Dyslipidemia In Obese Children Research Articles

Expression and Role of PDK4 on Childhood Dyslipidemia and Lipid Metabolism in Hyperlipidemic Mice.

Hyperlipidemia is a common metabolic disorder that can lead to cardiovascular disease. PDK4 is a key enzyme that regulates glucose and fatty acid metabolism and homeostasis. The aim of this study is to explore the correlation between PDK4 expression and dyslipidemia in obese children, and to find new therapeutic targets for hyperlipidemia in children. The expression of PDK4 in serum was detected by qRT-PCR. Receiver operating characteristic curve was used to analyze the relationship between PDK4 and dyslipidemia. Upstream miRNAs of PDK4 were predicted by the database and verified by dual luciferase reporter gene assay and detected by qRT-PCR. The hyperlipidemia mouse model was established by high-fat diet (HFD) feeding, and the metabolic disorders of mice were detected. PDK4 is poorly expressed in the serum of obese children. The upstream of PDK4 may be inhibited by miR-107, miR-27a-3p, and miR-106b-5p, which are highly expressed in the serum of obese children. Overexpression of PDK4 improves lipid metabolism in HFD mice. miR-27a-3p silencing upregulates PDK4 to improve lipid metabolism. In conclusion, PDK4 has a diagnostic effect on dyslipidemia in children, while lipid metabolism in hyperlipidemic mice could be mitigated by upregulation of PDK4, which was inhibited by miR-107, miR-27a-3p and miR-106b-5p on upstream.

Frequency of Dyslipidemia and Associated Risk Factors Among Obese Children and Adolescents in Turkey

Background: The chronic inflammatory state that occurs in obesity causes metabolic complications such as dyslipidemia, hypertension, insulin resistance, hepatosteatosis, and cardiovascular disorder. Dyslipidemia secondary to obesity, which is an important cause of morbidity, is a worldwide concern. Dyslipidemia has an essential role in the pathogenesis of cardiovascular disease (CVD). Objectives: The aim of this study was to determine the prevalence and risk factors associated with dyslipidemia in obese children and adolescents. Methods: This single-center, retrospective, cross-sectional study included 1,136 obese patients. Fasting lipid, liver transaminases, glucose, and insulin levels were measured, and ultrasound scans (US) were performed. Other clinical assessments included waist-to-hip ratio, blood pressure, and the presence of acanthosis nigricans and striae. Results: Dyslipidemia was present in 644 (56.7%) cases. Puberty, high body mass index (BMI), increased waist-hip ratio, increased homeostasis model of assessment for insulin resistance (HOMA-IR), high uric acid, and acanthosis nigricans were found to be risk factors for dyslipidemia. Conclusions: The prevalence of dyslipidemia in obese children was high and increased with puberty. Therefore, obese children and adolescents should be closely monitored for dyslipidemia that predisposes them to adolescent CVD.

Influence of subclinical hypothyroidism on metabolic parameters in obese children and adolescents.

BackgroundSubclinical hypothyroidism (SH) is a common condition in obese children. However, its effect on glucose and lipid metabolism in obese children remains controversial.PurposeThe present study aimed to investigate the association between SH and metabolic parameters.MethodsA total of 215 obese children and adolescents aged 6–18 years were included in this retrospective cross-sectional study. The patients’ anthropometric measurements such as thyrotropin (TSH), free thyroxine (fT4), fasting plasma glucose, and insulin levels, as well as homeostasis model assessment for insulin resistance (HOMA-IR) index, and lipid profiles were evaluated. The patients were allocated to the SH group (fT4 normal, TSH 5–10 mIU/L) (n=77) or the control group (fT4 normal, TSH<5 mIU/L) (n=138). The glucose and lipid metabolisms of the 2 groups were compared.ResultsSH was identified in 77 of 215 patients (36%). Mean body mass index was similar in both groups. The mean serum insulin, HOMA-IR, and triglyceride (TG) levels were higher and the mean high-density lipoprotein cholesterol level was lower in the SH group than in the control group (p=0.007, P=0.004, P=0.01, and P=0.02, respectively). A positive correlation was observed between TSH level and insulin level, HOMA-IR, and TG level.Conclusion SH was identified in some of the obese children and adolescents. A clear association was observed between SH, insulin resistance, and dyslipidemia in obese children.

