How to control a weight?

It has been established that the so called hypothalamus takes active part in the regulation of fat metabolism. In 1911 I.P.Pavlov expressed an idea about the existence of satiation center in the hypothalamus. He believed that the feeling of hunger and satiation depends on the filling of the stomach. To some extent this assumption is true now. In 1951 the Indian scientist B.K.Anand found out that satiation center of hypothalamus consists of two parts: the hunger center (appetite) which is located in the lateral nucleus, and satiation center which is in the median nucleus.

Stimulation of the hunger center by the weak flow makes animals look for food and absorb it without restraint, which leads to obesity. On the contrary, the stimulation of the satiation center causes the condition of pleasure in the animals and even bliss in full food refusal, but the result is exhaustion. As Anand indicated, the mechanism is not confined to satiety. The satiation center is connected with the hunger center by inhibitory nerve fibers. The hunger center is inhibited at the satiation. Such mechanism under the normal physiological conditions prevents people from overeating.

Both centers interact with the other parts of the brain, involving emotions and shaping behavior and habits. The selective destruction of the median nucleus (in rats, cats and primates) causes a strong hunger, the unrestrained desire for food and a great excess weight. Persistent refusal of food, exhaustion and starvation develops during the destruction of the lateral nucleus.

It was established that adrenalin-like transmitters of nerve impulses excite the satiation center and as a result there is a feeling of satiety. The drugs like benzedrine which were used during the war to suppress hunger and sleepiness, tried to use at peacetime, but unfortunately, it turned out that they have side effects, and at long administration it is not effective.

The satiation center is regulated by serotonin. It was started the development of the drugs which affected this center but the given drug - fenfluramine - causes many side effects and now is forbidden.

Different hormones may influence on the hunger center including vasointestinal polypeptide, intestinal enterohormones which are emitted in response to food and suppresse appetite, and others. A lot of mechanisms are known that regulates ingestion but not weight.

In 1994, the American scientist George Friedman discovered a new hormone leptin. It is synthesized by adipocytes when they are full of fat and as if are "full up". The leptin production is stimulated by insulin. Leptin "comes" to brain with blood flow and is caught by the median nucleus of the hypothalamus causing a feeling of satiety and the production of inhibitory signals which addressed to the hunger center. At the same time the production of a special neuropeptide Y is suppressed by the hunger center which stimulates feeding behavior, insulin production and, finally, the accumulation of fat in the adipocytes. Thus the circle closes: excess fat - the hunger suppression - the reduction of neuropeptide Y production - termination of insulin elimination and decrease of leptin elimination. It is on the contrary at the losing of weight.

In 1997 a group of scientists published an article which stated that at the excessive formation of leptin activates the sympathetic nervous system. This system which, in addition, working through the newly opened beta 3-adrenergic receptors (earlier it was considered that there was only two types), activates lipolysis of adipose tissue, i.e. its destruction with further burning (especially at visceral obesity).

It seems that the excessive fat accumulation indicates a little leptin in the body. But among the patients with primary obesity only about 20% have leptin deficiency, and 80% have this peptide in plenty. Apparently, in the latter the sensitivity to leptin is reduced, i.e. there is a lot of leptin but it helps a little. The same picture is observed in diabetes of the 2 type: there is a lot of insulin but cells do not react to it.

Lypostasis (the mechanism of fat balance) can be figuratively imagined as a barrel with two tubes. In the first tube the fat flows in, and in the second - flows out. At the primary obesity lypostasis moves the adjusting of the body weight (the tube with flowing out and burning fat in outlet) to the higher level accepting available fat amount as insufficient.

In general, the primary obesity is defined as the manifestation of absolute or relative leptin deficiency against the violations of dietary habits and hypodynamia.

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