According to the World Health Organization (WHO) more than 420 million people around the world suffer from diabetes and its dire consequences such as cancer, kidney failure, heart attacks. Prevalence of diabetes is growing rapidly around the world and there is an urgent need to better understand and stop the progress of diabetes. Researchers at the Garvan Institute of Medical Research in Australia have found that fat tissue could also be a source of the disease.
The discovery widens our understanding of diabetes from its earlier focus solely on liver and pancreas as the main source for the disease. The new findings, uncovered in mice, show that a particular protein known to be involved in diabetes, is not acting in the liver or the pancreas as was once assumed. Earlier studies have shown that the enzyme protein kinase C epsilon (PKCε) is important for the development of diabetes. Research on mice that have no PKCε produced anywhere in the body have resulted in them not developing diabetes-like symptoms. Even when fed with a high-fat diet (HFD) they were not found to become glucose intolerant — the inability to control blood sugar after eating, as the liver becomes ‘insulin resistant’ and no longer responds to pancreatic hormone insulin.
The researchers found that if PKCε production was removed from liver, the rats continued to develop diabetes when fed with HFD, but when PKCε was removed solely from fat tissue, the mice were protected from becoming glucose intolerant, similar to when PKCε was removed from the entire animal.
The study suggests that PKCε is not progressing diabetes from the liver, but is worsening the disease by acting from fat tissue. The new finding could have wide-ranging and complex implications for diabetes, including therapeutic interventions that block PKCε activity.
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