Obesity's effects extend all through the body, and the liver is one of the more serious victims. Poor diet can cause fat to build up in the organ, leading to chronic liver disease and other serious health issues like diabetes and heart disease. Now a team from Saint Louis University has found that switching off a particular protein decreased the body fat and improved the blood sugar levels of mice.

"Obesity and fatty liver disease are intimately connected and pose a severe public health burden, given their high and growing prevalence in both adults and children," says Angel Baldan, lead author of the study. "The toolbox to manage patients with a fatty liver is scarce, beyond lifestyle modifications, appetite suppressant drugs and major surgical procedures. Better medical interventions are sorely needed for these patients."

Such interventions may come in the form of better detection tests for liver diseases connected with obesity, and wearable devices that could boost visceral fat loss and improve blood sugar levels. For this study, the researchers investigated a certain protein associated with regulating how lipid droplets are metabolized.

"When I think of fatty liver disease, I think of fatty hepatocytes – liver cells," explains Baldan. "Each cell has many lipid droplets, and those droplets contain triglycerides. The lipid droplets aren't skinny-dipping in the cells, though. They are coated by proteins. One such protein is called 'fat-specific protein 27,' or FSP27."

The function of body fat is to store energy for later use. But what FSP27 does is prevent those lipids from mobilizing – being used – and instead encourages them to stay put in the cell. A high-fat diet increases the amount of FSP27 and, in turn, the amount of fat that builds up in the liver. Inversely, triglycerides can also accumulate as a result of fasting, which sees the body begin to process more stored fat, sending mobilized fat to the liver for processing.

Knowing this, the team hypothesized that shutting off FSP27 should reduce fat build-up. To test the idea, the researchers used two groups of obese mice, afflicted with high blood sugar and fatty liver disease. The difference was, one group was fed a high-fat diet, while the other mice were genetically modified. Some of each group were then treated with antisense oligonucleotides, polymers which essentially switch off FSP27.

As a result, both groups showed a significant decline in visceral fat, while improving insulin sensitivity at the level of the liver and fat tissue, and glycemic control throughout the body. But despite the improvements, triglyceride levels in the liver didn't decrease.

"This study suggests that turning FSP27 down has potential as a therapy for insulin-resistant obese or overweight patients," says Baldan.

The team plans to look into ways that the treatment could be applied to humans, and is also trying to find ways for the treatment to reduce the lipid build-up in the liver.

The research was published in the Journal of Lipid Research.