For the first time, scientists have described how diabetes drugs thiazolidinediones (TZDs) work on your pancreas. The study, published on the journal Diabetes and edited by the American Diabetes Association, has discovered and explained the pharmacological action of TZDs directly on the insulin-producing organ.
The study was led by professor Carme Caelles, from the Cell Signaling Research Group from the Department of Biochemistry and Molecular Biology (Faculty of Pharmacy), together with the team of Dr Ramon Gomis, from the Hospital Clínic of Barcelona (IDIBAPS). These researchers carried out tests with laboratory animal models to discover their results.
Insulin, produced by the pancreas, is the main hormone responsible for regulating your blood sugar levels. Type 1 diabetes, and a need for daily insulin administrations, develops when your pancreas does not produce enough insulin. Type 2 diabetes, on the other hand, is linked to being overweight and physically inactive, and occurs when your body is resistant to insulin, and does not use the hormone effectively. This is the diabetes type that the researchers looked at.
Type 2 diabetes is the most common form of diabetes, affecting the wellbeing of 85-90% of all diabetics. It often shows no poor-wellness symptoms at first, but leads to insulin resistance, which produces hyperglycaemia. This means that your tissues don’t answer the hormone signal and your cells therefore cannot absorb insulin. In response, your pancreatic β-cells produce extra insulin, and this can cause pancreatic hyperplasia. Drugs can improve your blood sugar control in diabetes, and the focus of this study was on TZDs, which are taken orally to reduce insulin resistance and exert insulin-sensitizing action directly on tissues.
Caelles explained, ‘the action mechanism of TZDs is not well known yet. Their receptor (the PPARγ) has been identified; but we do not know yet how they act at molecular level.’ Researchers have already established that TZDs inhibit JNK kinase (c-Jun N-terminal kinase, which inhibits your insulin signals), and Caelles added, ‘Then we proved that the pharmacological action of TZDs includes JNK inhibition and this effect is more effective on adipose tissues, where PPARγ is mostly expressed.’ So that’s JNK and tissues sorted, but what about the pancreas?
Caelles remarked, ‘we knew that pancreatic β-cells also have the receptor PPARγ, but now we know that TZDs have a role in central insulin resistance. All the pharmacological actions described were attributed to the receptor expression in peripheral tissues, such the adipose (peripheral insulin resistance).’ Thanks to this discovery, the team is now looking to analyse the physiologic and biochemical answer of β-cells in animal models in extreme conditions, such as a high-fat diet and peripheral insulin resistance. They also hope to uncover how the insulin resistance mechanism evolves in ageing.
Google+
Diabetes Drug And Your Pancreas: Study Finds The Answer
