OBJECTIVESome research has shown that C-reactive protein (CRP), leptin, soluble leptin receptor (sLR) and blood lipids are involved in the development of obesity. This study aimed to investigate the changes of leptin resistance, blood lipids and inflammatory response before and after the exercise therapy in children with obesity.

METHODSFifty-one obese children at ages of 12 years received an exercise therapy for 2 months. The levels of serum leptin, sLR, triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-sensitivity C-reactive protein (hs-CRP) were measured before and after the exercise therapy. Forty normal children served as the control group.

RESULTSCompared with the control group, serum levels of leptin, TG, TC, LDL-C and hs-CRP and the body mass index (BMI) in the obese group increased (p<0.01), while the serum level of sLR decreased significantly (p<0.05). The levels of hs-CRP, leptin, TC, TG, LDL-C and BMI in the obese group were significantly reduced after the exercise therapy (p<0.05). In the obese group, the serum leptin level was positively correlated with the levels of blood lipids and hs-CRP (p<0.05); serum levels of leptin and hs-CRP were negatively correlated with the sLR level (p<0.05); the hs-CRP level was positively correlated with the levels of blood lipids (p<0.01).

CONCLUSIONSLeptin resistance and the changes of blood lipids and inflammatory response are found in children with obesity. Exercise therapy can partially improve these changes.

Body Mass Index ; C-Reactive Protein ; analysis ; Child ; Exercise Therapy ; Female ; Humans ; Leptin ; blood ; Lipids ; blood ; Male ; Obesity ; blood ; therapy ; Receptors, Leptin ; blood

OBJECTIVETo investigate serum leptin level and its relationship with bone mineral density in obese children from Changsha City.

METHODSOne hundred and nineteen obese children and 103 normal children aged 7 to 12 years from five primary schools of Changsha City were enrolled. Obesity was assessed based on the body mass index (BMI). Dual energy X-ray absorptiometry (DEXA) was used to determine bone mineral density (BMD) and body composition. Serum leptin level was measured using enzyme-linked immunosorbent assay (ELISA).

RESULTSThe obesity group had higher height, weight, BMI, waist circumference and waist to hip ratio (WHR) compared with the normal group (p<0.01). BMD, bone mineral content (BMC), lean mass (LM), fat mass (FM), percentage of body fat (%BF) and leptin concentration in the obesity group were significantly higher than those in the normal group (p<0.01). Serum leptin level was positively correlated with BMD, BMC, LM and FM (r=0.528-0.903, p<0.01). Multiple stepwise regression analysis indicated that BMI and %BF were independent influencing factors for serum leptin level.

CONCLUSIONSObese children have higher serum leptin level. Serum leptin concentration is significantly correlated with BMD and body composition. BMI and %BF are independent influencing factors for serum leptin level in children.

Body Composition ; Bone Density ; Child ; Female ; Humans ; Leptin ; blood ; Male ; Obesity ; blood ; Regression Analysis ; Sex Characteristics

OBJECTIVETo evaluate the role of leptin in neointimal formation and related mechanisms.

METHODSFemoral arterial injury was induced in wild-type (Wt, n = 10), leptin-deficient (Lep(-)/-, n = 12), and leptin receptor-deficient (LepR(-)/-, n = 10) mice. Leptin treatment studies (tail vein injection of adenovirus expressing murine leptin on the RSV promoter, ad-leptin) were performed on Lep(-)/- (n = 5) and LepR(-)/- (n = 4) mice. Intimal (I) and medial (M) areas were measured and the ratio of I/M was calculated. Smooth muscle cells were detected by smooth muscle alpha-actin staining using an alpha-actin monoclonal antibody. Cellular proliferation was analyzed with BrdU Staining Kit and the number of BrdU-positive cells was counted manually. Plasma leptin level was measured by ELISA.

