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Obesity, overweight can lead to diabetes: study | Health
overweight and obese people They are more likely to develop diabetes, but the exact mechanism is not well understood.
A new study at the Washington University School of Medicine in St. Louis may help explain how excess weight contributes to diabetes and may provide researchers with goals to help prevent or prevent it. . slow down diabetes part of the population at risk. The findings suggest that many people with elevated levels of insulin, an early marker of diabetes risk, also have defects in enzymes critical to the processing of critical fatty acids from the diet.
The study was published January 11 in the journal Cell Metabolism.
Also read: Association between fast food consumption and liver disease: a study
“There are 30 to 40 million people in the United States with type 2 diabetes, and another 90 to 100 million have risk factors that predispose them to developing it. type 2 diabetes “This is an important step for the study of lipids,” said Senior Research Fellow Clay F. Semenkovich, M.D., Ph.D., director of the Department of Endocrinology, Metabolism, and Lipid Research at the School of Medicine. Signals that a problem might be occurring. If we can intervene before they actually develop diabetes, we may be able to prevent serious health problems such as: heart disease, chronic kidney disease, nerve damage, poor vision, and other problems ――To many people. “
Too much body fat signals the beta cells of the pancreas to secrete more insulin. The beta cells that secrete insulin to the point of failure can fail, leading to diabetes.
A study of human tissue samples, Prof. Semenkovic, Eileen E. and Michael M. Karl. Lead Author Dr. Guifang Dong, Senior Scientist. Xiaochao Wei, PhD, Associate Professor of Medicine. Other University of Washington researchers have found that insulin overproduction involves a process called palmitoylation. This is the process by which cells attach palmitic fatty acids to proteins.
Thousands of human proteins can bind to palmitic acid, but researchers have found that diabetes is the end result if this fatty acid is not removed from proteins in beta cells. Examining tissue samples from lean and overweight people, people with and without diabetes, they found that people with diabetes lacked the enzyme that removes palmitic acid from beta cells.
“Because this process goes wrong and the release of insulin from beta cells cannot be regulated properly, they oversecrete insulin,” Semenkovich explained. is partially controlled by
With colleagues David W. Piston, PhD, Edward W. Mallinckrodt Jr. Maria S. Remedi, PhD, Professor and Head of the Department of Cell Biology and Physiology, Professor of Medicine and Cell Biology and Physiology, and Fumihiko Urano , MD, PhD, Professor of Medicine and Pathology and Immunology, the research team genetically engineered mice lacking an enzyme called APT1, an enzyme that removes palmitate from proteins. Manipulated mice developed diabetes.
Impaired APT1 function contributed to diabetes risk, so the researchers collaborated with the university’s drug discovery center to screen and identify compounds that could increase the activity of the APT1 enzyme.
“We have identified several drug candidates and are pursuing them,” Semenkovich said. “We believe that increasing APT1 activity could reverse this process and potentially prevent at-risk people from progressing to diabetes.”
Semenkovich said the new discovery of targeting APT1 was an important step, but explained that APT1 is just one of many therapeutic targets.
“There are several ways that type 2 diabetes can develop,” he said. There appears to be a promising tool that may prevent
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