Small-for-gestational-age (SGA) infants have been the subject of much attention in the last decade. The current common definition of SGA is that the birth mass is below the 10th percentile or below -2 s of the average body mass for the same gestational age, but some data reports define SGA as birth mass or height below the 3rd or 5th percentile of the average height or body mass for the same gestational age. However, the most widely used criterion for the diagnosis of SGA is height or body mass below the -2 s for the same gestational age. SGA occurs in preterm, term, and expired infants, and has a high perinatal morbidity and mortality rate. It is estimated that 2.3-10.0% of infants worldwide are born prematurely. It is estimated that 2.3-10.0% of infants worldwide have SGA, and the incidence of SGA varies in different regions of China, about 7.5%. There are still many scholars equate SGA with intrauterine growth retardation syndrome (I UGR), in fact, the two concepts are different, I UGR mainly refers to the fetal growth pattern, which is used to describe the pathophysiological process of the formation of fetal growth and developmental backwardness. a shorter period of I UGR does not necessarily lead to SGA, i.e., SGA is not necessarily caused by I UGR. 1, the typing of SGA according to the time of damage typing SGA typing has many kinds, at present the most widely used is the clinical typing, that is, according to the time of fetal growth damage typing. (1) proportional type: accounting for 20% to 30%, the child’s body mass, length, head circumference is proportionally reduced, proportional body type. Often associated with genetic, metabolic defects and intrauterine infection. In early pregnancy growth is impaired, the organ cells mitosis is affected, the number of cells is reduced, the damage is irreversible, easy and congenital malformations and permanent growth retardation, but seldom and hypoglycemia and erythrocytosis, the prognosis is poor. (2) Non-proportional type: accounted for 70% ~ 80%, the child’s length and head circumference is not affected, but the subcutaneous fat disappears, showing malnutrition appearance. The impaired growth occurs in late pregnancy and is associated with maternal gestational hypertension syndrome (hyperemesis gravidarum) and placental insufficiency. The number of cells in each organ is normal, but due to insufficient nutrient supply, the cytoplasm is reduced and the cells become smaller. If appropriate nutrients are supplied, the damage is reversible, and the affected cells can return to normal size. 50% of the cells are associated with erythrocytosis, and may be associated with hypoglycemia. According to the definition of SGA, SGA can be divided into SGA with low birth height (SGAL), SGA with low birth mass (SGAW), and SGA with low height and mass (SGAL,W). Since the occurrence of SGA begins in the fetal period, fetal growth monitoring, ultrasonography to determine gestational age, estimation of fetal size, growth and development are important for the diagnosis of SGA. (1) Psychological problems: the intellectual development of some SGA after birth often lags behind that of children with normal birth mass, and the incidence of long-term physical, physical, neuropsychological developmental disorders is higher than that of healthy children. For example, the scores of psychological scales are lower than those of children of appropriate gestational age (AGA) [ 8 ], cognitive function is significantly reduced, and learning ability is low [ 102 11 ]. Studies have shown that the lack of growth catch-up is an important reason for the lower-than-normal psychological and intellectual performance of children with SGA. However, there is no clear research result on whether the cognitive dysfunction of SGA is due to the neurological developmental abnormality caused by the intrauterine environment or the influence of the postnatal social environment on the psychology of children with SGA. (2) Short stature: At birth, SGA lags behind healthy children of the same gestational age in height or body mass. Whether it is body mass or height, most of the SGA children start to catch up with the growth at 6 to 12 months of age, and at the age of 2 years, 85% to 90% of the SGA children’s height is within the range of healthy children of the same age, and about 15% of the SGA children can not catch up with the children of the same gestational age, and among the children who can not catch up with them, 50% of the children are of short stature in the adult stage, and the growth of the preterm SGA children does not catch up with the growth at birth obviously, and the growth of the preterm SGA children may not start to catch up until they reach the age of 6 years. Growth catch-up may not begin until 6 years of age. Studies have shown that the growth rate of body mass in SGA is significantly higher than that of full-term healthy fetuses at 2 years of age, and the growth rate of body length is significantly higher than that of full-term healthy fetuses at 1 year of age, which means that the catch-up of body mass in