Researchers from the University of Illinois at Chicago (UIC) College of Medicine have found that dysfunction in a single gene in mice causes fasting hyperglycemia, one of the major symptoms of type 2 diabetes. Their findings were reported online on December 30, 2013 in the journal Diabetes. If a gene called MADD (which codes for MAP kinase-activating death domain protein) is not functioning properly, insulin is not released into the bloodstream to regulate blood sugar levels, says Dr. Bellur S. Prabhakar, professor and head of microbiology and immunology at UIC and lead author of the paper. Type 2 diabetes affects roughly 8 percent of Americans and more than 366 million people worldwide. It can cause serious complications, including cardiovascular disease, kidney failure, loss of limbs and blindness. In a healthy person, beta cells in the pancreas secrete the hormone insulin in response to increases in blood glucose after eating. Insulin allows glucose to enter cells where it can be used as energy, keeping glucose levels in the blood within a narrow range. People with type 2 diabetes don’t produce enough insulin or are resistant to its effects. They must closely monitor their blood glucose throughout the day and, when medication fails, inject insulin. In previous work, Dr. Prabhakar isolated several genes from human beta cells, including MADD, which is also involved in certain cancers. Small genetic variations found among thousands of human subjects revealed that a mutation in MADD was strongly associated with type 2 diabetes in Europeans and Han Chinese. People with this mutation had high blood glucose and problems of insulin secretion – the “hallmarks of type 2 diabetes,” Dr. Prabhakar said.
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