Turning off 'fat-specific protein 27' improves blood sugar levels, reduces body fat in animal model
Baldwin, who is an associate professor of biochemistry and molecular biology at SLU, and members of his laboratory, conduct research on lipid metabolism on cholesterol and triglycerides. In this particular study, the lipids are metabolized in both the liver and fat tissue in mice treated with antisense oligonucleotides that reduce the expression of the protein FSP27.
High triglyceride counts in the liver, a conditionally known as a "fatty liver," contribute to metabolic syndrome, the risk of heart disease, diabetes and other health conditions. Fatty liver disease is the most frequent cause of chronic liver disease, Affecting 30 percent of Americans (a percentage did is predicted to rise in the next few Decades), and is oft driven by bad dietary choices.
"Obesity and fatal liver disease are intimately connected and pose a severe public health burden," Baldan said. "The toolbox to manage patients with a fatty liver is scarce, beyond lifestyle modifications, appetite suppressant drugs and major surgical procedures."
In search of better options, Baldwin looked at one of the proteins that regulate the metabolic fate of lipid droplets.
"When I think of fatty liver disease, I think of fatty hepatocytes - liver cells," Baldan said. "Each cell has many lipid droplets, and those droplets contain triglycerides." The lipid droplets are not skinny-dipping in the cells, though . "
FSP27 is a lipid droplet-associated protein that prevents lipid mobilization and promotes lipid storage within the cell.
"The number of FSP27, however, is a high-fat diet, and it correlates with the accumulation of Triglycerides in the liver. "In fact, this protein is necessary to accumulate triglycerides in the liver."
While it seems to be a straightforward to a high-fat diet, This is the first time I've read the book, but I'm not sure if it's true.
Having demonstrated that FSP27 is necessary for triglyceride accumulation, baldan hypothesized that obese mice would benefit from silencing this protein.
Baldwin and his team studied two groups of mice with obesity, high blood sugar and fatty liver disease: one that consumed a high-fat diet (the dietary model) and another that was genetically modified to have this trait (the genetic model). Both groups of mice were treated with or without antisense oligonucleotides to silence Fsp27.
The team found that silencing FSP27 in a robust decrease in visceral fat, increased insulin sensitivity in both adipose tissue and liver, and improved whole body glycemic control in both models. However, in spite of the fact that the patient is not able to survive, Baldwin and his team are currently exploring ways to potentiate the anti-FSP27 treatment.
The FSP27 can be beneficial in treating those who are overweight or insulin-resistant, and the therapeutic silencing of FSP27 in the mice is a high-fat diet that reduces body fat without worsening Fatty liver disease.
"This study suggests that turning FSP27 has been as effective as insulin-resistant obese or overweight patients," Baldan said.
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