Diabetes, metabolic syndrome, and obesity are an epidemic facing much of the world (specifically the western nations) today. A major contributing factor to this is the Western Diet or SAD (Standard American Diet) which is high in sugar and high in fat.
The association between these diets and obesity has long since been established, however, the role of the gut microbiome has only recently been defined. In a study published in Cell in August of 2022, researchers at the Columbia University Irving Medical Center have identified one of the roles of the microbiome within mice when it comes to protecting against metabolic syndrome, diabetes, and obesity.
To do so, mice were fed the equivalent of a typical Western Diet, high in fat and high in sugar, and the effect was stark. Within four weeks the mice began displaying the signs and symptoms of metabolic syndrome, such as weight gain and insulin resistance.
Prior to beginning the diet a sample of the gut microbiome was taken and measured. After four weeks another sample was collected and the researchers found stark differences between the two samples. There was a steep decline in the amount of filamentous bacteria within the gut, which coincided with a similar decline in the amount of Th17 cells, a cell that is in part responsible for regulating uptake of lipids through the epithelium of the stomach.
To test whether it was the high fat or high sugar part of the diet that was responsible for the decline of filamentous bacteria the researchers repeated the study with a high fat low sugar diet and a high sugar low fat diet. It was found that the filamentous bacteria were only depleted in the high sugar diet, with the high fat low sugar diet having no effect on the population within the microbiome or the amount of Th17 cells.
The relationship between the microbes and the Th17 cells was tested further when mice that lacked the filamentous bacteria to begin with were fed a low sugar diet. These mice, despite the low sugar diet having previously been shown to not effect Th17 cell population, still displayed a decreased amount of the cells and were susceptible to the typical phenotype changes associated with metabolic syndrome.
The researchers concluded that the Th17 cells were commensal to certain types of filamentous bacteria within the gut microbiome and provided some protection against the development of metabolic syndrome.
Whilst this study has only been performed on mice it is a key stepping stone on the way to understanding how the microbiome in humans and other animals can effect, both negatively and positively, our immune system and our health.