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?

What is the purpose of body fat? We all have it, some of us a little more than others. As we grow older, some of our diets fall out of balance with our energy needs causing our white fat cells to become swollen.

White fat cells secrete leptin, adiponectin and resistin. Leptin and adiponectin work together in suppressing appetite. Resistin is the newest discovered - and has been found to participate in the inflammatory response and resistence to insulin. It also triggers an immune response to irritation, so it may be the fat cells attempt to shut your piehole because we're not gonna take it. As the white fat cells take on excessive calories they begin swelling, resulting in an inflammatory response.

Inflammation, by definition, is a protective attempt to remove the injurious stimuli (excess calories) and initiate the healing process. As the fat cells dispatch hormones signaling inflammation - one could hypothesize that Type 2 diabetes is a response to an imbalanced diet - calories in versus calories out. So what do our white fat cells do for us? They are designed to store energy for use in times of need. When your body is sending out DEFCON signals of inflammation - I'd say that is a time of need, indeed. Would inducing ketosis till the swelling goes down help?

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.

A small molecule has been identified that controls diabetes in mice and may pave the way to the development of easier treatment for adult-onset diabetes.

This key molecule, called Boc5, can stimulate insulin function and reduce body weight by 20%. The molecule stimulates the production of the glucagon-like peptide1 (GLP1), responsible for metabolizing glucose. The study intended to discover ways to sensitize insulin by stimulating production of GLP1. Boc5 is not powerful enough to become a diabetes or weight loss drug. But researchers suggest that similar compounds could join the latest generation of diabetes drugs, called "incretin mimetics." The first FDA-approved incretin mimetic was Byetta. A second such drug, with the generic name liraglutide, is in clinical trials.

The problem with the existing FDA approved incretin mimetic treatments is that they are large molecules that must be administered through injection. Boc5 is a small fry with big potential. Being a smaller molecule gives hope for a new generation in diabetes treatment in the form of a pill many of us would be happy to swallow.

Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.

SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.

This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.

Elixir Pharmaceuticals is a company focused on age-related diseases such as diabetes and obesity. Elixir released new data on research that ultimately could lead to a treatment for type 2 diabetes.

The research explains the role of ghrelin, a hormone secreted by the stomach. Ghrelin controls appetite by increasing levels before meals and decreasing levels after meals. A lack of sleep produces ghrelin, which stimulates appetite and creates less leptin which, amongst its many other effects, suppresses appetite. Research scientists have developed an anti-obesity vaccine, which is directed against the hormone ghrelin. The vaccine uses the immune system antibodies to prevent ghrelin from reaching the central nervous system, thus producing a desired reduction in weight gain.

The research conducted by Elixir, as well as the obesity vaccination, shows compelling evidence that ghrelin plays a pivotal role in metabolic regulation. Scientists have shown pharmacologic inhibition of the ghrelin receptor results in a reduction in fasting glucose levels, reduction in insulin resistance, and weight loss. This could lead to victorious battle for science in the war on obesity.