How to lose weight fast in 2 weeks

How to lose weight fast in 2 weeks

  study the normal metabolism in the body. For example: lactose metabolism (milk sugar) and normal galactose are studied by studying metabolism in patients who have no ability to break down galactose. Researchers over the years have also come to realize that there are physiological conditions that mimic a disease. Example: Use hunger research as diabetes research (creating keto bodies, etc.). And so whenever there is a defect in metabolism, researchers try to learn from it about normal metabolism. The syndrome described below is another example.

Some people have a defect (Lipodistrophy-Lipodistrophy), because of which they have no adipose tissue at all. Defects suffer from partial or complete loss of body fat. This defect can be hereditary or acquired - HIV patients sometimes develop this syndrome. The problems that people with low fat tissue make us realize that fat tissue is an important organ of importance to our health. Catapult in adipose tissue can cause similar health problems to those caused by fat proliferation.
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The most obvious symptom of the defects is the external appearance. The loss of subcutaneous fat and the overgrowth of the muscles causes the defects to become very lean and lean. Another phenomenon is the hormonal equilibrium violation that can cause excessive growth to height. Syndrome sufferers suffer from constant hunger. Normally, body fat regulates appetite by producing the hormone leptin. Without leptin the person feels like he is starving. Lack of fat storage in the defect causes very high blood lipid levels and therefore 100 times the incidence of heart disease in the general population. Scientists who have studied this phenomenon have found ways to treat some of the symptoms, such as dieting. Another solution, which is still experimental, is to give leptin injections to prevent the constant hunger.

The researchers found another aspect of the impairment that at first seemed very strange to them. All those with syndrome develop type 2 diabetes which is also the disease that develops as a result of obesity. Remember - type 1 diabetes is caused by the immune system that destroys the pancreas cells of insulin, which is the hormone that regulates blood glucose entry into cells. The initial cause of type 2 diabetes is insulin resistance.

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How can a complete deficiency in adipose tissue cause the same disease caused by excess adipose tissue?
At first glance it seems absurd. As mentioned above, insulin resistance is the major cause of type 2 diabetes, which means that cells do not respond well to the insulin command to absorb sugar. When this happens, blood glucose levels rise and can cause a variety of problems that we talked about when we talked about diabetes.

Because of the high blood glucose levels found in type 2 diabetics, the researchers first thought it was a carbohydrate metabolism disease. Today there is much scientific evidence that this is a disease of fat metabolism. If the body cannot properly store the fat whether the fat reservoir is full (obesity) or if it is non-existent (lipodystrophic), the cells cannot respond to the insulin command. The researchers call it fat-lipotoxicity. This insight can offer new ways to treat type 2 diabetes.

Most of the new insights into type 2 diabetes have come from lipodystrophic syndrome research. These patients cannot store fat in the normal way and so their body directs the fat to muscle or liver tissue and there it starts to cause problems. A similar process occurs in obese people.

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You should know the great benefit of the fatty tissue in our bodies. This tissue stores the fatty acids until we need them. But adipose tissue is not bottomless. If we over-eat for years, the reservoirs fill up and the excess fatty acids overflow to the muscle tissue just as it does in the lipodystrophy locks. When their fatty acids or prodrugs accumulate in muscle cells, they activate insulin resistance. This is why all obese sufferers also have insulin resistance. Insulin resistance is very significant in muscle cells, as they are the most important blood glucose consumer and therefore their resistance is the most important cause of type 2 diabetes.

Normally, the insulin secreted from the pancreas as a result of the gland being stimulated by the glucose, binds to the receptor located on the outer surface of the muscle cell. This binding triggers a sequence of signals that trigger the cell's various responses to insulin. The most important response is the transfer of glucose carriers from the intracellular reservoirs to the outer membrane of the cell from which they can enter the glucose into the cell. For people with obesity and probably also for lipodystrophy, excess fatty acids poison the process in a way that is not yet clear to researchers. Probably a key step is to turn the fatty acids into a ceramide (tying the sugar chain to the fat and not going into the formula). Excess fatty acids mean increased formation of ceramide. Researchers have shown that ceramide interferes with the movement of glucose carriers toward the outer membrane of the cell and activates molecules that block the signal transfer of insulin within the cell.

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Lamaride has another form of effect on the development of diabetes mellitus 2. It appears to destroy the pancreatic insulin cells. In the early stages of the development of insulin resistance, these cells compensate for the decrease in insulin response by increasing its formation. The ceramide causes the pancreas cells to activate their self-destruct mechanism and thus the pancreas's ability to produce insulin decreases. Experiments in animals have shown that leptin prevents this damage. As mentioned above, researchers believe that people with obesity have deficiencies in leptin production and one of the suggested solutions to prevent their incessant hunger is leptin injection.