The main pathogenetic role in the development of
obesity plays a dysfunction of the cerebral cortex
and the hypothalamus and first of all the nerve formations in
posterior hypothalamus, which are part of the food center –
ventromedial and ventrolateral nuclei. Defeat ventro
medial nucleus – “centers of satiety” – leads to excitation
ventrolateral nuclei – “appetite centers.” Increased
the step of food (carbohydrates, fats) due to the excitement of pi
ganglion center leads to a lack of active physical
the accumulation of fat in fat depots.
Essential in the development of obesity may have
decrease in lipolysis (fat splitting) due to predominance
the tone of the parasympathetic division of the autonomic nervous system
system over sympathetic. This leads to the stimulation of insulin production by the p-cells of the pancreatic islets (
Langerhans) followed by obesity. It is believed that
factor contributing to increased insulin secretion and
obesity, is (3-endorphin. Last synth
zyrazov cells of the adenohypophysis. The role of endocrine factors in
The development of normal obesity is small. However, in the development of simp
of tomato obesity to endocrine factors are given
war value. Due to insufficient production of fatty
lysing hormones: ACTH, TSH, STG, thyroxin and triiodothyro
Nina, adrenaline, norepinephrine and glucagon – occurs from below
lipolysis. This is the reason for insufficient use.
Fat depot as an energy source. Development of fat
first of all, symptomatic obesity,
decrease in production of sex hormones, which leads to
the shift of glucose metabolism in the pentose cycle, as well as the increase
production of glucocorticoids that increase glycogen deposition
in the liver and consequently inhibiting lipolysis. Excess
the deposition of fat most often leads to cardiac damage
vascular system, respiratory system with possible development
heart or pulmonary heart disease, impaired
functions of the gastrointestinal tract, liver, etc. When ozire
An increase in the absolute amount of the total and
extracellular fluid with its simultaneous decrease in
intracellular space. Intracellular dehydration
increases with body weight and becomes the most
pronounced with III and IV degrees of obesity (V. P. L a sh w and n).