition has been strongly correlated with the rapid influence of gut microbiota (DiBaise et.al, 2012). High fat diets have been found to increase bacteroidetes and firmicutes which of course has been found to increase our body’s free fatty acids. These bacteria interact with Toll-like receptor (TLRs) which enhance diet induced obesity and possible insulin resistance (Tsukumo et al, 2007)
Therefore, there has been a large role of microbiota in inducing many responses that could possibly lead to obesity in the long term consequence.
Type II Diabetes
Previously as seen in the obesity correlation with gut microbiota, it is evident that drastic changes in microbiota can inevitably cause glucose intolerance within in human and animal subjects. High fat diets induce obesity and secondary to that is the development of type II diabetes. Type II diabetes occurs with high insulin resistance within the body in which glucose is constantly produced from the liver through the action of glucagon. When the body is unable to reduce blood glucose levels, the patient develops hyperglycemia and hyperinsulinemia which eventually leads to type II diabetes. Microbiota somewhat plays a large role in the development of type II diabetes. Studies show that bacteriodes and ruminococcus were dominant strains that contributed to the disease. Many observations were found including;
- 1) a reduction of butyrate-producing bacteria;
- (2) an increase in mucus degradation thereby potentially impairing gut barrier function (decrease in A muciniphila and increase in R gnavus)
- (3) an increase in oxidative stress.
These findings were commonly found in a mice that were induced with artificial sweetener exposure. From these findings, artificial sweeteners might play a role in inducing all these diseases instead of preventing it, which was the purpose of its original use. The role that the gut microbiota play has been triggered by a profound dysbiosis and are the main contributors to long term complications such as diabetic retinopathy, kidney toxicity, atherosclerosis and diabetic foot ulcers. Zhang & Zhang, 2013 suggested that the gut microbiome interferes with carbohydrate metabolism and host immunity adaptation which gives rise to the development of diabetes. Moreover, as mentioned, gut microbiota has been associated with a triggered low-level inflammatory state and this is a catalysing factor for development of type II diabetes. It has also been found that there has been an overaccumulation of gut derived bacterial inflammatory molecules which has also been thought to accelerate the inflammation in type II diabetes (Zhang & Zhang, 2013).