The Assessment of the Neutrophil-lymphocyte Ratio and Platelet-lymphocyte Ratio in Dyslipidemic Obese Children

Objective: Childhood obesity is one of the most important children’s health problems that is gradually increasing all over the world. Dyslipidemia which coexists with obesity is a risk factor for atherosclerotic diseases in adulthood. In this study, the usability of the neutrophil-lymphocyte ratio (NLR) and the platelet-lymphocyte ratio (PLR) in predicting dyslipidemia, a serious complication of obesity, in children was investigated. Material and Method: 207 cases aged between 11-17 years who were diagnosed with obesity at the Pediatrics Clinic of our hospital and 50 cases with no disorders whose complete blood count was performed for routine purposes were retrospectively investigated. The genders, ages, and examination findings of the cases were recorded. In obese children, leukocyte, hemoglobin, platelet, mean platelet volume, neutrophil and lymphocyte levels were evaluated in the complete blood count performed at the first admission. The neutrophil-lymphocyte ratio and the platelet-lymphocyte ratio were calculated. Preprandial blood glucose and preprandial insulin, serum aminotransferase values, and the lipid profile were recorded. Results: While dyslipidemia was determined in 99 (47.82%) of 207 cases who were diagnosed with obesity, it was not determined in 108 (52.18%) cases. The systolic blood pressure, diastolic blood pressure, and preprandial insulin level were higher in cases with dyslipidemia than the group without dyslipidemia. The PLR average of the dyslipidemic group was 112.75±39.11, the PLR average of the non-dyslipidemic group was 104.78±31.38, and the PLR average of the control group was 110.20±39.35, and there was no statistically significant difference between the PLR averages of the groups (p=0.353). The NLR average was 1.52±0.69 in the dyslipidemic group, 1.66±0.81 in the non-dyslipidemic group, and 1.72±1.26 in the control group. No statistically significant difference was observed between the NLR averages of all three groups (p=0.295). Conclusion: In this study, no relationship was determined between the PLR and NLR and dyslipidemia in obese children.

The relationship between serum FGF-23 concentration and insulin resistance, prediabetes and dyslipidemia in obese children and adolescents.

Background Obesity is known to cause metabolic disturbances including insulin resistance, dyslipidemia and alters bone mineralization. The effects of obesity on fibroblast growth factor 23 (FGF-23), which is important in bone mineralization, have not yet been clarified. Our aim was to investigate the association between FGF-23 concentration and obesity-associated dysmetabolism. Methods Subjects comprised 46 obese children and adolescents. The same number of age-matched, healthy controls were recruited. Markers of bone mineralization and glucose metabolism were measured. Thyroid function and insulin resistance were investigated in both groups. In obese subjects; an oral glucose tolerance test (OGTT) was performed and hemoglobin A1c and lipid fractions were measured. Bone mineral density and hepatic steatosis were investigated. Results Serum FGF-23, α-klotho and 1,25(OH)2D3 concentrations were significantly lower while fasting insulin, fasting glucose, C-peptide and alkaline phosphatase (ALP) concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) were significantly higher in the obese group compared to controls. A significant negative correlation was observed between free tri-iodothyronine (fT3) and both FGF-23 and α-klotho in the obese group. Significant negative correlation was found between FGF-23 and C-peptide and a positive correlation was found between FGF-23 and high density lipoprotein-cholesterol (HDL-c) in the obese subjects with impaired glucose tolerance (IGT). Significant negative correlations were found between FGF-23 and both fasting insulin levels and C-peptide levels in the obese subjects with hepatic steatosis. Conclusions In our study, insulin resistance-associated hyperinsulinism and/or lower 1,25(OH)2D3 levels, both present in obese children and adolescents, may lead to decreased serum FGF-23 concentrations in obese subjects.

Effect of Low Carbohydrate Versus Low Fat Diet in the Treatment of Dyslipidemia in Obese Children With Metabolic Syndrome

Effect of Low Carbohydrate Versus Low Fat Diet in the Treatment of Dyslipidemia in Obese Children With Metabolic Syndrome

