Insulin Resistance in Obese People
Obesity often leads to insulin resistance, a condition that can lead to development of type 2 diabetes.
Obesity often leads to insulin resistance, a condition that can lead to development of type 2 diabetes. Researchers at Monash University in Australia have now discovered that behind this result could be a protein called factor derived from the pigment epithelium (FDEP) that is secreted by fat cells.
The authors, who publish their work in the journal Cell Metabolism, provide evidence suggesting that specifically blocks the action of this protein could eliminate some of the complications of obesity.
Explains Matthew Watt, director of the study, “with the obesity increases the release of FDEP fat, leading to higher levels of FDEP in the blood. FDEP it sends a signal to other body tissues, producing insulin resistance in muscle and liver, a major defect that leads to the development of type 2 diabetes.
The high level of FDEP is also associated with an increased release of fatty acids from fat stores, which causes increased levels of blood lipids. This dyslipidaemia could be associated with other complications including cardiovascular disease.
Moreover, according to Watt, found that treatments designed to block the action of FDEP in obese mice reduced the levels of lipids in the blood of animals and eliminated part of their resistance to insulin.
In the current study, researchers conducted an analysis of molecules secreted by fat cells and found that FDEP was one of the most abundant. Watt notes that were established especially in the protein because earlier evidence from other laboratories and himself had shown that FDEP is elevated in the blood flow in patients with type 2 diabetes than those who remain sensitive to insulin.
“We also observed in another study that when mice lost weight by caloric restriction or intervention with drugs, the FDEP of fat cells was reduced,” said Watt.
Now researchers report that levels of FDEP in fat and blood were greater in mice that are obese for different reasons. Levels of FDEP decreased when the animals lost weight. Lean mice to be injected FDEP also respond less to insulin and showed signs of inflammation in the muscles and liver. The authors found that long-term, FDEP contributes to fatty acid levels in blood levels.
“These fatty acids are then mobilized to the muscle and liver, where they accumulate. The accumulation of fat in muscle and liver is harmful because it can cause insulin resistance,” says Watt.
According to investigators, the observed in mice is particularly exciting because it has been recently discovered that the FDEP circulation was higher in people with metabolic syndrome, a set of risk factors including excess abdominal fat, high cholesterol, hypertension and resistance to insulin, and in those with type 2 diabetes.