RESULTSThe I/M ratio of Lep(-)/- and LepR(-)/- mice was significantly lower than that in Wt separately (Lep(-)/- vs. Wt = 0.80 +/- 0.14 vs. 1.50 +/- 0.22, P < 0.01; LepR(-)/- vs. Wt = 0.55 +/- 0.20 vs. 1.50 +/- 0.22, P < 0.05). Plasma leptin level was significantly increased in Lep(-)/- and LepR(-)/- mice post leptin treatment. I/M was significantly increased in Lep(-)/- mice receiving ad-leptin compared with untreated Lep(-)/- mice (P < 0.05), while I/M was similar between LepR(-)/- mice with and without ad-leptin treatment (P > 0.05). The changes on number of positive alpha-actin and BrdU stained smooth muscle cells were consistent with the neointimal formation findings in various groups.

CONCLUSIONSMice lacking leptin or the leptin receptor were protected from neointimal formation following vascular injury. Leptin treatment increased neointimal formation in Lep(-)/- but not in LepR(-)/- mice, suggesting leptin receptor activation and vascular smooth muscle cell proliferation played a pivotal role on neointimal formation post-injury in this model, giving an evidence that high plasma leptin level is a risk factor for neointimal formation.

Actins ; analysis ; Animals ; Cell Proliferation ; Leptin ; blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular ; pathology ; Receptors, Leptin ; metabolism ; Tunica Intima ; pathology

In order to explore the effect and underlying mechanism of hypoxia on body weight, the effect of intermittent moderate hypoxia on high-fat diet-induced obesity was observed in mice, and the role of leptin in hypoxic effect was identified. Healthy Kunming mice were divided randomly into 4 groups (n=20 in each group). The control group: the mice were fed normally under the normal oxygen pressure. Hypoxia group: the mice were fed normally, and given intermittent moderate hypoxia training. Obesity group: the mice were fed diet rich in fat and sugar under the normal oxygen pressure. Hypoxia + obesity group: the mice were fed diet rich in fat and sugar, and given intermittent moderate hypoxia training. After 40 d of feeding and training, the body weight of mice was determined, and the average increasing rate of body weight in each group was calculated and normalized with food intake. Meanwhile, plasma leptin level was measured with ELISA method, and fatty degeneration and leptin receptor expression in liver were observed by Sudan III staining and immunohistochemistry, respectively. The obesity mouse model was successfully established with increases in body weight, plasma leptin level and distribution of adipocytes in the liver. The average body weight and density of adipocytes in the liver in hypoxia and hypoxia + obesity groups decreased obviously, while plasma leptin level and leptin receptor expression in the liver were increased. It is suggested that intermittent moderate hypoxia reduces body weight through elevating plasma leptin level and/or enhancing leptin receptor expression in the liver.
Adipocytes ; cytology ; Animals ; Body Weight ; Female ; Hypoxia ; metabolism ; pathology ; Immunohistochemistry ; Leptin ; blood ; Liver ; chemistry ; Mice ; Mice, Obese ; Obesity ; metabolism ; pathology ; Receptors, Leptin ; analysis

OBJECTIVETo explore the effects of obesity on the peak level of luteinizing hormone (LH) in the gonadotropin-releasing hormone (GnRH) agonist test and obesity-related hormones in girls with central precocious puberty (CPP).

METHODSThree hundred and thirty-three girls with CPP who underwent the GnRH agonist test between 2012 and 2014 were classified into three groups: normal weight (n=123), overweight (n=108), and obesity (n=102), according to body mass index (BMI). The sexual development indices were compared between the three groups. Twenty girls were randomly selected from each group for evaluation of the serum levels of leptin, sex hormone binding globulin (SHBG), neurokinin B, and kisspeptin. The correlation of BMI with the levels of various hormones was assessed using Pearson correlation analysis.

