Diabetes is one of the most rampant diseases in the world and millions of people across the globe are suffering from it. Diabetes is a condition where a person has high blood glucose or blood sugar. This increase can be either due the inadequate insulin production or because of the body cells' incapability to properly react to insulin, or both. A recent study has unearthed another factor that can trigger diabetes.According to a recent study published in the Journal, 'Molecular and Cellular Biology', a certain enzyme called 12-lipoxygenase is the culprit behind triggering diabetes. Researchers at the Indiana University School of medicine have found that 12-LO causes obesity-induced oxidative stress in the pancreatic cells that leads to pre-diabetes and diabetes. The drugs that can interfere with this enzyme can prevent or even reverse diabetes. The enzymatic action by 12-lipoxygenase (12-LO) is the last step in the production of certain small molecules that harm the cell."Our research is the first to show that 12-LO in the beta cell is the culprit in the development of pre-diabetes, following high fat diets," said principal investigator Raghavendra Mirmira from Indiana University's school of medicine.The researchers carried out experiments on mice. They genetically engineered mice that lacked the gene for 12-LO exclusively in their pancreas cells. Mice were divided into two groups, one that were genetically engineered and lacked the enzyme and the other that were not. Both the groups were either fed a low-fat or high-fat diet. Mice from both the groups -who were on the high fat diet- developed obesity and insulin resistance.
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However on examining the pancreatic beta cells of both types of mice, it was found that those from the genetically engineered mice were intact and healthy while those from the controlled mice group showed oxidative damage, demonstrating that 12-LO and the resulting hydroxyeicosatetraenoic acid (HETEs) caused the beta cell failure.HETEs harm the mitochondria, which then fail to produce sufficient energy to enable the pancreatic cells to manufacture the necessary quantities of insulin.
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