Obesity is a common group of metabolic syndrome. When the body eats more calories than calories, the excess calories are stored in the body in the form of fat, which exceeds the normal physiological requirements, and when it reaches a certain value, it becomes obesity. Normal male adult fat tissue weight accounts for 15% to 18% of body weight, and women account for 20% to 25%. With the increase of age, the proportion of body fat increases accordingly. Regarding the method of evaluating obesity, if there is no obvious cause, it is called simple obesity, and those with a clear cause are called secondary obesity.
Common cause
Excessive diet, too little fat metabolism, genetics, etc.
Common symptoms
Simple obesity has a slow weight gain and rapid increase in secondary short-term; often combined or aggravated hypertension, coronary heart disease, diabetes, hyperlipidemia, cholelithiasis, etc.
Cause
The external cause is mainly due to excessive diet and too little activity. Calorie intake is more than calorie expenditure, making fat synthesis more important than obesity. It is obese due to disorder of fat metabolism.
Genetic factor
The incidence of simple obesity in humans has a certain genetic background. Some studies have suggested that one of the parents is obese, and the child's obesity rate is about 50%; both parents are obese, and their child obesity rate rises to 80%. Human obesity is generally considered to be polygenic, and heredity plays a prone role in its pathogenesis. The formation of obesity is also related to the interaction of lifestyle behavior, feeding behavior, hobbies, climate and psychosocial factors.
2. Neuropsychiatric factors
It is known that there are two pairs of nerve nuclei associated with feeding behavior in the hypothalamus of humans and various animals. One pair is the contralateral nucleus, also known as the satiety center; the other pair is the ventrolateral nucleus, also known as the hunger center. When the center is full of excitement, there is a feeling of fullness and refusal to eat. When it is destroyed, the appetite increases greatly. When the hunger center is excited, the appetite is strong, and when it is destroyed, it is anorexia and refuses to eat. The two regulate each other, restrict each other, and are in a state of dynamic equilibrium under physiological conditions, so that the appetite is regulated in a normal range and maintains a normal body weight. When the lesion occurs in the hypothalamus, whether it is the sequela of inflammation (such as meningitis, encephalitis), trauma, tumor and other pathological changes occur. If the ventromedial nucleus is destroyed, the ventrolateral nucleus function is relatively phlegm and then gluttony. Causes obesity. Conversely, when the ventrolateral nucleus is destroyed, the ventromedial nucleus functions relatively sputum and then anorexia, causing weight loss.
Cause
The external cause is mainly due to excessive diet and too little activity. Calorie intake is more than calorie expenditure, making fat synthesis more important than obesity. It is obese due to disorder of fat metabolism.
Genetic factor
The incidence of simple obesity in humans has a certain genetic background. Some studies have suggested that one of the parents is obese, and the child's obesity rate is about 50%; both parents are obese, and their child obesity rate rises to 80%. Human obesity is generally considered to be polygenic, and heredity plays a prone role in its pathogenesis. The formation of obesity is also related to the interaction of lifestyle behavior, feeding behavior, hobbies, climate and psychosocial factors.
2. Neuropsychiatric factors
It is known that there are two pairs of nerve nuclei associated with feeding behavior in the hypothalamus of humans and various animals. One pair is the contralateral nucleus, also known as the satiety center; the other pair is the ventrolateral nucleus, also known as the hunger center. When the center is full of excitement, there is a feeling of fullness and refusal to eat. When it is destroyed, the appetite increases greatly. When the hunger center is excited, the appetite is strong, and when it is destroyed, it is anorexia and refuses to eat. The two regulate each other, restrict each other, and are in a state of dynamic equilibrium under physiological conditions, so that the appetite is regulated in a normal range and maintains a normal body weight. When the lesion occurs in the hypothalamus, whether it is the sequela of inflammation (such as meningitis, encephalitis), trauma, tumor and other pathological changes occur. If the ventromedial nucleus is destroyed, the ventrolateral nucleus function is relatively phlegm and then gluttony. Causes obesity. Conversely, when the ventrolateral nucleus is destroyed, the ventromedial nucleus functions relatively sputum and then anorexia, causing weight loss.
3. Endocrine factors
Many hormones such as thyroxine, insulin, and glucocorticoids regulate food intake, so it is assumed that these hormones may be involved in the pathogenesis of simple obesity. Obesity leads to hyperinsulinemia to insulin resistance, and hyperinsulinemia lowers the insulin receptor and increases insulin resistance, thereby forming a vicious circle. Increased insulin secretion can stimulate the increase in food intake, while inhibiting the decomposition of fat, thus causing accumulation of fat in the body. Sex hormones may play a role in the pathogenesis of simple obesity.
Eating too much can produce excessive intestinal inhibitory peptide (GIP) by stimulating the small intestine, and GIP stimulates islet beta cells to release insulin. In the case of hypopituitarism, especially when the growth hormone is reduced, the gonads and thyroid dysfunction caused by the reduction of gonadotropin and thyroid stimulating hormone are reduced, a special type of obesity may occur, which may be related to a decrease in fat mobilization and a relatively increased synthesis. Clinically, obesity is more common in women, especially those who are maternal or menopausal women or oral female contraceptives, suggesting that estrogen is associated with fat anabolism. When the adrenal cortex is hyperactive, cortisol secretion increases, promotes gluconeogenesis, increases blood sugar, stimulates insulin secretion, and thus increases fat synthesis, while cortisol promotes fat breakdown.
 
3. Endocrine factors
Many hormones such as thyroxine, insulin, and glucocorticoids regulate food intake, so it is assumed that these hormones may be involved in the pathogenesis of simple obesity. Obesity leads to hyperinsulinemia to insulin resistance, and hyperinsulinemia lowers the insulin receptor and increases insulin resistance, thereby forming a vicious circle. Increased insulin secretion can stimulate the increase in food intake, while inhibiting the decomposition of fat, thus causing accumulation of fat in the body. Sex hormones may play a role in the pathogenesis of simple obesity.
Eating too much can produce excessive intestinal inhibitory peptide (GIP) by stimulating the small intestine, and GIP stimulates islet beta cells to release insulin. In the case of hypopituitarism, especially when the growth hormone is reduced, the gonads and thyroid dysfunction caused by the reduction of gonadotropin and thyroid stimulating hormone are reduced, a special type of obesity may occur, which may be related to a decrease in fat mobilization and a relatively increased synthesis. Clinically, obesity is more common in women, especially those who are maternal or menopausal women or oral female contraceptives, suggesting that estrogen is associated with fat anabolism. When the adrenal cortex is hyperactive, cortisol secretion increases, promotes gluconeogenesis, increases blood sugar, stimulates insulin secretion, and thus increases fat synthesis, while cortisol promotes fat breakdown.
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