(A) causes of morbidity

1. Inside because of the inherent factors of human fat metabolism disorder Erzhi obesity.

(1) genetic factors

Epidemiological survey showed that: simple obesity tend to some family disease. Both parents are obese, they are suffering from simple obesity in children born to both parents than those of normal-weight children born to a high 5 to 8 times. Vanllallie of 1333 was born in 1965 and 1970 conducted a longitudinal survey of children also found that obese parent, with her children grew older, they exceed the normal ratio of (odd ratio) also increases, 1 ~ 2-year-old obese children to adults of early obesity 1.3,3 ~ 5-year-old obese 4.7,6 ~ 9-year-old obese 8.8,10 ~ 14 years of age 22.3,15 ~ 17-year-old is 17.5.

(2) Neuropsychiatric factors

Known human hypothalamus with a variety of animals, the existence of two pairs of feeding behavior with the nucleus. A pair of the contralateral ventral core (VMH), also known as the satiety center; another pair of ventral lateral nucleus (LHA), also known as the hunger center. Satiety center a sense of excitement when saturated antifeedant, destroyed the significant increase in appetite; hunger and excitability when the appetite strong, destroyed the anorexia refuse to eat. Both are interrelated and regulation, mutual restraint, in a state of homeostasis under physiological conditions, so that appetite regulation in the normal range, while maintaining normal body weight. The moment when the lesions occur in the hypothalamus, regardless of the sequelae of inflammation (such as meningitis, encephalitis later), trauma, tumors and other pathological changes, such as the ventromedial nuclear devastation, then the ventral lateral nuclear capabilities without the relative hyperactivity and bulimia bored , causing obesity. On the contrary, when the ventral lateral nuclear devastation, then the function of the relative hyperfunction ventromedial nucleus and loss of appetite, causing weight loss. In addition, the district with the more advanced anatomy of nervous tissue is closely linked, the latter feeding center can also be a degree of regulation. The role of the hypothalamus at blood-brain barrier is relatively weak, the anatomical characteristics of the blood in a variety of biological activity easy migration to the area and thus have an impact on the feeding behavior. These factors include: glucose, free fatty acids, norepinephrine, dopamine, 5 – HT, insulin. In addition, psychological factors often affect the appetite, the central function of prey are subject to mental state, when the spirit of over-excited or nervous and sympathetic adrenergic nerve stimulation, when (especially the dominant receptor α), loss of appetite restrained; when the vagus nerve excitability The increase in insulin secretion, the appetite often hyperactive. Ventromedial nucleus of the central sympathetic and ventral lateral nucleus of the parasympathetic center, both in the pathogenesis of this disease play an important role.

(3) hyperinsulinemia

Hyperinsulinemia in obesity in recent years, the pathogenesis of eye-catching. Obesity and hyperinsulinemia often coexist, but the general opinion of hyperinsulinemia caused by obesity. Hyperinsulinemia of obese insulin release is about 3 times normal.

Insulin significant role in promoting fat accumulation, it was believed that insulin can be used as an indicator of the overall fat content, and in a certain sense, can be used as the monitoring of obesity factor. Some even say that, plasma insulin concentration and the overall fat content was a significant positive correlation.

(4) The brown adipose tissue abnormalities

Brown adipose tissue were only discovered in recent years a kind of fat tissue, and mainly distributed in the subcutaneous and visceral white adipose tissue around the corresponding. Brown adipose tissue distribution is limited, only distributed in the inter-scapular neck, back, axillary, mediastinal and renal around the light brown appearance of their organizations, the cell volume change is relatively small.

White adipose tissue is an energy storage form of excess body the energy stored in the form of a neutral fat, the body can take when the hydrolysis of neutral fat within the fat cells to use. White fat cell volume with the release energy and storage can be changed greatly.

Brown adipose tissue in function is a kind of heat production of organs, that is, when the body ingestion or by cold stimulation, the fat-burning brown fat cells to determine the level of the body’s energy metabolism. In both cases that were termed feeding-induced heat and cold-induced heat.

Of course, the function of this particular protein affected by many factors. Thus, brown adipose tissue thermogenesis in this organization directly involved in the total body heat regulation, excess body heat will be distributed to the in vitro, so that tends to balance the body’s energy metabolism.