RESULTSThere was no significant difference in mean age at diagnosis between the three groups; however, the bone age was significantly higher in the overweight and obesity groups than in the normal weight group (P<0.05). The peak level of LH in the GnRH agonist test and SHBG level in the normal weight group were significantly higher than those in the overweight and the obesity groups, while the serum levels of leptin and neurokinin B were significantly lower in the normal weight group than in the overweight and the obesity groups (P<0.05). BMI was negatively correlated with the peak level of LH in the GnRH agonist test and SHBG level (P<0.05), and positively correlated with the levels of leptin and neurokinin B (P<0.05).

CONCLUSIONSThe effects of BMI on the result of the GnRH agonist test and levels of obesity-related hormones should be taken into account in girls with precocious puberty.

Body Mass Index ; Child ; Female ; Gonadotropin-Releasing Hormone ; agonists ; Humans ; Leptin ; blood ; Luteinizing Hormone ; blood ; Neurokinin B ; blood ; Obesity ; blood ; Puberty, Precocious ; blood ; Sex Hormone-Binding Globulin ; analysis

OBJECTIVETo study the correlation between obesity and hypersensitive C-reactive protein (hsCRP), leptin, and insulin sensitive index (ISI) in children.

METHODSThe subjects included 69 obese volunteers and 30 age and gender-matched normal volunteers who were recruited from 13702 children aged 2 to 18 years in Xiangtan City by sampling survey. The body mass index (BMI), hsCRP, leptin, fasting plasma glucose (FPG), and fasting insulin (INS) were tested, and then the ISI was calculated. The results between the obese and normal children were compared. The correlation between the parameters was evaluated.

RESULTSThe values of hsCRP, leptin and INS in obese children were significantly higher than those in the normal controls (P < 0.01), but the ISI in obese children was significantly lower than that in normal controls (P < 0.01). The BMI was significantly positively correlated with the values of hsCRP, leptin and INS (r=0.225, P < 0.05; r=0.776, P < 0.01; r=0.568, P < 0.01), but was significantly negatively correlated with the ISI (r=-0.889, P < 0.01). There was a positive correlation between the value of hsCRP and the values of FPG and INS (r=0.429, P < 0.01; r=0.206, P < 0.05), and there was a negative correlation between the value of hsCRP and the ISI (r=-0.889, P < 0.01). The value of leptin significantly positively correlated with the values of INS and BMI, and significantly negatively correlated with the ISI.

CONCLUSIONSInsulin resistance and leptin resistance exist in obese children. The inflammatory factors such as CRP and leptin may be involved in the pathogenesis of obesity.

Adolescent ; Blood Glucose ; analysis ; Body Mass Index ; C-Reactive Protein ; analysis ; Child ; Female ; Humans ; Insulin Resistance ; Leptin ; blood ; Male ; NF-kappa B ; physiology ; Obesity ; blood

OBJECTIVETo study the changes of serum leptin (LEP) and vascular endothelial growth factor (VEGF) in children with congenital heart disease(CHD) and their roles in CHD.

METHODSForty-eight children with acyanotic CHD (ACHD group), 20 age-matched children with cyanotic CHD (CCHD group) and 20 healthy children (control group) were enrolled. The ACHD group was subdivided into two groups with (n=20) or without concurrent heart failure (n=28). Serum LEP, VEGF, total protein and albumin levels and body mass index (BMI) were measured.

RESULTSSerum total protein and albumin levels were not apparently different in all CHD children from healthy controls, but there was a significant difference in the BMI between them (p<0.01). Serum LEP and VEGF levels and the ratio of LEP/BMI in all CHD children were significantly higher than those in healthy controls (p<0.01). Compared with the ACHD group without heart failure, the serum LEP and VEGF levels and the ratio of LEP/BMI in the CCHD and the ACHD with heart failure groups increased significantly (p<0.01). In the ACHD group, serum LEP level was positively correlated with BMI (p<0.01). In the CCHD group, there were positive correlations between serum LEP level and serum VEGF level (p<0.01) and between hemoglobin concentration and serum VEGF level (p<0.01). Arterial oxygen saturation was negatively correlated with serum VEGF (p<0.01) and LEP levels (p<0.01) in the CCHD group.

