News article

Chronic intake of Western diet kills mice

Posted:  Monday, June 23, 2014

Mice that were fed high fat western diets died from lethal lung damage, these mice were engineered without the required immune system receptors to recognize pathogens. Cornell researchers studied the impact of western diets have on humans; that has been causing an epidemic of obesity and metabolic syndrome causing high mortality rates in humans.

However, after closer inspection the death of the mice can be attributed to the production of a group of gut bacteria that released toxins into the blood stream causing lung haemorrhaging.

Although the research linking the high fat diets, immunity and gut bacteria is its nascent stage, researchers are consider this achievement as they have opened up new avenue of research.

The researchers Ling Qi et al, main focus was to understand and study the effects of obesity and how it can lead to insulin resistance (or metabolic syndrome) followed with inflammation in turn causing diabetes.

Ling Qi associate professor of nutritional sciences and the principal author of the paper along with Yewei Ji, a postdoctoral fellow, and Shengyi Iris Sun, a graduate student, who are all co-authors, suggested that “With this study, the role of gut bacteria in the mortality of obese patients can be explored,”

The mice were fed high fat diets by Qi and his colleagues, as they attempted to reduce inflammation that is a natural response in engineered mice without receptors. Though the mice got fat, the engineered mice developed and died of pulmonary damage. Through this study researchers found that administration of the antibiotics prevented death.

“We know that [toxins from] gut bacteria are sufficient to cause pulmonary damage,” Qi said. “We don’t know how the bacteria becomes prolific” in the engineered mice, he added.

Both engineered and control mice were put in the same cage to determine whether the control mice would suffer the same fate. As mice are known to eat faeces, the control mice also developed pulmonary damage and subsequently died due to it. The faeces were strained and the fluid was injected into the control mice and they suffered the same fate. So Qi and his colleagues were able to infer that toxins were causing the lung damage. Interestingly, the engineered mice that were fed low fat diets lied a healthier life and thus suggested that the morality rate is based on the diet.

“We believe that bacteria proliferation is related to high-fat diets and a lack of immune system surveillance in the engineered mice,” said Ji. “The results of this study may help dietary choices in immune-compromised patients such as those under radio- and chemotherapy,” added Sun.

Qi and his colleagues will do more research and determine the effects of gut bacteria and also try and identify the bacterial toxins and identify antibiotics that are effective against these bacteria. After further research Qi et al will be able to determine whether there is a co relation between the inflammation and metabolic syndrome which are the main causes of diabetes.