How to find obesity?
The cause of human obesity has not been eliminated before, and there are some factors to consider, such as heredity, nervous system, eating habits, and metabolic disorders.
In particular, energy supply and demand disorders, as well as endocrine regulation dysfunction.
The specific pathogenesis is the same, that is, the dietary energy intake is more than the body consumption, and excess is formed. The excess energy is stored in the body in a small amount, and the slight tissue is increased to form obesity.
First, primary obesity: 1.
Genetic factors Obesity is often associated with heredity.
According to statistics, the normal incidence of obesity in children with parental weight increases by 10%; one parent is obese, the incidence of obesity in both children is obese, and the incidence of obesity in children is as high as 70%.
The same as lecithin grows in the same environment, its body weight is similar; even in different environments, its body weight is smaller than the difference between the isoflavones.
Obese patients are not only hereditary, but also the location of the adult and the state of bone metabolism.
The genetic height of obesity is still manifested in a small number of cells and/or an increase in cell volume.
Diet, lifestyle and social factors often have a history of increased diet, reduced food intake, eating sweets or eating in the middle of each meal causes excess energy.
In the same transient state, there is a habit of sleeping on food and eating more.
Physical activity is too low or bed rest due to fractures, tuberculosis, hepatitis or other causes, resulting in low consumption and obesity.
Especially after people reach middle age, the amount of physical labor is gradually decreasing, and there is often a fracture of the tibia.
Most people develop obesity after stopping regular exercise.
In addition, the energy consumption of obese people is significantly different from that of normal people. When resting and slightly active, the energy used is less than that of normal people; in the same diet, anabolism is more advanced than normal; the basal metabolic rate is relatively reduced, resulting in reduced energy consumption and obesity.
Changes in the social environment have a certain relationship with the occurrence of obesity.
Before liberation, due to low living standards, the incidence of obesity was very low.
After liberation, the incidence of obesity has increased dramatically through improved life.
Family education is related to childhood obesity.
The study found that the only child or the youngest child in the family is prone to obesity.
First and foremost, it is wrong to think that the baby is getting too much fatter, the child is over-nutrition from breastfeeding; excessive love, bad habits, such as snacks, especially candy sweets; and other nutrients stimulate appetite and increase food intake;Lack of necessary physical exercise.
The pre-recognized over-nutrition of children is a preliminary cause of extra years for children and adults.
Second, secondary obesity has obvious complications of endocrine abnormalities, including secondary obesity, including hypothalamic obesity, pituitary obesity, hypothyroidism, Cushing’s syndrome, hyperinsulinemia, and hypogonadism., polycystic ovary syndrome and congenital hereditary obesity.
There are two kinds of nucleus regulating the feeding activity in the hypothalamus. The ventral nucleus is the center of satiety. When excited, the nucleus is full and the food is absent. The ventrolateral nucleus is the obesity center. When the excitement increases, the appetite increases, and they are related to each other.Under physiological conditions, it is in a state of dynamic equilibrium, which makes the appetite in the normal range and maintains normal body weight.
When the hypothalamus is damaged, such as inflammation, injury, new biological stimulation and other pathological changes, the satiety center of the hypothalamic diarrhea nucleus is destroyed, the inhibition of the ventromedial nuclear metabolic center is relieved, and more food is eaten, easy to survive, andA lot of time to eat and lead to obesity.
At the same time, there may be fatigue, lethargy, and low sexuality. Most of these patients have hypogonadal hypoplasia, lack of secondary syndrome, and women have menstrual disorders, amenorrhea, and infertility.
The most common cause of hypothalamic obesity in children is cranial tube tumor, which is ruptured in adults, caused by trauma and new biological stimuli.
Treatment is mainly to treat the primary cause of hypothalamic obesity.
The hypothalamic and high-level nerve activity satiety center is located in the hypothalamic ventral nucleus, and the feeding center is located in the hypothalamic ventral nucleus. There are nerve fiber connections between them, which are functionally related to each other and related to each other.
Animal experiments have shown that these two centers are affected by sugar, traces and amino acids in the body.
Therefore, when the hypothalamic malformation or certain metabolic changes in the body can affect the appetite center to eat more food, resulting in obesity.
This is the initial stage of hypothalamic syndrome.
In simple obesity, it is thought that there is a functional change in the hypothalamus.
The high level of neural activity in the cerebral cortex affects the appetite center of the hypothalamus through neurotransmitters and plays a role in regulating fatigue and satiety.
Mental factors often affect appetite, and the function of the appetite center is subject to mental state.
When the spirit is over-stressed and the adrenergic nerve is stimulated with sympathetic stimulation, the appetite is inhibited. When the vagus nerve is excited and the copying secretion is increased, the appetite is hyperthyroidized.It is known that stimulating hypothalamic diarrhea reduces nuclear secretion to promote increased secretion, so the appetite is hyperthyroidism; stimulation of the ventral nucleus inhibits insulin secretion and strengthens glucagon secretion, so the appetite decreases.
