A study has explained why sleep loss may contribute to the development of obesity and type 2 diabetes. Think appetite.

The study found that sleep loss reduced glycogen release from the liver. Since the patient was still awake, requiring energy (and none was being supplied) - the islets withheld production of insulin to sustain existing blood sugar. The aftermath of this suspended glucose metabolism resulted in increased hunger. Yikes.

This study may hint at reasons behind the dubious freshman fifteen for a lot of college students. Can the body adapt to being up all night studying and snacking without jolting the counter regulatory response of metabolism?

Today I compose an ode in remembrance for our islets of Langerhan. Their job is far more complex than balancing blood sugar. They balance everything in our metabolism, starting with the hormones that tell us to eat or stop eating. The islets of Langerhan house 4 critical cell groups: beta cells, alpha cells, delta cells, and gamma cells - also referred to as the PP cells and D1 cells.

Beta cells are activated by a rise in glucose which results in secreting insulin. As this insulin lowers the blood glucose, amylin is also released. Amylin supports the stability of blood glucose levels by slowing the rate that digested glucose enters the bloodstream. The alpha cells are the opposite - they are responsible for preventing hypoglycemia by secreting glucagon. Glucagon helps maintain the level of glucose by causing the liver to release stored glucose. Delta cells secrete somatostatin, which is like the hold button of the alpha-beta cell connection, restraining the release of insulin and glucagon. The last of our Langerhan lineup, and seemingly the least understood, is the gamma cells, PP and D1. These cells affect appetite through the secretion of ghrelin or leptin. Ghrelin is a stimulant for appetite and feeding. Leptin is a hormone that suppresses appetite and speeds up metabolism.

To recap Team Langerhan: beta cells respond to rising blood glucose with insulin, alpha cells respond to falling blood glucose with glucagon. Delta cells respond to perfect balance in blood glucose by suppressing insulin and glucagon, and the gamma cells keep an appetite on an even keel with ghrelin and leptin. If the initial blood glucose lowering medicine prescribed affects any one of these hormones (as you can see it does) - it is definitely causing an imbalance in metabolism. As we memorialize the islets of Langerhan- let us consider all they have done for us. Pay tribute to your islets of Langerhan by doing all that is naturally possible to restore metabolic balance in the future. I have a few ideas - but your job today is complete. You are enlightened. Please have a happy and safe Memorial Day!

Neuropeptide regulating appetite may help in developing new diabetes treatments. The neuropeptide called melanin concentrating hormone (MCH) plays a role in the growth of insulin-producing beta cells and the secretion of insulin. MCH is found in the brain and regulates energy balance and appetite.

A previous study conducted at Joslin found an association between high levels of MCH and an increase in the number of beta cells in mice. When we eat food, our body needs more insulin. When MCH induces appetite, it simultaneously increased insulin secretion. This calls upon the beta cells and enhances their growth. If the proteins that mediate the growth mechanism can be identified, it could lead to the development of new drugs that would enhance beta cell growth to treat type 1 and type 2 diabetes.

Sounds great! However, this sounds similar to the function of SYMLIN, which is the synthetic form of amylin. Amylin is a hormone secreted by beta cells at the same time as insulin. If you've heard of Byetta - you've heard of Amylin Pharmaceuticals, the makers of SYMLIN. The researchers at Joslin and the guys at Amylin should get together and do lunch. They might have a lot to discuss between this research and the development of yet another biotechnological blockbuster drug.

Overeating can shut down a natural brain function that is key to preventing common cardiovascular and diabetic diseases..

Researchers found that chronic overeating can overwhelm the neural pathway that regulates the amount of fats flowing into the bloodstream from the liver. The liver is partly responsible for regulating fats entering the blood stream. It produces triglyceride fats the body can turn into LDL (bad) cholesterol, which can cause arteriosclerosis and blood vessel blockage. Glucose can enter the brain when levels are elevated in the bloodstream. When glucose enters the brain, it is broken down into an acidic substance known as lactate. Lactate signals the liver to stop making fat. It appears that chronic overeating can overwhelm the brain's ability to metabolize glucose into lactate. When lactate is no longer produced -- the signal to stop the liver from releasing fat into the blood stops, too. As small arteries get clogged, they create the circulatory problems common in type 2 diabetes, linked to overeating, obesity, and limb amputations.

Smaller portions, less glucose in the brain, better traffic flow. After all - nobody likes getting mixed signals. Let's do all we can to keep the lines of communimcation (and our arteries) open.