Bäckhed investigates how bacteria interact with their mammalian hosts. He is currently a professor at University of Gothenburg, and also an appointed professor at University of Copenhagen and has been guest Professor at University of Oslo. Bäckhed's vision is to prevent and cure cardiovascular disease using the gut microbiota.

Website: https://backhedlab.org/

#1: The gut microbiota as an environmental factor that regulates fat storage

The gut microbiota plays an important role in processing dietary polysaccharides. When adult germ-free mice were colonized with a normal microbiota, they experienced a significant increase in body fat and insulin resistance within a short period, despite eating less. The microbiota promotes the absorption of monosaccharides from the gut, leading to the production of new fat in the liver. A protein called Fasting-induced adipocyte factor (Fiaf) is suppressed in the gut by the microbiota, and this suppression is necessary for the microbiota-induced accumulation of fat in adipocytes. The research suggests that the gut microbiota is an important environmental factor affecting energy utilization and storage in the body.

Bäckhed, Fredrik, et al. "The gut microbiota as an environmental factor that regulates fat storage." Proceedings of the national academy of sciences 101.44 (2004): 15718-15723.

#2: Mechanisms underlying the resistance to diet-inducedobesity in germ-free mice

The gut microbiota is essential for metabolic function and acts as another organ for our human metabolic system. Because of the obesity epidemic, there is increased instrest in how the micriobiome affects energy balence. 

In this experiment, it was found that germ-free (GF) mice are protected against obesity from consuming a Western-style, high sugar, high fat diet. This is associated with their higher levels of AMPK, which is responsible for fatty acid oxidation. However, it was also found that GF mice lacking fasting-induced adipose factor (Fiaf) are not protected from diet-induced obesity, despite having normal AMPK levels compared to wild type. This suggests that GF mice are protected from diet-induced obesity by two complementary but independant mechanisms: elevated levels of Fiaf, and increased AMPK activity. This suggests the microbiome is able to influence both sides to the obesity scale.

What is most interesting is the makeup of the microbiome. When a percentage of Bacteroidetes increase, the Firmicutes decrease by a cooresponding degree, and vice versa. Higher levels of Bacteroidetes have coorelated to lean humans, while higher levels of Firmicutes have been coorelated to obese humans.

Bäckhed, Fredrik, et al. "Mechanisms underlying the resistance to diet-induced obesity in germ-free mice." Proceedings of the National Academy of Sciences 104.3 (2007): 979-984. 

#3: Diet-Induced Obesity Is Linked to Marked but Reversible Alterations in the Mouse Distal Gut Microbiome

This experiment explores the relationship between diet, gut microbes, and energy balance using an obese mouse model fed a Western diet. The diet caused an increase in a specific group of microbes, which was reduced with weight control diets. Transplanting these microbes into lean mice led to increased fat storage. The study used metagenomics and biochemical analysis to uncover features that give these microbes an advantage in a Western diet. The research demonstrates how combining metagenomics, mouse models, and dietary changes can reveal insights into the gut microbiota's unknown members.