CONCLUSIONSBoth VEGF and LEP play roles in the pathophisiological process of CHD. VEGF and LEP are associated with the development of heart failure in children with ACHD.

Body Mass Index ; Child ; Child, Preschool ; Female ; Heart Defects, Congenital ; blood ; Hemoglobins ; analysis ; Humans ; Infant ; Leptin ; blood ; Male ; Oxygen ; blood ; Vascular Endothelial Growth Factor A ; blood

OBJECTIVETo study blood Leptin level of 154 (78 male, 76 female) Chinese obese/non-obese children aged 0 - 14 years during 1999 - 2001.

METHODSThe gender- and age-specific distribution pattern of Leptin and its relationship with anthropometric parameters (waist circumference, waist/hip ratio, lean body mass, fat mass, body fat percentage, BMI/Kaup index etc.) and blood insulin level were recorded.

RESULTS(1) The blood Leptin level in healthy non-obese kids ranged from 1.01 - 29.92 (ng/ml), the mean values and SD were 2.99 +/- 2.13 (ng/ml) [90% confidence interval was 1.36 - 14.21 (ng/ml) in boys and 1.74 - 21.17 (ng/ml) in girls]. There was no significant difference in the blood Leptin level between serum and plasma. (2) The blood Leptin level was higher in overweight/obese kids than that in non-obese kids (P < 0.001). (3) There was significant difference in the blood Leptin levels between boys and girls groups (P = 0.023), especially in non-obese group (P = 0.004). The multiple regression analysis showed that there was no correlation between gender and blood Leptin level when body fat factor was added (P = 0.138, 0.241, 0.990), but there was still a strong correlation between blood leptin level and BMI, FM and BF% (P < 0.001). (4) There was a correlation between blood Leptin level and age (P = 0.005), especially in overweight/obese group and in girls (P = 0.001). The blood Leptin level rose from early puberty, especially in girl group (P = 0.045). There was significant difference in blood Leptin level in different age groups (P < 0.001) (5) There were strong positive correlation between blood Leptin level and BMI, BM and FM%, a weak correlation with LBM, and no correlation with W/H ratio in boys and a positive relationship in girls. The Quatatic equation was better than the linear equation in description of the correlation mentioned above. (6) There was a correlation between blood Leptin from 0 to 7 yr and birth weight (P = 0.001), after 7 yr of age this correlation disappeared (P = 0.456). (7) A positive correlation was seen between blood Leptin level and blood insulin level (P < 0.001).

CONCLUSIONThe blood Leptin level of 0 - 14 years old children is consistent with the level of growth of adiposity tissue and the degree of adiposity rebound.

Adolescent ; Age Factors ; Birth Weight ; physiology ; Body Constitution ; Body Mass Index ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Insulin ; blood ; Leptin ; blood ; Male ; Multivariate Analysis ; Regression Analysis ; Sex Factors

BACKGROUNDLeptin is a protein mainly secreted by adipocytes, and the major function of leptin was its role in body weight regulation. It is suggested that increased levels of circulating leptin may contribute to anorexia in pathologic conditions including chronic obstructive pulmonary disease (COPD). Recent studies have provided evidence for a link between leptin and proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha). This study aimed to explore the role of serum leptin in the malnutrition of COPD patients, and to observe the changes of serum leptin levels during acute exacerbation, also to investigate relationship between leptin and TNF-alpha.

