A new study of the Faculty of Medicine of the University of Washington in St. Louis (United States) can help explain how excess weight can contribute to diabetes and can provide researchers with an objective to help prevent or delayDiabetes in some people at risk.
The findings, which have been published in the magazine 'Cell Metabolism', suggest that many people with high insulin levels, an early score of the risk of diabetes, also have defects in an important enzyme for the processing of a key fatty acid of thediet.
"Between 30 and 40 million people in the United States they have type 2 diabetes, and another 90 to 100 million have risk factors that make them prone to develop type 2 diabetes in the future," said principal researcher Clay F. Semenkovich, Director of the Division of Endocrinology, Metabolism and Lipid Research of the Faculty of Medicine.
"Many at risk of diabetes have high insulin levels, a distinctive seal of insulin resistance and a sign that problems can be brewing. If we could intervene before they really develop diabetes, we could prevent significant health problems, such asheart disease, chronic kidney diseases, nerve damage, loss of vision and other problems, in a large number of people, "he said.
When a person has too much body fat, he tells the beta cells of the pancreas that they secrete more insulin.When insulin levels rise and remain high, the body can become insulin resistant and, finally, beta cells that secrete insulin can fail, which leads to diabetes.
Studying human fabric samples, Semenkovich, Professor Irene E. and Michael M. Karl;the first author Guifang Dong, PhD, senior scientist;Xiaochao Wei, Associate Professor of Medicine;and other researchers at the University of Washington found that insulin overproduction involves a process called palmitilation.This is the process by which cells join the fatty acid palmitate to proteins.
Thousands of human proteins can be joined to the palmitate, but the researchers discovered that when this fatty acid is not eliminated from proteins in beta cells, the final result is diabetes.When examining tissue samples of thin or overweight people, with and without diabetes, researchers found that people with diabetes had deficiency of an enzyme that eliminates the palmitate of beta cells.
"Hypersecretan insulin because this process goes wrong and cannot properly regulate the liberation of insulin from beta cells. The regulation of insulin release is partly controlled by this process of palmmitilation," said Semenkovich.
