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UCSD study clarifies insulin's role in blocking release of energy in patients with type II diabetes

Type II diabetes using medicines called insulin sensitizers, so that the body becomes more sensitive to using its own insulin, rather than compensating for insulin resistance by making more.

In order to understand the mechanisms of insulin resistance present in Type II diabetes, the researchers used a new breed of cellular enzyme reporter to track PKA. The reporter is a “marker?protein, created with special fluorescent tags so that scientists can physically view the protein under a microscope and watch how the live cell activates PKA in real time. The PKA is normally activated inside the adipocyte cell, the major site of energy storage in the body where many aspects of metabolism are controlled. There, energy is stored in the form of triglycerides, commonly known as fat. If a person is obese, excess triglycerides are stored in the adipocytes. The new study shows that insulin weakens the normal linkage between catecholamine receptors and the turn-on of PKA.

“If insulin levels get too high for too long a time ?which happens in many patients with type II diabetes –the normal catecholamine signal that triggers fat breakdown and energy release can be drowned out. This can lead to excessive energy storage in the adipocyte,?said Hupfeld. “This may be one reason why chronic obesity and Type II diabetes are often seen together.?/p>

“By correcting this hormonal imbalance, researchers may at some point improve treatment options for both obesity and Type II diabetes,?said Hupfeld.


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Source:UCSD


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