Dyslipidemia in Childhood Obesity: A Review

Childhood obesity has become epidemic in developed as well as developing countries. Apart from genetic factors, changes of lifestyle like consumption of excess calorie rich food, lack of physical activity and increased screen time are major contributing factors for childhood obesity. Many co-morbid conditions like cardiovascular, metabolic, neurological, hepatic, pulmonary, orthopedic, and renal disorders are associated with childhood obesity. It has both immediate medical complications as well as long term health consequences in later life. The most hazardous consequences like the cardiovascular disorder occur due to early athrosclerotic process which is accelerated due to dyslipidemia. As a result dyslipidemia is an important etiologic factor for development of cardiovascular disease (CVD), which is a leading cause of death in adulthood throughout the world. As abnormal vascular changes begins in childhood, and as dyslipidemia is an significant risk factor for CVD, screening and treatment of dyslipidemia in obese children and adolescents are an important health issue to prevent development metabolic syndrome and its consequences.&#x0D; Bangladesh J Child Health 2018; VOL 42 (3) :148-154

Secondary Dyslipidemia In Obese Children - Is There Evidence For Pharmacological Treatment?

BackgroundLong-term safety, effectiveness and criteria for treatment with statins in children are still unclear in clinical practice. There is very limited evidence for the use of medication to treat children with dyslipidemia secondary to obesity who do not respond well to lifestyle modification.ObjectiveSystematic review of randomized clinical trials of statin use to treat children and adolescents with dyslipidemia secondary to obesity.MethodsWe performed a search in PubMed, EMBASE, Bireme, Web of Science, Cochrane Library, SciELO, and LILACS for data to evaluate the effect of statins on: improvement of surrogate markers of coronary artery disease in clinical outcomes of adulthood; increased serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipropotein B (APOB); and decreased serum levels of high-density lipoprotein cholesterol (HDL-C) from inception to February 2016. Participants were children and adolescents.ResultsOf the 16793 potentially relevant citations recovered from the electronic databases, no randomized clinical trials fulfilled the inclusion criteria for children with dyslipidemia secondary to obesity.ConclusionsWe found no specific evidence to consider statins in the treatment of hypercholesterolemia secondary to obesity in children. The usual practice of extrapolating findings from studies in genetic dyslipidemia ignores the differences in long-term cardiovascular risks and the long-term drug treatment risks, when compared to recommendation of lifestyle changes. Randomized clinical trials are needed to understand drug treatment in dyslipidemia secondary to obesity.

Vitamin D deficiency and insulin resistance as risk factors for dyslipidemia in obese children.

Dyslipidemia is one of the major complications of obesity; vitamin D deficiency and insulin resistance are attending metabolic complications in dyslipidemic obese children. Objective. To determine if vitamin D deficiency and insulin resistance are risk factors for dyslipidemia in obese children. This study was conducted in the Department of Pediatrics at Bagcilar Training and Research Hospital in Istanbul, Turkey between 2014 and 2015. Obese patients whose age range was 8-14 were included in the study. The serum triglyceride, total cholesterol, low-density lipoprotein cholesterol, highdensity lipoprotein cholesterol, fasting glucose, insulin, alanine aminotransferase, vitamin D levels were measured; a liver ultrasonography was performed. Homeostatic model assessment (HOMA-IR), was used to calculate insulin resistance. 108 obese children were included; 39 (36.11%) had dyslipidemia. The average fasting blood glucose (88.74 ± 7.58 vs. 95.31 ± 6.82; p= 0.0001), insulin level (14.71 ± 12.44 vs. 24.39 ± 15.02; p= 0.0001) and alanine aminotransferase level (23.45 ± 11.18 vs. 30.4 ± 18.95; p= 0.018) were significantly higher in the children with dyslipidemia. In the dyslipidemic obese children, the average hepatosteatosis rate and HOMA-IR level were higher; 28 (71.9%) had hepatosteatosis, 37 (94.87%) had insulin resistance; the vitamin D levels were <20 ng/ml in 69.3%. Vitamin D deficiency was significantly more common (p= 0.033). The multivariate regression analysis confirmed that the increase in the HOMA-IR level (p= 0.015) and the low vitamin D level (p= 0.04) were important risk factors for dyslipidemia. Obese children in our region exhibit low vitamin D and increased HOMA-IR levels, which are efficient risk factors of dyslipidemia.