An obvious high-level neurological activity is the hypothalamic appetite center and replication secretion through autonomic nerves, and the boots produce polyphagia or anorexia.
Endocrine factors In addition to hypothalamic factors, other endocrine hormone disorders in the body can also cause obesity.
Among them, insulin changes are recognized as the most critical part of the pathogenesis of diabetes, followed by changes in adrenocortical hormone.
(1) Insulin insulin is a hormone secreted by islet β cells.
Its function is to promote the synthesis of glycogen in hepatocytes, inhibit gluconeogenesis; promote the uptake of glucose into feces by micro-cells, and inhibit the decomposition of feces.
The latter two roles are particularly important in the pathogenesis of obesity.
The characteristics of insulin secretion in obese patients are as follows: 1 The fasting basal value is higher than normal or normal high level; 2 During the oral glucose tolerance test, plasma insulin is further increased with the increase of blood glucose; 3 plasma peak is often later than the blood sugar peak.So after the meal 3?
Hypoglycemia can occur in 4 hours.
In recent years, it has also been found that the number and affinity of insulin receptors in hypertensive patients are reduced, and insulin insensitivity and resistance are present.
Due to the insensitivity and resistance of insulin, in order to meet the needs of glucose metabolism, it must be maintained at a high level, and hyperinsulinemia means that a small number of cells and a few metabolisms mean that the corresponding micro-synthesis increases, the decomposition decreases, and further development is made.
After obesity loses to normal, plasma plasma levels and insulin receptors return to normal, indicating that this change is secondary.
(B) Adrenal Glucocorticoid Adrenal glucocorticoid is a hormone secreted by the adrenal cortical bundle, and is mainly leather alcohol in the human body.
Simple obesity may have a certain degree of adrenal hyperfunction, plasma cortisol is normal or elevated; and in secondary obesity, Cushing’s syndrome plasma cortisol is significantly increased.
As plasma cortisol increases, blood sugar rises, causing an increase in the increase, resulting in excessive micro-synthesis and excessive formation.
Because the trunk and limbs of adult tissue are different in response to insulin and cortisol, they are obese.
(3) Growth hormone Growth hormone is a protein hormone secreted by the anterior pituitary. It promotes protein synthesis, mobilizes storage assistants and anti-insulin action, but in the early stage of action, it still acts as an insulin-like one.
Growth hormone and insulin have complementary effects in the regulation of glucose metabolism.
If the growth hormone is reduced, the insulin action is relatively dominant, alternating with small synthetic increments, resulting in obesity.
It is gradually confirmed that the basal level of growth hormone in diabetic patients is low, and the secretion reaction under stimulating conditions such as arginine, hypoglycemia, obesity and physical activity is also low, and as a result, a large amount of energy cannot be slightly decomposed in neonates and sports activities.
If fasted for 2 days, normal human plasma growth hormone increased from 10 μg / liter to 15 μg / liter, while obese people rose from 2 μg / liter to 5 μg / liter.
This change will gradually increase and disappear and return to normal.
(4) The relationship between thyroid hormone thyroid hormone and obesity is not clear.
Obese people generally do not have thyroid dysfunction, unless the basal metabolic rate may be slightly lower than normal, and does not mean thyroid dysfunction.
Occasionally the two merged.
(5) The male hormone of gonadotropin is mainly testosterone, and more than 90% is synthesized and secreted by testes.
In women with ovarian, adrenal synthesis and secretion.
Estrogen and progesterone are mainly synthesized and secreted by the ovaries.
Sex hormones do not directly affect abnormal metabolism.
The proportion of female body mass is higher than that of males. The percentage of female body impurities is significantly higher than that of males. Except for individual parts, the thickness of the relative parts of males is generally doubled.
In women during pregnancy, menopause, male or male livestock after castration, complications appear obesity.
But the mechanism is still unclear.
It is believed that menopausal obesity is associated with excessive secretion of pituitary gonadotropins.
After the animal castration, the guide island hypertrophied, causing increased replication and promoting unfortunate synthesis.
In addition to a small number of hypogonadal obesity, generally obese people do not have sex hormone secretion disorders.
(6) Platelet glucagon Glucagon is secreted by islet α cells, and its action is opposite to that of insulin, inhibiting accidental synthesis.
Whether plasma glucagon is disturbed in diabetic patients remains to be studied.
(7) Catecholamine catecholamines are produced by the brain, sympathetic nerve endings, chromaffin tissues, mainly adrenal medulla, which can promote micro-decomposition. The cerebral cortex regulates hypothalamic function through catecholamines and serotonin. The sympathetic nerves regulate secretion through catecholamines.
Fecal tissue in obese patients is not sensitive to catecholamine hormones, but returns to normal after weight loss.
In short, the causes of obesity are multifaceted, such as genetic predisposition, eating habits, physical activity reduction and mental factors are important reasons.