5. Other

Eating too much of the small intestine can be stimulated by excessive intestinal gastric inhibitory polypeptide (GIP), GIP stimulated pancreatic β-cell to release insulin. In hypopituitarism, especially growth hormone reduced gonadotrophic and thyroid-stimulating hormone induced reduction in gonadal, thyroid dysfunction may occur a special type of obesity may be related to the mobilization of fat reduction in the relative increase in the synthesis. Clinical obesity in women and more especially by the mother or the female menopause or oral contraceptives are likely to occur, suggesting synthesis of estrogen and fat metabolism. Adrenal cortex hyperfunction, the increased cortisol secretion, promoting gluconeogenesis, blood glucose increased, stimulating increased insulin secretion, so an increase in fat synthesis, while promoting fat decomposition of cortisol.

2. External to eating too much and too little activity-based.

Day of eating more than consumption of calories needed for energy, divided by the liver and muscle glycogen in the form of storage, is an almost completely converted to fat, body fat stored in the library, mainly in triglycerides, due to glycogen reserves are limited, Therefore, body fat, the major storage form of heat. Such as regular intake of excess neutral fat and sugar, makes fat synthesis to accelerate and become external causes of obesity, often in the case of too little activity, such as the cessation of physical activity, reducing manual labor or disease, bed rest recovering from , emerging economies such as obesity, post-natal recuperation.

In short, the simple cause of obesity is not clear. May include genetic and environmental factors, a variety of factors, including the results of the interaction. But regardless of the cause why, the incidence of simple obesity is certainly greater than the energy intake of energy consumption.

Simple Obesity can cause many adverse metabolic disorders and diseases. Such as hyperlipidemia, impaired glucose tolerance, hyperinsulinemia, hyperuricemia. Obese persons, the following diseases: hypertension, coronary heart disease, stroke, atherosclerosis, type 2 diabetes, gallstones and chronic cholecystitis, gout, bone joint disease, endometrial cancer, postmenopausal breast cancer, gallbladder cancer, male colon, rectal and prostate cancer incidence rates are higher. Respiratory syndrome may occur to reduce the pulmonary ventilation, cardiopulmonary dysfunction syndrome (Pickwickian syndrome) and sleep apnea syndrome. In severe cases, can lead to hypoxia, cyanosis and hypercapnia.

(B) the pathogenesis of

In obesity because of the inherent factors of human fat metabolism disorder Erzhi obesity, its pathogenesis and genetic factors, neuropsychological factors, hyperinsulinemia, brown adipose tissue abnormalities and other relevant.

1. Genetic factors common type of simple obesity may be a multi-genetic disease, genetic disease in their playing a role in prone, the parents of their children who were normal weight, risk of obesity, about 10% of the parents of obese whose child obesity rate is about 50%; parents, the two sides are obese, their children’s obesity rates rose to 80%, identical-twin children suffering from obesity, with the risk of close to 100%, but was unable to determine its genetic model. The adopted child obesity had no such a high prevalence, it can not simply acquired by lifestyle factors, such as an explanation.

Leptin (leptin), also known as fat-suppression element, the body obese gene (ob gene) of the encoded protein, is synthesized by fat cells and secretion of a hormone. Leptin and orexin (orexin) the change involved in the pathogenesis of obesity, which are a major role in the hypothalamus of both roles opposite peptide, leptin, so that loss of appetite, increased energy to lose weight, orexin to stimulate eating behavior leading to obesity. Physiological circumstances, when an increase in food intake, fat storage increases, the increase in leptin secretion by the hypothalamus so that the body a series of reactions occur, such as loss of appetite, energy consumption and increase in sympathetic activity increased, the increase in fat breakdown, synthesis reduced, so much weight. When the body is hungry, leptin secretion reduce, but also through the hypothalamus there was a series of protective responses such as increased appetite, reduced energy consumption, body temperature lower, while orexin secretion increases, stimulating eating behavior, in order to maintain body weight will not reduce the too. Obesity in humans, only about 5% may be ob gene synthesis of the existence of anomalies, which in some patients showed an absolute lack of leptin, the obese more than 95% of the principal exception of endogenous leptin resistance, leptin receptor and receptor After the disorder led to increased leptin secretion was secondary, at this point that some similar type 2 diabetes.

