Obesity 'linked to onset of diabetes'

Obesity 'linked to onset of diabetes'

Obesity 'linked to onset of diabetes'


A new study has revealed that fat cells release a protein, called pigment epithelium-derived factor, that makes muscle and liver ignore insulin, triggering a chain of events and interactions that lead to development of Type 2 diabetes.

Prof Matthew Watt of Monash University, who led the team, said: "When PEDF is released into the bloodstream, it causes the muscle and liver to become desensitised to insulin. The pancreas then produces more insulin to counteract these negative effects.

"This insulin release causes the pancreas to become overworked, eventually slowing or stopping insulin release from the pancreas, leading to Type 2 diabetes.

"It appears that the more fat tissue a person has the less sensitive they become to insulin. Therefore a greater amount of insulin is required to maintain the body's regulation of blood-glucose.

"Our research was able to show that increasing PEDF not only causes Type 2 diabetes like complications but that blocking PEDF reverses these effects. The body again returned to being insulin-sensitive and therefore did not need excess insulin to remain regulated."

 
According to the scientists, identifying the link is a significant breakthrough in explaining the reasons why obesity triggers the onset of Type 2 Diabetes.

"Until now scientists knew there was a very clear pattern and had strong suspicions that a link existed between the two conditions, but our understanding of the chain of events caused by the release of PEDF shows a causal link.

"Type 2 diabetes patients will benefit knowing the two conditions are linked. We already know that weight-loss generally improves the management of blood glucose levels in diabetes patients.

"Researchers can now move forward knowing this link exists and we can begin to design new drugs to improve the treatment of Type 2 diabetes," Prof Watt said.

The findings are published in the latest edition of the 'Cell Metabolism' journal.

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