METHODSSeventy-two COPD patients and 34 control subjects participated in this study. Seventy-two COPD patients were divided into 3 groups: group COPD IA (patients without malnutrition during acute exacerbation, n = 25), group COPD IB (patients without malnutrition during stable disease, n = 29), group COPD II (patients with malnutrition during stable disease, n = 18). To eliminate the effect of sex differences, all patients and controls were male. Body mass index (BMI), percent ideal body weight (IBW%), triceps skin-fold thickness (TSF), mid-upper arm circumference (MAC), mid-upper arm muscle circumference (MAMC), serum leptin and TNF-alpha levels, serum prealbumin (PA), serum transferrin (TF), serum albumin (Alb), total lymphocytes count (TLC), forced expiratory volume in one second (FEV(1)), maximal inspiration pressure (MIP) and maximal expiration pressure (MEP) were measured in all participants. Leptin levels were measured by radioimmunoassay. TNF-alpha levels were measured by ELISA. The between group difference and correlation of these parameters were analyzed.

RESULTSSerum leptin levels were significantly lower in group COPD II [(4.07 +/- 3.42) ng/ml] than in group COPD IB [(9.72 +/- 6.67) ng/ml] and controls [(8.21 +/- 5.41) ng/ml] (P < 0.05). There was no statistically significant difference in serum leptin levels between group COPD IA [(10.82 +/- 6.40) ng/ml], group COPD IB [(9.72 +/- 6.67) ng/ml] and controls [(8.21 +/- 5.41) ng/ml]. There was no statistically significant difference in serum TNF-alpha levels between group COPD II [(8.03 +/- 3.37) pg/ml], group COPD IA [(8.90 +/- 1.60) pg/ml], and group COPD IB [(7.25 +/- 2.08) pg/ml]. There was no significant correlation between leptin and TNF-alpha in any group.

CONCLUSIONSLeptin was not involved in anorexia and weight loss of COPD patients. There was no statistically significant difference in serum leptin levels between COPD patients during stable stage and acute exacerbation, and there was no significant correlation between TNF-alpha and leptin during the regulation of the energy balance in COPD patients.

Adult ; Aged ; Anorexia ; etiology ; Humans ; Leptin ; blood ; Male ; Malnutrition ; blood ; etiology ; Middle Aged ; Pulmonary Disease, Chronic Obstructive ; blood ; complications ; Tumor Necrosis Factor-alpha ; analysis ; Weight Loss

OBJECTIVETo investigate the influence of lead exposure in rats during the developmental stage on the expression of leptin in plasma, cerebrospinal fluid, and hippocampus, as well as investigating whether leptin is associated with the mechanism of cognitive impairment induced by lead exposure.

METHODSThe rat model of cognitive impairment after chronic lead exposure was established by adding lead acetate into drinking water. According to the concentration of lead acetate in drinking water, the rats were divided into control (0 ppm), low-lead (50 ppm), medium-lead (200 ppm), and high-lead groups (1 000 ppm), with 16 rats in each group. Atomic absorption spectrometry was used to measure the content of lead in the plasma, cerebrospinal fluid and hippocampus. ELISA was used to measure the level of leptin in the plasma and cerebrospinal fluid. Immunohistochemistry was used to observe the distribution of leptin protein in the hippocampus. Western blot was used for relative quantification of leptin proteins in the hippocampus.

RESULTSCompared with the control group, the lead exposure groups showed significant increases in the content of lead in blood, cerebrospinal fluid, and hippocampus (P<0.01), as well as significant reductions in the levels of leptin in plasma and cerebrospinal fluid (P<0.05). The results of immunohistochemical staining showed that leptin was mainly distributed in the cytoplasm of pyramidal neurons in the hippocampal CA region. The results of Western blot showed that compared with the control group, the three lead exposure groups showed a slight increase in the protein expression of leptin in the hippocampus (P>0.05).

CONCLUSIONSLead exposure can reduce the levels of leptin in plasma and cerebrospinal fluid in rats, which may be associated with the mechanism of cognitive impairment induced by lead exposure.

Animals ; Apoptosis ; drug effects ; Cognition ; drug effects ; Female ; Hippocampus ; chemistry ; drug effects ; pathology ; Lead ; blood ; toxicity ; Leptin ; analysis ; blood ; cerebrospinal fluid ; Male ; Rats ; Rats, Sprague-Dawley