March 22, 2013

Less X-box More Glucose Trouble in T2D

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xboxWhat role does endoplasmic reticulum (ER) stress play in high blood glucose in T2D? When you bring X-box into the equation, the answer is clear. A new study published in Diabetes shines the light on X-box. 

The endoplasmic reticulum (ER) is important in maintaining  level blood sugar. When ER stress is observed, the beta cells continue to regulate blood glucose by releasing X-box binding protein 1 (XBP1).

All cells in the body that have a nucleus have ER. The ER is like a vascular network that connects to the nucleus. XBP-1 is part of the endoplasmic reticulum (ER) stress response. When the ER is stressed, it triggers XBP-1 as a response that helps blunt the blow.

Alpha cells are the cells that counteract beta cells. Beta cells secrete insulin to lower blood glucose. Alpha cells secrete glucacon to raise blood glucose.  When ER is stressed, this impairs the alpha and beta cells from balancing blood glucose.

Researchers wanted to understand the role of XBP1 in alpha and beta cells. They created knock-out alpha cells, lacking XBP1. Researchers found that the XBP1 deficiency in alpha cells causes an imbalance in the release of insulin and glucagon.

What does this mean for glucose regulation? We need XBP1 to be present to counteract the stress imposed on ER to regulate glucose. A little X-box never hurt anyone. Invariably, this study shows it helps people with T2D.

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