SGA is more persistent. (3) Metabolic problems: The risk of insulin resistance (I R), type 2 diabetes mellitus (T2DM), dyslipidemia and cardiovascular disease in adult SGA children is higher than that in AGA children, especially those with a family history of T2DM or metabolic syndrome (MS), and the mechanism of this is not yet clearly defined, and a large number of studies have suggested that the I R is the key. Hales et al. suggested that, in the intrauterine environment, the fetus adopts a protective mechanism due to malnutrition: in order to ensure the nutritional development of important organs (brain, lungs, etc.), it selectively reduces the growth rate of some organs (kidneys, liver, pancreas, etc.), which leads to endocrine dysfunction of pancreatic β-cells, decrease in the number and function of glucose transporters in skeletal muscle, decrease in glucose uptake, decrease in insulin sensitivity, and thus cause I R. Another viewpoint is that I R is related to growth catch-up, which is a key factor for I R in SGA. Another view is that I R is related to growth catch-up. A study revealed that growth catch-up may be related to I R. In this study, individuals with low birth mass reached normal levels at 7 years of age after growth catch-up, but the mortality rate of patients with coronary atherosclerotic heart disease was very high in this group. Stono et al. studied insulin sensitivity at birth and 1 year of age of SGA children and found that fasting insulin, area under the insulin curve, early insulin sensitivity, and insulin concentration were significantly lower in SGA children who had growth catch-up. Fasting insulin, area under the insulin curve, and early insulin secretion were higher in children with SGA and AGA without catching up, and fasting insulin was higher in children with SGA than in children with SGA and AGA without catching up, suggesting that IR can occur as early as 1 year of age and is related to catching up in terms of body length. Ibanez et al. suggested that some children with SGA continued to gain excess fat even after completing the process of body mass catch-up, and the accumulation of excess fat caused I R. At the same time, I R led to the accumulation of extra fat and the formation of central obesity, early onset of puberty, precocious puberty, and polycystic ovary syndrome. I R may be related to the common post-receptor signaling pathway of growth hormone (GH) and insulin. Growth and development are mainly regulated by the GH2 insulin-like growth factor 2 1 (IGF2 1) axis, and GH promotes hepatic secretion of IGF2 1, which, in combination with insulin-like growth factor-binding protein 2 3 (IGFBP2 3), mediates the growth and metabolic regulation of GH.The umbilical cord blood levels of IGF2 and IGFBP2 3 of children with SGA are lower than those of children of normal gestational age, and the birth weights of these children are also lower than those of children of normal gestational age, while the lengths and placental weights of these babies are lower than those of babies of normal gestational age, and the birth weights of the fetuses are also lower than those of babies with GH, The cord blood IGF2 and IGFBP2 3 levels are lower than those of normal fetal age, and fetal birth mass, body length and placental weight are positively correlated with IGF2 1 and IGFBP2 3 levels, thus, IGF2 1 and IGFBP2 3 play important roles in the growth and development of children with SGA. GH may be directly involved in and mediate the IR of SGA. GH and insulin share a common post-receptor signaling pathway, the phosphatidylinositol 3-kinase (PI 3K) pathway, which is a metabolic effector of insulin, and the Akt/protein kinase B (PKB) pathway, which is an effector of insulin, is an effector of insulin. Akt/protein kinase B (PKB) is a key signaling molecule in the PI 3K pathway to achieve its biological effect, SGA mice in the basal state of P2 Akt significant expression of the body’s response to insulin stimulation is low, blockade of the upstream signaling protein of the post-receptor pathway of the GH JAK2 and then insulin stimulation results showed that the Akt response to insulin was significantly improved to a level close to the normal level, confirming that the GH signaling mediated or aggravated the I R. I R is the basis for the development of MS in adults and is the link between low birth mass and T2DM. In a study of 296 newborns, a polymorphism in the β3 2 AR gene, Trp64Arg, was found to correlate with insulin sensitivity in SGA. Angiotensinase (ACE) gene I/D polymorphism was associated with neonatal birth mass and insulin sensitivity at 3 d. The two polymorphisms had a synergistic effect on neonatal insulin sensitivity, and the lowest insulin sensitivity was found in those who had both ACE gene DD genotype and β3 2 AR Arg64 genotypes. It was also pointed out that there is no correspondence between genotype and phenotype in human polygenic diseases, and that genetic factors and environmental factors work together to determine the insulin sensitivity of newborns, resulting in I R. 3. Treatment of SGA Children