Etiology and mechanism of obesity

  The etiology of human obesity has not been elucidated so far, and there are several factors to consider, such as genetic, neurological, dietary habits, and metabolic disorders. In particular, energy supply and demand imbalance, and endocrine regulation malfunction, etc.. Specific pathogenesis is consistent, that is, dietary energy into more than the amount of body consumption, the formation of excess, excess energy in the form of fat stored in the body, increased adipose tissue, the formation of obesity.
  A, genetic factors
  Obesity is often related to heredity. According to statistics, both parents are normal weight of their children obesity incidence of 10%; two parents in one obese, children obesity incidence of 50%;
  Both parents are obese, the incidence of obesity in children up to 70%. Identical twins grow up in the same environment, their weight is similar; even if they grow up in different environments, their weight difference is also smaller than the difference between heterozygotic twins. Obese patients not only have heredity of obesity, but also have heredity of fat distribution site and bone state. Obesity genetic tendency is also expressed in the number of fat cells and (or) cell volume increase.
  Second, diet, living habits and social environment factors
  Obese people often have a history of increased diet, eating larger amounts of food, like to eat sweets or add food in the middle of each meal caused by excess energy. In the same calorie situation, have the bedtime before eating and dinner more food habits. The physical activity is too little or because of fracture, tuberculosis, hepatitis or other reasons and bed rest, calorie consumption is less and cause obesity. Especially after middle age, the amount of physical work gradually decreases, and often fat congestion exists in the abdomen and buttocks.
  Most people stop regular exercise after that is developed into obesity. In addition, obese people’s energy consumption and normal people have obvious difference, rest and light activity with less energy than normal people; the same diet under the circumstances of anabolic than normal people hyperactive; basal metabolic rate is relatively low, resulting in less energy consumption, causing obesity.
  Social environment change and obesity occurrence have certain relationship. Before liberation, due to the low standard of living, the incidence of obesity is very low. After liberation, with the improvement of life, the incidence of obesity increased sharply. Family education is related to childhood obesity. Research found that only child or the youngest child in a family is prone to obesity. The main reason is the wrong belief that infant feeding the fatter the better, children from the nursing period on over-nutrition; overindulgence, develop bad habits, such as snacks, especially candy sweets too much; unnecessary nutritional drugs to stimulate appetite, increase the amount of food; lack of necessary physical exercise. It has been recognized that children’s over-nutrition is the main cause of obesity in children and adults.
  Third, the hypothalamus and advanced neural activity
  The satiety center is located in the ventral medial nucleus of the hypothalamus, the feeding center is located in the ventral lateral nucleus of the hypothalamus, they have nerve fiber connection, in the function of mutual regulation, mutual constraints. Animal experiments have shown that these two centers are influenced by sugar, fat and amino acids in the organism. Therefore, when hypothalamic lesions or certain metabolic changes in the body can affect the appetite center to occur overeating, resulting in obesity. This is the main cause of hypothalamic syndrome. In the case of simple obesity, the hypothalamus is mostly considered to have functional changes.
  The higher neural activity of the cerebral cortex affects the appetite center of the hypothalamus through neurotransmitters and plays a role in regulating hunger and satiety. Mental factors often affect appetite, and the function of the appetite center is limited by mental state. When the adrenergic nerves are stimulated with sympathetic excitation due to excessive mental stress, appetite is suppressed;
  When the vagus nerve is excited and insulin secretion is increased, the appetite is hyperactive. It is known that stimulation of the median nucleus of the hypothalamus promotes insulin secretion, so appetite is hyperactive; stimulation of the median nucleus of the abdomen inhibits insulin secretion and enhances glucagon secretion, so appetite is reduced. It shows that the senior neural activity is through the vegetative nerve influence hypothalamus appetite center and insulin secretion, and then produce overeating obesity or anorexia emaciation.
  Fourth, endocrine factors
  In addition to hypothalamic factors, other endocrine hormone disorders in the body may also cause obesity. Among them, insulin changes are recognized as the most critical link in the pathogenesis of obesity, followed by changes in adrenal cortical hormones.
  (A) insulin Insulin is a hormone secreted by pancreatic beta cells. Its function is to promote hepatocyte glycogen synthesis and inhibit gluconeogenesis; promote adipocyte uptake of glucose for fat synthesis and inhibit lipolysis. The latter two roles are particularly important in the pathogenesis of obesity. Insulin secretion in obese people is characterized by.
