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Rachel and her husband chose to adopt a baby instead of meeting the challenges of handling a high risk pregnancy and Rachel’s type 1 diabetes at the same time. She shares their thought process and ultimate happy ending about the decision to bring a child into their lives.
Hosting Hardball on MSNBC and The Chris Matthews Show keep Chris Matthews working long hours. But Matthews got a lesson in priorities and made some life changes when he was diagnosed with type 2.
Olivia and her dog both have diabetes and today they comfort and encourage each other through the rigors of dealing with the disease. Plus, find out what it means when your domestic pet is diagnosed with diabetes.
Smoking has severe effects on your diabetes and your health. Learn why diabetes and smoking are an especially bad combination and get some tips from the experts on how to quit.
CGM is a relatively new technology, but the information it provides is invaluable. Find out what CGM offers and whether it could help you.
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Latest Type 2 Issues Articles
The word leptin comes from the Greek word leptos, meaning thin. A hormone produced by fat cells, it binds to a spot in the brain known as the satiety center, thereby announcing to the brain that the body has had enough to eat, that plenty of energy is stored in the fat, and that there is no need to eat any more right now. In short, its effect on the brain is to reduce appetite.
Obese people have a lot of stored fat, and they produce unusually high levels of leptin. Unfortunately, their leptin doesn't work like it's supposed to. Why that occurs was the subject of recent research about leptin's effects on beta cells, performed by scientists at the Joslin Center. Previous test tube studies have found leptin receptors in the pancreas as well as the brain. When leptin binds to the pancreas receptors, it inhibits insulin secretion in the beta cells; that is, it keeps insulin levels from getting too high.
To figure out why that mechanism fails to work in obese people, the researchers engineered themselves some mice that lacked leptin receptors in the pancreas. Those mice showed improved glucose tolerance, greater insulin secretion, and beta cell growth. Since leptin keeps insulin levels from getting too high, the lack of leptin action apparently enhanced beta cell functioning and promoted insulin secretion.
Then the researchers put those engineered mice and some control mice on a high fat diet. Both groups of mice grew obese, but, oddly enough, the mice without the leptin receptors developed glucose intolerance and insulin resistance, both of which are way stations on the road to diabetes.
The researchers speculate that leptin resistance in pancreatic beta cells somehow contributes to high insulin levels, beta cell failure, and the consequent glucose intolerance experienced by obese people. Future studies will look at the interaction of insulin and leptin signaling in beta cells in an effort to further explain the relationship between diabetes and obesity.
Sources: Joslin Diabetes Center, October 2007; Wikipedia; Journal of Clinical Investigation, September 2007
Categories: Professional Issues, Type 2 Issues
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