with SGA have different complications at different ages, and the monitoring indicators are different, so the treatment is also different. The incidence of respiratory distress in neonatal SGA is high, so we should be prepared for rescue. Due to intrauterine nutritional deficiency, liver glycogen storage is reduced and insulin level is elevated, hypoglycemia is easy to occur after birth, especially in children with non-proportional SGA, and early treatment is recommended. Intrauterine nutritional deficiencies have a certain impact on brain tissue development. Early temperament assessment of newborns with SGA can be performed after birth for early detection of problems and targeted early intervention. From 6 months to 2-3 years of age, most of the children with SGA start to catch up with their growth. Since too fast catching up of SGA can lead to IR, obesity, T2DM and cardiovascular complications in adults, theoretically, a healthy dietary structure control is beneficial to the height and body mass of SGA during the catching up period, and avoiding too fast catching up can reduce the risk of IR and other complications. At the same time, we monitored the growth and development, blood IGF2 1, IGFBP2 3, blood glucose, insulin level, calculated the I R index, and carried out the necessary interventions as early as possible. For children with good natural catch-up, blood pressure, fasting blood glucose, insulin and other indexes should be monitored to prevent the occurrence of cardiovascular and metabolic diseases; for those who have not achieved satisfactory catch-up, GH treatment should be carried out. The study proved that GH treatment did not accelerate the growth of growth-restricted infants immediately after birth, and the levels of IGF2 1 and IGFBP2 3 related to insulin insensitivity were monitored at the same time, and they did not change. However, most studies have demonstrated that the earlier the prepubertal child receives growth hormone treatment, the more significant the effect is [ 13 ]. Therefore, the timing of treatment is very important. Since most children with SGA experience growth catch-up in the early postnatal period, which ends at the age of 2 years, and rarely occurs after the age of 3 years, the indications for GH treatment of children with SGA should be mastered. In Europe, the recommended criteria are: (1) birth mass < - 2 s; (2) height < - 2.5 s; (3) age > 4 years; and (4) growth rate < 0 s. The U.S. Food and Drug Administration (FDA) approved in July 2001 the use of GH as a long-term treatment for children with SGA who have lagged behind in growth and who have not experienced sufficient catch-up growth by 2 years of age. Early therapeutic growth is proportional to the initial dose of GH, with higher doses resulting in more rapid growth, and the optimal dose recommended by the FDA is 0.48 mg/(kg/week) [equivalent to 0.2 I U/(kg/d), 0.067 mg/(kg/d)] for 2-6 a. If catch-up growth or pubertal growth has been achieved, the dose can be adjusted to 0.24-0.48 mg/(kg/week) [0.067 mg/(kg/d)]. (kg/week) [0.7-1.4 I U/(kg/week)]. Before starting treatment, it is recommended to test blood IGF2 1, IGFBP2 3, fasting lipids, insulin, fasting blood glucose, and blood pressure. During the course of treatment, growth should be monitored and serum IGF2 1, fasting blood glucose, insulin, and blood pressure should be monitored at all times. Although the dose of GH plays an important role in the final height, the age of starting the treatment, the height and the median height of the parents should not be ignored, therefore, the dose of GH should be individualized, and the rate of height growth in the first year should be observed to know the effect of GH treatment. In order to achieve the best results, GH treatment should be continued, and the growth rate will slow down after discontinuation. Regardless of whether GH deficiency exists or not, children with SGA treated with high doses of GH had higher growth rates and improved lifelong heights, and had relatively few adverse effects of GH treatment, such as a negative feed-back increase in food intake due to a decrease in lipocalin levels. After long-term GH treatment, the intelligence and psychosocial function of children with SGA will be improved. The muscle tissue of children with SGA was increased, muscle motor function was strengthened, and body fat tissue was reduced. Systolic and diastolic blood pressure are reduced, and total cholesterol, atherosclerotic index (AI) and low-density lipoprotein (LDL) are lowered, which can reduce the incidence of cardiovascular disease. There are some unfavorable aspects and long-term complications of GH treatment.IFG2 1 and IGFBP2 3, insulin level of SGA children had a significant increase after GH treatment, and insulin sensitivity decreased, which led to the occurrence of glucose intolerance, and the emergence of IR.Although blood glucose, glycosylated Hb, insulin level and so on would be mildly increased after GH treatment, but most of them were still within the normal range. Metabolic changes can be reversed by stopping the drug.