  (i) fasting basal values higher than normal or normal high levels ;
  (ii) During the oral glucose tolerance test, plasma insulin rises even further with the increase in blood glucose;
  (3) The peak of plasma insulin is often later than the peak of blood glucose, so hypoglycemic reactions can occur 3-4 hours after meals. In recent years, it has been found that the number and affinity of insulin receptors in obese patients are reduced, and insulin insensitivity and resistance exist. Because of insulin insensitivity and resistance, insulin must be maintained at a high level in order to meet the needs of glucose metabolism, and hyperinsulinemia will increase fat synthesis and decrease fat decomposition for adipocytes and fat metabolism, which will further develop obesity. After obese people lose weight to normal, plasma insulin levels and insulin receptors can return to normal, indicating that this change is secondary.
  (B) adrenal glucocorticoid adrenal glucocorticoid is the hormone secreted by the adrenal cortex bundle, in the human body mainly for cortisol. Simple obese people can have a certain degree of adrenocortical hyperfunction, plasma cortisol normal or elevated; and in secondary obesity, Cushing’s syndrome plasma cortisol is significantly elevated.
  Due to the increase in plasma cortisol, blood glucose rises, causing insulin to rise, the latter leading to excessive fat synthesis and the formation of obesity. Because the adipose tissue of trunk and extremities has different responsiveness to insulin and cortisol, it is centripetal obesity.
  (C) growth hormone growth hormone is a protein hormone secreted by the anterior pituitary gland, which has the function of promoting protein synthesis, mobilizing storage fat and anti-insulin, but at the initial stage of action, it also shows insulin-like effect. There is a mutual antagonism between growth hormone and insulin in the regulation of glucose metabolism. If growth hormone is reduced, insulin action is relatively dominant, which can lead to increased fat synthesis and obesity. It has been confirmed that the basic level of growth hormone in obese patients is reduced as well as the secretion response under the stimulation conditions of arginine, hypoglycemia, starvation and physical activity is also low, as a result, a large amount of energy cannot come from lipolysis during starvation and physical activity. If fasting for 2 days, plasma growth hormone rises from 10 to 15 micrograms/liter in normal subjects and from 2 to 5 micrograms/liter in obese individuals. This change will return to normal as obesity disappears.
  (iv) Thyroid hormones The relationship between thyroid hormones and obesity is unclear. Obese people generally do not have abnormal thyroid function, and even though the basal metabolic rate may be slightly lower than normal in obese people, it does not mean that the thyroid gland is underactive. Occasionally, a combination of the two is seen.
  (E) gonadal hormone Male hormone is mainly testosterone, more than 90% of which is synthesized and secreted by the testes. In women, it is synthesized and secreted by the ovaries and adrenal cortex to a lesser extent. Estrogen and progesterone are mainly synthesized and secreted by the ovaries. Sex hormones themselves do not directly contribute to fat metabolism.
  The amount of body fat in women is more than that in men, and the percentage of body fat in women is significantly higher than that in men, and the thickness of subcutaneous fat is generally doubled than that of the corresponding parts in men, except for individual parts. Obesity can occur in women during pregnancy, menopause, and in men or after male livestock depopulation. However, the mechanism is not clear. It is thought that menopausal obesity is related to excessive secretion of pituitary gonadotropins. The islets of the pancreas are hyperplastic and hypertrophied after menopause, and insulin secretion increases, promoting fat synthesis. In addition to a few hypogonadal obesity, general obese people do not have disorders of sex hormone secretion.
  (F) glucagon Glucagon is secreted by pancreatic islet alpha cells, and its effect is opposite to insulin, inhibiting fat synthesis. Whether there is disorder of glucagon in obese patients is to be studied.
  (VII) catecholamine Catecholamine is generated by brain, sympathetic nerve endings, chromophobic tissue mainly adrenal medulla, can promote lipolysis, cerebral cortex through catecholamine and 5hydroxytryptamine regulation of hypothalamic function, sympathetic nerve through catecholamine regulation of insulin secretion. Obese patients’ adipose tissue is insensitive to the action of catecholamine hormones, but can return to normal after weight loss.
  In short, the etiology of obesity is multifaceted, such as genetic tendency, dietary habits, reduced physical activity and mental factors, are important reasons.