Obesity in children and adolescents has become a public health problem of global concern and often continues into adulthood. The incidence of metabolic syndrome increases with the rate of obesity. Epidemiologic studies have found that habitual sleep length is associated with the development of type 2 diabetes, heart disease, and even with morbidity and mortality. Sleep length in children and adolescents has been decreasing over the last 20-30 years, and the decrease in sleep length parallels the increase in their body weight. The relationship between sleep length and metabolic syndrome in children has become a hot topic. Recent advances in research on sleep length and metabolic syndrome in children and adolescents are summarized below. First, the metabolic syndrome in children and adolescents Reaven first proposed the concept of X’syndrome (later called metabolic syndrome), that a variety of metabolic abnormalities occurring at the same time than a single occurrence of cardiovascular disease or type 2 diabetes mellitus risk is more significant; insulin resistance and obesity is the core cause of X’syndrome. In 2003 Cook et al. defined metabolic syndrome in children and adolescents for the 1st time based on the National Cholesterol Education Program (NCEP ATPIII). The prevalence of metabolic syndrome in normal-weight children and adolescents is similar to that of adults, 3%-4%; however, the prevalence in the obese population is 26%-49%. This wide variation in prevalence rates between studies is related to the choice of different diagnostic criteria. A harmonized definition of the metabolic syndrome in children and adolescents is important for epidemiological studies. In 2007, the International Diabetes Organization proposed a diagnostic definition of metabolic syndrome in children and adolescents in order to standardize the diagnostic criteria: children <10 years of age are not diagnosed with metabolic syndrome. However, children with waist circumference ≥90% of normal for that age group and a concomitant history of type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, or obesity require treatment. Children/adolescents between the ages of 10 -16 years with a waist circumference ≥90% of normal for that age group and concurrent presence of at least 2 of the following 4: (1) triglycerides ≥1.7 mmol/L; (2) high-density lipoprotein cholesterol (HDL-C) <1.03 mmol/L; and (3) systolic blood pressure ≥130 mmHg (l mmHg = 0.133 kPa) or diastolic blood pressure ≥85 mmHg; (4) fasting blood glucose ≥5.6 mmol/L or diagnosed diabetes. In adolescents aged >16 years, the diagnostic criteria for metabolic syndrome were consistent with those for adults, with waist circumference ≥94 cm in males and ≥80 cm in females, and the concurrent presence of at least 2 of the following 4 items: (1) triglycerides ≥1.7 mmol/L; (2) for males: HDL-C <1. 03 mmol/L, and for females; HDL-C <1.29 mmol/L, or who had started treatment for hyperlipidemia; (3) systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥85 mmHg; or have been diagnosed or are being treated for hypertension; (4) impaired fasting glucose tolerance or have been diagnosed with type 2 diabetes. Sleep length and metabolic syndrome The relationship between sleep length and metabolic syndrome is not clear in adults, some studies point out that the occurrence of metabolic syndrome and sleep length is U-shaped relationship, that is, sleep length is too short or too long people suffering from metabolic syndrome risk is higher; some studies suggest that the occurrence of metabolic syndrome risk is higher in adults with longer sleep length. There is little research on the relationship between sleep length and metabolic syndrome in children or adolescents. There are a few studies that have linked sleep length to insulin resistance and waist circumference, but the results are inconsistent. Some studies suggest that too much or too little sleep in children or adolescents is associated with an increased risk of insulin resistance, and too little sleep is associated with increased waist circumference. There are also studies suggesting that the length of sleep in children and adolescents is not related to the occurrence of metabolic syndrome. 1, sleep length and obesity: obesity is a central factor in metabolic syndrome, obese children metabolic syndrome risk is 10-15 times that of normal weight children. The decrease in sleep length in children and adolescents in the last 30 years has been parallel to the increasing obesity rate. 2005, a US study showed that 45% of adolescents were sleep deprived (<8 h/night) and 31% had borderline sleep length (8-9 h/night). The main cause of reduced sleep duration in children and adolescents is environmental and lifestyle changes, rather than reduced sleep requirements due to intrinsic biological factors within individuals. The results of current studies on the relationship between sleep length and obesity in children are relatively consistent, with many studies supporting the trend of a negative linear correlation between sleep length and body mass index (BMI), i.e., the shorter the sleep length of a child, the greater his or her BMI; and vice versa. However, the consistency of findings on the relationship between sleep length and obesity in adolescents is poor. A portion of the findings suggest a linear negative correlation between BMI and sleep length in adolescents. However, some of the findings suggest a U-shaped relationship between BMI and sleep length in adolescents, i.e., both short and long sleep length adolescents have increased BMI. In addition, some studies suggest that there