Obesity exert a central role in the development of metabolic syndrome, NAFLD and a cardiovascular morbidity.
Examining the diagnostic role of serum visfatin levels as a novel indicator in childhood obesity and evaluating the risk of fatty liver and poor glycemic condition showed that Visfatin promotes B cell maturation and inhibits neutrophil apoptosis.The synthesis and secretion of Visfatin is regulated by Interleukin–6 (IL–6),growth factors, glucocorticoids, and TNF-α and up regulated in the course of pro-inflammatory cytokines release, under inflammatory conditions, by hyperglycemia and hypoxia [15,16] and down regulated by insulin, somatostatin and statins.
In the present study, the BMI correlates closely with total body fat (TBF), which is in previous studies estimated using dual-energy x-ray absorptiometry (DEXA) scanning in children who are overweight and obese.
DBP it was significantly higher in obese children, obesity likely contribute to the increase levels of insulin and insulin-like growth factor I which may increase blood pressure ,also Visfatin can promote vascular smooth muscle inflammation and play a potential role in vascular dysfunction and inflammation in some metabolic disorders.
Nageswari et al.,,(2007) found higher DBP values in the obese group children and hypothesized that higher DBP in obese children could be due to higher vasoconstrictor tone and/or increase in the cardiac output owing to increased circulatory load on heart. As a consequence of increase in BMI.However, Divković. et al.,(2014)proved that overweight/obese children had significantly higher systolic blood pressure compared to eutrophic children, while DBP showed no difference in both groups.
In the present study, NAFLD was significant higher in the obese children compared with overweight &healthy children. NAFLD is one of manifestations of metabolic syndrome. Risk factors associated with NAFLD include dyslipidemia, central obesity, type–2 diabetes mellitus, and insulin resistance (IR). NAFLD however, remains a diagnosis of exclusion, so other causes of chronic liver disease must be ruled out, especially HCV, alcoholic liver disease, and Wilson’s disease (in young Patients).In contrast to our study, Ludwig et al.,(1980) proved that, rarely, physical examination reveals hepatomegaly.
Our results showedmild to moderate elevations in transaminases two to five times the upper limits of normal in overweight and obese agreeingwith the results of Ekstedtet al.,(2017)&Li Hui-ling et al.,(2015)who found The ALT and AST levels of the obese children were higher than the overweight group and explained that patients with NAFLD have insulin resistance (IR) which increases lipolysis from the adipose tissue. The resulting FFA will be taken up by the liver and can cause lipid peroxidation so increase production of inflammatory cytokines. Also accumulation of fat in the liver is a result of increased triglyceride synthesis, decreased triglyceride export through very-low density lipoprotein (VLDL), and reduced beta-oxidation. [24, 25]
Higher total cholesterol, LDL and TG were detected in obese and overweight children compared with control groups and also in the obese children was higher than overweight ones. While HDL was higher in healthy children who show normal levels of HDL which has a cardiovascular protective function confirming the higher risk of cardiovascular complication in other two groups, this is in agreement with Holst-Schumacher et al.,(2009) who found higher mean serum concentrations of triglycerides but lower mean serum levels of HDL cholesterol in obese children compared to controls and demonstrated the alteration of lipoprotein levels and compositions are related to the greater risk of cardiovascular disease associated with obesity.
Obesity-related hyperlipidemia is primarily characterized by increased levels of plasma free fatty acids and triglycerides, decreased levels of HDL with abnormal low-density lipoprotein (LDL) composition. 
Higher mean fasting blood glucose level (FBG) and HbA1Cwere found in overweight and obese compared to healthy ones and this confirming that obesity is a risk factor for impaired glucose tolerance, this is similar to that described by Elghaffar et al.,(2010) who found that fasting blood sugar were significantly higher in obese children compared to non-obese controls and between the obese children and overweight children reflecting the relation between obesity & hyperglycemia as blood sugar concentrations increased with increasing adiposity.
Insulin resistance is defined as the decreased ability of tissues to respond to insulin action and one of the insulin-responsive tissues is adipose tissue, insulin stimulates storage of triglycerides in adipose tissue through promoting the differentiation of
pre-adipocytes to adipocytes, increasing the uptake of glucose and fatty acids derived from circulating lipoproteins and lipogenesis in mature adipocytes, and inhibiting lipolysis. 
Insulin resistance is feature of metabolic syndrome and is a major predictor of the development of type 2 diabetes. Visfatin is important to normal insulin secretion, but its relationship with diabetes risk and progression is still a matter of debate. Thus, Visfatin may be a compensatory mechanism or part of the pathophysiology of diabetes. 
In adipokines, Visfatin is over expressed in the route of adipocyte differentiation and can significantly regulate insulin secretion, insulin receptor phosphorylation. [31, 32]
Serum Visfatin was higher in obese &overweight patients compared with controls. Also it was higher in patients who develop metabolic syndrome (dyslipidemia, NAFLD and IR).The accumulation of body fat, particularly in a visceral distribution reduces the sensitivity to insulin in skeletal muscle, liver tissue, and adipose tissue; this “insulin resistance” predisposes to glucose intolerance, hypertriglyceridemia and low levels of HDL.The presence of NAFLD itself is a significant predictor of serum Visfatin levels as reported by Dahl et al.,(2010). In insulin resistance a direct relationship between plasma Visfatin level and type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site differ from that of insulin and causes hypoglycemia by stimulating glucose utilization in adipocytes and myocytes and reducing glucose release from liver. 
However, Fukuharaet al.,(2005) and Li Hui-ling et al.,(2015) found that Type 1 diabetic children and adolescents had a significantly lower Visfatin level compared to controls and no difference of serum Visfatin levels between the healthy and overweight children and the difference only was between the healthy and obese children [35,25],also Ihsan et al.,(2017) published that overweight/obese individuals there was negative relation between Visfatin level and anthropometric and lipid profile parameters, which can be explained by functional healthy fat tissue in this early life time even in a group of patients with increased body fat.
In our study there was a significant difference between the obese children and healthy ones in the ultrasonographic findings of NAFLD and between the obese children and overweight ones with the frequency of 65.6% and 26.7%, respectively. Lipid accumulation in the liver leads to hepatic inflammation and cytokine production. 
Both Jarrar et al.,(2008) and Younossi et al.,(2011) showed significantly lower serum visfatin levels in NAFLD obese patients compared with patients with simple steatosis obese ones, overall, three studies suggested a protective role of visfatin in NAFLD progression.[7, 37]
Our results showed the receiver-operating characteristic curve for serum Visfatin as a predictor of fatty liver in obesity, it shows an area under the curve (AUC) of 0.82 at cut off value for serum Visfatin of > 126.5 ng/ml, this mean sensitivity of 78.1% and specificity of 61.4% of serum Visfatin as a predictor of fatty liver disease in obese children.