Anatomy of Obesity

Anatomy of Obesity: As we age we understand that our bodies tend to gain weight much easier. We also find that it can be much harder to take that weight off. Is there a reason why this is true? If so, is there anything that can be done to reverse the effects?

Metabolism
This has typically been thought of as the culprit in weight gain. If a person gains weight it is often said that their metabolism has become slower with age. While this might be true it doesn’t appear to be the full story.

Introducing Leptin
The secretion of leptin is a function of various glands within the body. The role of insulin is to manage excess blood glucose by determining how to use the glucose (either stored fat or immediate fuel for energy). The role of leptin is to work to suppress hunger (leptin means thin). This may be that magic element that could help us all lose weight, but when we feed our appetite to excesses leptin does something drastic.

The Scars
According to ScienceDaily.com Leptin released a protein called SPARC. “It is thought that leptin, in an attempt to balance energy levels in the body, could trigger SPARC to limit the storage of fat. SPARC can do this by increasing the formation of scars in fat tissue, which can prevent fat being stored safely in the body.”



The researchers are from the University Hospital Aintree, the University of Warwick and Sweden. They discovered that diabetics have an increased level of SPARC, which essentially adds insult to injury.

The Cycle
Insulin is released to manage blood glucose. Leptin is released to suppress the appetite. SPARC is released to stop excess energy from storing as fat. The resulting effect is internal scarring in the fat cells that reduces the effective use of insulin and leptin and potentially the over production of both.

When fat is not stored safely in the body the individual becomes more prone to Type 2 diabetes. Professor John Wilding explains, “We tested fat tissue of patients at University Hospital Aintree and found that an increase in leptin also increases SPARC levels, which reduces the safe storage of fat through the development of abnormal tissue scarring. Scarring of fat tissue is known to increase as we gain weight and we found that this is exacerbated by leptin, as well as an increase in insulin, produced by the pancreas.”

Dr Katarina Kos was the lead author of the research, and she further explained, “Leptin is produced in fat cells to regulate appetite, but the body becomes resistant to the effects of appetite reduction in obese patients. Leptin continues to increase in response to overall fat mass and promotes scarring through increased SPARC levels. Once scarring occurs, the excess nutritional energy from fat cannot be taken up by fat cells and so remains in the blood and begins to gather around organs. As a result, fat cells of people classified as obese, may not fulfill their natural purpose to store fat.”

As a body becomes more obese it is less sensitive to Leptin. When Leptin has to work too hard it releases SPARC that may serve to make fat cells less receptive to accepting fat. This leaves excess blood glucose flowing through the veins, which signals the pancreas to send more insulin. The result of this tiered approach to normal body management is a body that is more susceptible to Type 2 diabetes.

Researchers recommend a reduced calorie diet, which has proven to lower levels of SPARC in the bloodstream. This may also lead to new medical advances in treating both obesity and diabetes.