are gender differences in the relationship between sleep length and obesity, with sleep length being negatively associated with obesity in male adolescents but not in females. The reason for the gender difference may be that obesity is mostly defined by waist circumference in studies of children and adolescents. After puberty, fat accumulates more centrally in the hips in females, so using waist circumference as an indicator of obesity is less sensitive in females than in males. However, the shortcoming in many studies is the determination of sleep length by asking about the length of subjective sleep time, and only one study of 7-year-old children and three studies of adolescents have applied somatic dynamographs to record more objective sleep length. A large number of epidemiological data suggest that sleep length is related to the occurrence of obesity, but it does not indicate that there is a causal relationship between the two. 2, sleep length and insulin resistance: insulin resistance is another core factor of metabolic syndrome in addition to obesity. At present, the results of research on the relationship between sleep length and insulin resistance are not consistent. Some studies point out that too short sleep length is associated with insulin resistance; some studies point out that too long sleep length is associated with insulin resistance; and some studies conclude that there is a U-shaped relationship between sleep length and the risk of insulin resistance. Currently, the mechanism of short sleep length and insulin resistance has been studied more clearly, and it is believed that obesity is one of the important intermediary mechanisms that mediate short sleep length and insulin resistance. Short sleep causes a decrease in leptin secretion and an increase in hunger hormone secretion, which leads to an increase in appetite and food intake, resulting in weight gain and obesity, which in turn leads to insulin resistance. In addition, short sleep causes increased cortisol secretion and increased sympathetic nervous system excitability, which may increase the risk of insulin resistance. However, the mechanism by which excessive sleep length is associated with the development of insulin resistance remains unclear. There are hypotheses that excessive sleep length is a sign of comorbid conditions, such as depression. Low levels of activity and low socioeconomic status have also been reported to be associated with excessive sleep length. In addition, cytokines may be a possible mechanism mediating excessive sleep length and insulin resistance. It has been noted that for each additional th of habitual sleep duration, levels of C-reactive protein and interleukin-6 were elevated by 8% and 7%, respectively, and that chronic elevation of inflammatory cytokine levels is associated with an increased risk of developing diabetes. Therefore, excessive habitual sleep duration may affect glucose metabolism by altering the regulation of these inflammatory cytokines. 3. Sleep length and metabolism-related hormones: Sleep length is associated with changes in the levels of metabolism-related hormones, which may affect BMI levels. There is a growing body of experimental research in adults that confirms that sleep length affects body weight by altering neuroendocrine control of appetite. Leptin is a hormone secreted by white fat cells that has an inhibitory effect on eating and stimulates energy expenditure. Gastric hunger hormone is a hormone secreted by the stomach that acts in the opposite way to leptin and has the effect of stimulating appetite, increasing hunger, producing fat and increasing body weight. In addition to leptin and gastric hunger hormone being related to the regulation of hunger and appetite, both are affected by sleep length. When sleep length decreases, it causes a decrease in leptin secretion and an increase in gastric hunger hormone secretion, which causes an increase in hunger, motivation to eat, and appetite, which causes weight gain. In addition, in obese children, decreased sleep length is associated with increased fasting insulin levels and peak insulin levels and insulin resistance. Third, sleep length, obesity and metabolic syndrome in sleep disorders Obesity and metabolic syndrome are the most common co-morbidities in children and adolescents with insomnia and short sleep length. In a study on sleep debt, 11 young male subjects were subjected to partial sleep deprivation (4 h of sleep per night), prolonged sleep (12 h of sleep per night) and normal sleep (8 h of sleep per night). During the sleep-restricted phase, subjects showed significantly impaired glucose tolerance and a significant decrease in the acute response of insulin to glucose and in the effective utilization of glucose, compared to when the subjects were fully asleep. Insulin sensitivity also tended to decrease, but there were no statistically significant differences. On the other hand, sleep length is a valid predictor of obesity in prepubertal children, both in cross-sectional and longitudinal studies. Obesity is a major high-risk factor for sleep apnea. Sleep breathing disorders are associated with the development of insulin resistance and low levels of systemic inflammatory response, which in turn are important causes of metabolic syndrome. In summary, appropriate sleep length in children and adolescents plays an important role in the proper functioning of normal metabolism, hormone secretion, and appetite regulation, and reasonable sleep length and good sleep quality are conducive to the maintenance of normal body weight and the reduction of metabolic disorders.