Tolerance test the glucose is a standard method to identify diabetes. But a new study offers another method that can detect diabetes much earlier.
Every year diabetes kills 3.4 million people worldwide, and it is expected that this figure will continue to grow. He kills people in secondary diseases such as heart disease, stroke and kidney failure. And the longer the diabetes is not controlled, the greater the risk of developing these diseases, so early detection is vital.
Diabetes occurs when the body can no longer regulate blood sugar levels. Blood sugar is controlled by insulin, a hormone produced in the pancreas. This hormone reduces the level of glucose in the blood, forcing the body’s cells to absorb it, where it is stored or used for energy.
There are two main forms of diabetes: type 1 and type 2. Type 1 is an autoimmune disease in which the body destroys cells in the pancreas that produce insulin. Type 2 is a progressive disease in which the body first becomes resistant to insulin. Initially, the body produces more insulin to control the blood sugar level, but eventually the pancreas wears out, and the level of glucose in the blood becomes dangerously high.
Fat as a new token
In type 2 diabetes the body’s cells become resistant to insulin before the development of diabetes. This led the scientists from the University of Cambridge to wonder, is it possible to detect early stages of disease, when the body is resistant to insulin, but before the pancreas wears out, and the level of glucose in the blood increases. Scientists have focused on the study of how the body becomes immune to insulin. To do this, they examined the fat, not glucose.
It is known that obesity is the leading cause of type 2 diabetes. It is believed that one of the reasons why obesity causes diabetes is the inability of adipose tissue to work properly.
Healthy fat tissue absorbs the fat we eat and stores it until then, until needed for fuel, for example, at night when we sleep. When people with obesity eat, their fat tissue does not absorb fat. Instead, the fat is directed to other organs such as liver and muscle where it causes insulin resistance.
Insulin acts as a warning device and is attached to the receiver on the outside of cells called insulin receptors. Insulin receptor activates numerous other signals within the muscles or liver to tell them what to do, for example: to make glucose. But when the cell is full of fat, it drowns out the signals. Fat cells do not react to insulin, making them insulin-resistant. The body tries to circumvent this by increasing the amount of insulin to force the cells to accept the necessary glucose.
Strong evidence
The concept that defective adipose tissue can cause insulin resistance and diabetes is supported by data from people with lipodystrophy – a condition in which the body lacks fatty tissue. People with this condition have severe insulin resistance and diabetes.
It is important to note that adipose tissue of humans with obesity are also poorly excreted during sleep, and this means that people with obesity have to consume a lot of glucose at night to provide the body with energy.
A test that doctors use to diagnose diabetes is called a test of glucose tolerance. Usually it is held in the morning on an empty stomach. Then, give the man a drink containing glucose (sugar), and blood samples over the next two hours.
People (and mice) are classified as having diabetes if the test detects high levels of glucose in the blood. But researchers believe that some people with obesity to successfully pass the testbecause their fat tissue does not emit a sufficient amount of fat, and their body is programmed to use glucose in times of famine, for example when they sleep.
Conversely, if we give people, suffering from obesity, a large portion of food, the fat that they have stored in the fatty tissue will be supplied to organs such as muscles, and cause insulin resistance, causing glucose levels in the blood rise.
Test Milksheyk
To find out how fat causes insulin resistance and diabetes, the scientists used mice that lacked the gene for PPARy2. Deletion of a gene prevents fat tissue to absorb and release fat, mimicking what is observed in people with obesity.
Despite the fact that their fat is not working properly, it was discovered that mice that lacked PPARy2 perfectly healthy according to the test on glucose tolerance. Scientists wanted to know whether it is possible to detect faulty fat using the test to a large portion of food. But here is the problem: how to force the mouse to eat more food?
Researchers interested in the fact that mice usually pretty meager diet, mostly feed them breadcrumbs. When the mice were transferred to a more varied diet high in fat, they began to eat twice more than usual during the first 24 hours. The scientists collected blood samples before and after 24 hours of overfeeding to make sure that the level of blood glucose and insulin increased.
It should be noted that the method of overfeeding have been tested both in normal mice and those that lack the PPARy2. In normal mice, insulin levels increased twice, and the level of blood glucose remained in the normal range. But in mice that lack the PPARy2, after overfeeding, not only increased blood sugar levels, but insulin levels about ten times, which indicates damage to their metabolism.
It is important to note that tests were performed on young mice, which is equivalent to a 20-year-old people at the age when tests for glucose tolerance were normal. Finally, scientists have determined that when mice with defective adipose tissue had reached middle age, they become metabolic patients, even when eating healthy foods. Samuel Virco, senior research fellow, University of Cambridge, their comments summed up the results of the study:
Our research suggests that some people detect a metabolic disease much earlier, if you replace the glucose in the test for tolerantnosti calorie dairy cocktail, which, besides glucose, sideritis and protein. The next step will be a comparison of ability test for glucose tolerance and shake test прогнозироватьбудущееразвитиедиабета people.