Association between obesity and lipid profile in children 10--12 years of age

Background Worldwide prevalence of obesity in children hasbeen increasing. Together with dyslipidemia and hypertension,obesity is associated with higher risk of cardiovascular morbiditylater in life.Objective The aim of this study was to assess associationbetween obesity and occurrence of dyslipidemia in 10-12 yearsold children.Methods We performed a cross sectional study on 53 obese and53 non-obese children matched for age and gender in Yogyakarta.Obesity was defined as body mass index (BMI) at or above the95th percentile of the CDC 2000 reference. The levels of totalcholesterol, LDL-cholesterol, HDL-cholesterol and triglyceridewere measured. Dyslipidemia was defined as increased level oftotal cholesterol, LDL-cholesterol, triglyceride and decreasedlevel of HDL-cholesterol.Results Obese children had higher risk of increased level oftriglyseride, i.e. RR 2.6 (95% CI 1.6 to 4.4), P&lt;O.OOl anddecreased level ofHDL-cholesterol, i.e. RR 17.8 (95%CI 14.0 to20.1), P=0.003. Overall, relative risk for dyslipidemia in obesechildren was 5.2 (95%CI 4.2 to 5.9), P=0.002, higher than innon-obese children.Conclusion Compared to non-obese children, obese children havehigher risk of dyslipidemia, particularly hypertriglyceridemia andhypo-HDL.

Resistin, inflammation and dyslipidemia in obese children and adolescents

Introduction: Childhood obesity is related to cardiovascular diseases and diabetes mellitus type 2 in later life. Resistin, an adipokine primarily secreted by monocytes and tissue macrophages in humans, is considered to be associated with these conditions. The Aim: To examine the correlations between resistin concentration and anthropometric parameters, lipid status, inflammatory markers and parameters of insulin resistance in obese children and adolescents. Material and Methods: The study included 66 patients (40 boys, 26 girls), which underwent anthropometric measuring and laboratory testing (glucose level, total cholesterol, high-density lipoprotein cholesterol (HDL-cholesterol), low-density lipoprotein cholesterol (LDL-cholesterol), triglycerides, uric acid, high-sensitivity C-reactive protein (hsCRP) and glycosylated hemoglobin (HbA1c). Insulin resistance was estimated with HOMA-IR (homeostasis model assessment of insulin resistance). Results: We determined that 63.3% of our patients had dyslipidemia, while hsCRP and uric acid levels suggested an ongoing inflammation. We established that there was a correlation between resistin concentration and waist to hip ratio (WHR) (r=0.294, p<0.05), as well as between resistin concentration and HOMA-IR (r=0.293, p<0.05). Also, uric acid levels correlated with obesity parameters. While comparing parameters by gender we found a significant difference in height (p<0.01), WHR (p<0.001), uric acid levels (p<0.01) and HOMA-IR (p<0.01). Conclusion: Our results show a link between obesity, inflammation and dyslipidemia in children and adolescents. In the future, resistin could become a significant clinical marker for evaluation of cardiometabolic risk.

Combined dyslipidemia in obese children: Response to a focused lifestyle approach

Combined dyslipidemia (elevated triglyceride [TG] ± non-high-density lipoprotein cholesterol [non-HDL-C] ± total cholesterol [TC] ± low-density lipoprotein cholesterol [LDL-C] ± reduced high-density lipoprotein cholesterol [HDL-C]) is seen in >40% of obese children. Primary recommended treatment is weight loss with limited reports of any other approach. In children with combined dyslipidemia, evaluate the response to a clinical protocol focused on diet composition change and increased activity with no direct weight loss approach. Retrospective review of lipid profile and growth parameter changes in patients 6 to 18years of age with diagnosis of combined dyslipidemia seen between December 31, 2009, and December 31, 2011, managed with this protocol through 2 follow-up visits. Combined dyslipidemia diagnosed when ≥2 lipid values exceed the upper limit of normal for TC, TG, non-HDL-C, or LDL-C ± HDL-C below the lower limit of normal. Fifty-three patients were identified, 55% male, 92% obese, mean age 12.1±3.4years with mean follow-up 9.2months. Lipid parameters (mean±SD, mg/dL) improved significantly (P<.001): TC 209±39 to 181±32; TG 255±119 to168±99; non-HDL-C 167±35 to 138±30 and LDL-C 121±43 to 106±30. HDL-C was unchanged. Body mass index decreased in 58% and mean body mass index decreased 0.67kg/m(2) (P<.05). Focused lifestyle changes significantly improved combined dyslipidemia in obese children. With no direct weight loss approach, body mass index decreased in 58%.