2. Neuropsychiatric factors, with a variety of animals, human beings exist in the hypothalamus and feeding behavior of two pairs of the nucleus. A pair of the ventral medial nucleus, also known as the satiety center; another pair of ventral lateral nucleus, also known as the hunger for the hub. Satiety center a sense of excitement when saturated antifeedant, destroyed the significant increase in appetite; hunger and appetite, excitability, when strong, destroyed the anorexia refuse to eat. Both are interrelated and regulation, mutual restraint, in a state of homeostasis under physiological conditions, so that appetite regulation in the normal range, while maintaining normal body weight. When the meningitis, encephalitis sequelae, trauma, tumors and other pathological changes, such as the hypothalamic ventromedial lesions occur in the nuclear destruction of the ventral lateral nuclear capabilities relative hyperactivity and bulimia without disgust, causing obesity. On the contrary, when the ventral lateral nuclear devastation, then the function of the relative hyperfunction ventromedial nucleus and the fear eating, causing weight loss. In addition, the district with the more advanced anatomy of nervous tissue is closely linked, the latter feeding center can also be a degree of regulation. The role of the hypothalamus at blood-brain barrier is relatively weak, the anatomical characteristics of the blood in a variety of biological activity easy migration to the area and thus have an impact on the feeding behavior. These factors include: glucose, free fatty acids, norepinephrine, dopamine, 5 – HT, insulin. In addition, psychological factors often affect the appetite, the central function of prey are subject to mental state, when the spirit of over-excited or nervous and sympathetic adrenergic nerve stimulation, when (especially the dominant receptor α), loss of appetite restrained; when the vagus nerve excitability The increase in insulin secretion, the appetite often hyperactive.

3. Endocrine system changes in patients with obesity, high levels of plasma insulin, glucose load-stimulated insulin levels are high, suggesting that hyperinsulinemia may cause obesity caused by eating more. Hyperinsulinemia of obese insulin release is about 3 times normal. Insulin significant role in the promotion of fat accumulation and its role in the promotion of body fat increased role through the following links:

(1) to promote glucose into the cell, and thus synthesis of neutral fat.

(2) suppression of fat in fat cells to use. It should be noted that some obese people do not exist with hyperinsulinemia, speculated that the cause of obesity is multifaceted.

Facchinetti, etc. In the 13 obese children, it was discovered elevated levels of plasma β-endorphin, and can not be dexamethasone suppression and, correspondingly β-endorphin in obese children is not corticotropin-releasing hormone (CRH) in control, whereas the opiate antagonist naloxone can eat the phenomenon disappears. Obesity on insulin resistance caused by hyperinsulinemia, and hyperinsulinemia can increase insulin receptor down-regulation of insulin resistance, and thus a vicious cycle. An increase in insulin secretion, can stimulate food intake increased, while inhibiting fat breakdown, thus causing accumulation of body fat.

4. Abnormal brown adipose tissue brown adipose tissue is mainly distributed in the inter-scapular neck, back, axillary, mediastinal and renal around the light brown appearance, the cell volume change is relatively small. Brown adipose tissue is a functional organ heat production, while the β3-adrenergic receptor expressed mainly in brown fat, through its role in thermogenesis and the promotion of lipolysis play a role in energy balance and fat storage regulation, the study found, β3 adrenal gland Su-adrenergic receptor gene mutation, and its expression in brown fat obstacles, heat effect and promoting fat decomposition significantly weakened, leading to obesity, increased fat storage.

5. Other eating too much can be produced by excessive stimulation of the small intestine of intestinal gastric inhibitory polypeptide (GIP), GIP stimulated pancreatic β-cell to release insulin. In hypopituitarism, especially growth hormone reduced gonadotrophic and thyroid-stimulating hormone induced reduction in gonadal, thyroid dysfunction, may occur a special type of obesity may be related to the mobilization of fat reduction in the relative increase in the synthesis. Adrenal cortex hyperfunction, the increased cortisol secretion, promoting gluconeogenesis, blood glucose increased, stimulating increased insulin secretion, so an increase in fat synthesis, while the cortisol promote fat break down, due to the different parts of the body adipose tissue and insulin sensitivity of the cortisol sex may be different, the limbs of the role of cortisol in the mobilization of fat, the more sensitive face and neck, and trunk fat synthesis to insulin are less sensitive to the mobilization of the fatty tissues of the limbs and re-deposited on trunk decomposition to form a typical concentric肥胖. Hypogonadism, whether women after menopause, male class of testosterone with or without testosterone the performance of patients with both obesity may be related to disturbance of fat metabolism. In short, the hormone is an important factor in regulating fat metabolism, especially the triglycerides synthesis and mobilization of decomposition by the hormone through the regulation of the enzyme and to determine their increase or decrease trends.