Obesity is a disease in which energy intake is greater than consumption, resulting in excessive accumulation of body fat. Clinically can be divided into simple obesity and secondary obesity two categories. Simple obesity refers to those who are caused by excessive diet and too little activity, accounting for the vast majority of obesity in pediatric period. In recent years, due to the development of social economy and the improvement of diet structure, the incidence of this disease in China has a tendency to increase. The survey in Shanghai area shows that the incidence of simple obesity is 15.0% for boys and 11.0% for girls. Secondary obesity refers to those caused by brain diseases, endocrine disorders and some rare hereditary syndromes. Whether it is simple obesity or secondary obesity, the physical development and sexual development of the affected children in adolescence can produce adverse effects. In addition, childhood obesity if not timely control, the future can develop into diabetes, coronary heart disease, hypertension and liver and gallbladder disease, etc., so should cause enough attention. The etiology of simple obesity 1, long-term caloric intake too much and too little activity Most of the children with hyperphagia and overeating, but the activity is too little, the energy intake exceeds the consumption for a long time, and the excess is stored in the body in the form of triglycerides and leads to obesity. At present, it is thought that the child’s appetite is strong and the activity is too little may be caused by the abnormal function of the hypothalamus feeding and weight regulation center. 2, obesity gene, leptin and its related links abnormal obesity belongs to polygenic disease, its pathogenesis may involve a number of related genetic abnormalities and environmental factors (including diet structure, living habits, etc.) the combined effect. Recent studies have revealed that adipocytes are capable of synthesizing and secreting a protein hormone consisting of 146 amino acid residues with a relative molecular mass of 16,000, called leptin (Leptin). Its gene, the obesity gene, is located in humans at the q31 locus on chromosome 7. The receptor for leptin is composed of 1,165 amino acid residues and is most abundant in the cytosol of the hypothalamic arcuate nucleus. Its gene is localized in humans at locus p32 on chromosome 1. As a peripheral signal reflecting the volume of adipose tissue and the energy metabolic status of the body, leptin is transmitted to the feeding and weight regulation center of the hypothalamus and is involved in the regulation of the body’s feeding behavior and energy metabolic balance. Under normal conditions, when adipose tissue increases and energy balance is positive, serum leptin level increases and binds to leptin receptors in hypothalamus, which can activate melanocortin and corticotropin-releasing hormone (CRH) system, while inhibiting neuropeptide Y (neuropeptide Y) system, causing reduced feeding and increased activity, accelerated metabolism and increased energy consumption. Conversely, when adipose tissue is reduced and energy balance is negative, serum leptin level decreases, which activates the neuropeptide Y system and inhibits the melanocortin and corticotropin-releasing hormone systems, causing increased food intake and decreased activity, slowed metabolism and decreased energy consumption. In children with obesity, the normal interrelationship between leptin and the hypothalamic feeding and weight regulation centers is disturbed. Studies have shown that a minority of familial obesity is caused by mutations in the leptin gene or the leptin receptor gene, but the majority of children with simple obesity have normal genes. Serum leptin levels are significantly higher and correlate positively with body mass index (BMI), but the child still has a high appetite and low activity, showing a significant positive energy balance, indicating a significant leptin resistance in the body. At present, it is believed that simple obesity is likely to be caused by abnormalities in the postreceptor link of leptin, i.e., abnormalities in the function of the hypothalamic feeding and weight regulation center, which is manifested by overactive neuropeptide Y system and too low activity of melanocortin and corticotropin-releasing hormone system.