Polygenic background of dyslipidemia in obese children

Polygenic background of dyslipidemia in obese children

Frequency of secondary dyslipidemia in obese children

This paper reports the frequency, type, and degree of dyslipidemia in obese children before therapeutic intervention. The relationships between lipid values and weight status, as well as lipid values and physical fitness, of these children were also investigated. The initial examination of the Freiburg Intervention Trial for Obese Children (FITOC) measured the values of triglycerides (TG), total cholesterol (C), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in 546 obese children aged 7-12 (body mass index [BMI] > 97th percentile), and compared these values with those of the age- and sex-specific reference group in the Lipid Research Clinics Population Studies Data Book (LRC). Four groups were selected according to the following scheme: A, Normolipidemia; B, Hyper-LDL-cholesterolemia alone; C, Hypo-HDL-C + hypertriglyceridemia; D, Combined hyperlipidemia = Hyper-LDL-C + hypertriglyceridemia. Body mass index, BMI-SDS (corrected BMI), and physical performance in watt/kg body weight were measured. A total of 45.8% of the overweight children showed an abnormal lipid profile. Ten percent of the children had high LDL-C levels (group B), while 15% had increased LDL-C and increased TG (group D) (higher prevalence in boys). In 18.9% we found increased TG, combined with decreased HDL-C values (group C). Obese children are at risk of dyslipoproteinemia and related diseases. Children with the highest BMI-SDS and lowest physical fitness have the lowest HDL-C values and increased TG, indicating a higher risk for the metabolic syndrome.

Assessment of atherosclerotic cardiovascular risk and management of dyslipidemia in obese children

As the prevalence of childhood obesity increases there is potential for an increase in prevalence and an earlier onset of coronary artery disease. Comorbidities of obesity such as dyslipidemia, insulin resistance syndrome, hypertension, sedentary lifestyle or associated lifestyle factors, like tobacco smoke exposure may result in premature onset of atherosclerosis. Obese children may have other diseases, which can also accelerate the development of atherosclerosis. As clinical atherosclerotic cardiovascular disease does not manifest in obese children, assessment of non-invasive markers of vessel function and structure may be helpful in further stratifying risk and in monitoring effects of intervention. Broad social and cultural changes outside the scope of the health sector are probably most effective in curtailing the epidemic of obesity and thus minimizing its cardiovascular manifestations. Pediatric health care providers should be diligent in screening and providing counseling regarding potential cardiovascular risk factors. Lifestyle alterations resulting in optimal weight management are of foremost importance in preventing the cardiovascular effects of obesity. A select group of children may be at high risk of premature cardiovascular disease despite rigorous implementation of these measures. These children may benefit from pharmacological therapy of dyslipidemia, insulin resistance syndrome or hypertension. Statins have been proven to be effective in decreasing blood low-density lipoprotein cholesterol levels in children and appear safe in the short-term, but their effect in eventually altering the timeline of atherosclerotic cardiovascular disease manifestations in adult life or its associated mortality and morbidity is unclear. The effect of risk factor modification on vascular functional and structural end points will continue to be a resource for evidence-based therapy in these children in the absence of hard clinical outcomes data. This article addresses an overview of assessment of atherosclerotic cardiovascular risk in obese children, but is restricted to an overview of the management of one risk factor - dyslipidemia.

Challenges of Existing Pediatric Dyslipidemia Guidelines

Existing guidelines for screening and managing lipoprotein abnormalities in children and adolescents are based on a consensus document published over 15 years ago by the National Cholesterol Education Program (NCEP) Expert Panel on Blood Cholesterol Levels in Children and Adolescents.1 This document was based on evidence that elevated levels of low-density lipoprotein (LDL) cholesterol are highly correlated with development of atherosclerotic cardiovascular disease (ASCVD) in adults and on pathological data suggesting that dyslipidemia in children and adolescents was associated with early arterial plaque development. The panel recommended 2 strategies to address abnormal lipoprotein levels in children: a population-based approach (dietary recommendations) and a targeted screening approach (selective screening based on family history of ASCVD and/or parental hypercholesterolemia). The guidelines recommended dietary and lifestyle interventions for children with elevated LDL cholesterol levels. They proposed that drug therapy only be considered when LDL cholesterol levels are ≥190 mg/dL or ≥160 mg/dL with concomitant ASCVD risk factors (≥2) or with a family history of ASCVD. Article p 32 Since the initial publication of the existing guidelines, many significant challenges have emerged that deserve attention. First, accumulating data suggest that the guidelines significantly underestimated the number of children who would be targeted for lipoprotein screening. Second, the guidelines do not account for variations in lipids due to race, gender, and pubertal status, all of which are known …

Das Metabolische Syndrom: Eine neue Kinderkrankheit?

Overweight and obesity in children and adolescents have become a major public health problem in recent years throughout the world. The medical consequences of obesity may manifest as an increase in the prevalence of the metabolic syndrome in children and adolescents putting them at increased risk for future cardiovascular diseases. Obesity can cause insulin resistance and might disturb glucose homeostasis eventually leading to type 2 diabetes in susceptible patients. Insulin resistance is also involved in the pathogenesis of dyslipidemia in obese children characteristically presenting as hypertriglyceridemia and low HDL cholesterol. Even elevated blood pressure might be present in obese kids. Here we present a 12-year-old boy diagnosed with the metabolic syndrome. The diagnostic criteria of the metabolic syndrome in children and adolescents are discussed. Thoughts about pathophysiology and therapeutic options are offered.

Longitudinal Analyses among Overweight, Insulin Resistance, and Cardiovascular Risk Factors in Children

It has been questioned whether insulin resistance or obesity is the central abnormality contributing to the cardiovascular risk factors dyslipidemia and hypertension in obesity. We studied weight status [SD score (SDS)-BMI], lipids (triglycerides, low-density lipoprotein- and high-density lipoprotein-cholesterol), blood pressure, and insulin resistance index [as homeostasis model assessment (HOMA) model] over a 1-year period in 229 obese white children (median age 12 years). Any degree of decrease in HOMA was associated with significant decreases in triglycerides (p < 0.001), systolic blood pressure (p < 0.001), and diastolic blood pressure (p < 0.001), whereas the children with different changes in HOMA did not differ significantly in their weight changes. Only the children in the highest quartile of weight reduction (decrease in SDS-BMI > 0.5) demonstrated a significant decrease in systolic blood pressure (p < 0.001), diastolic blood pressure (p < 0.001), and triglycerides (p = 0.012), and an increase in high-density lipoprotein-cholesterol (p = 0.023), whereas with a lower degree of weight loss, there were no significant changes in cardiovascular risk factors. In contrast with a lower degree of weight loss, a reduction of >0.5 SDS-BMI was associated with a significant decrease in HOMA (p < 0.001). Because blood pressure and triglycerides decreased with any degree of decrease in HOMA, independently of changes in weight status, these findings support the hypothesis that insulin resistance is the central abnormality contributing to these cardiovascular risk factors. Therefore, improving insulin resistance seems more important than reducing overweight to prevent or treat hypertension and dyslipidemia in obese children.

Increased cutaneous blood flow but impaired post-ischemic response of nutritional flow in obese children

It is well known that cardiovascular risk factors and dyslipidemia along with obesity can be identified early in life. Serum lipids and lipoproteins influence skin vessel reactivity in adults. The purpose of this study was to investigate the cutaneous microcirculation and its correlation to dyslipidemia in obese children. Thirty-four obese children and an equal number of age- and sex-matched healthy children were enrolled in this study. Laser Doppler flowmetry and dynamic capillaroscopy were performed to measure total cutaneous blood flow and nutritional blood flow, respectively. A significantly higher cutaneous baseline flow and peak flow after a 1-min arterial occlusion was noticed in obese group as compared to normal control. Results of dynamic capillaroscopy revealed values of resting capillary blood cell velocity that did not differ from controls but a significantly lower peak CBV after a 1-min arterial occlusion in obesity. Plasma lipids examination showed a high triglycerides and low high density lipoprotein cholesterol levels in obesity. Pearson analysis detected no significant correlations between pCBV, baseline flow and peak flow and dyslipidemia in obesity. These results may be explained by the fact that the duration of dyslipidemia in our study population was not long enough to cause vascular damage or the dyslipidemia was not pronounced enough to have an impact on skin vessel activity tests. It is also possible, that the combination of methods used in the present study was not sensitive enough to detect an existing correlations between flow values and high triglycerides/low HDL-cholesterol values in the obese group. Our results suggest that all the responses of the cutaneous microcirculation were mainly due to physiological compensatory rather than pathological reactions in young obese children. The results of cutaneous microcirculatory assessment in obese children provide follow-up parameters for assessing the risk of cardiovascular diseases later in life.