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Leptin Concentrations (leptin + concentration)

Distribution by Scientific Domains

Medical Sciences	59%
Life Sciences	40%

Distribution within Medical Sciences

Diabetes	13%
Pediatrics	10%
Andrology	6%
10 Other Subdomains	48%

Kinds of Leptin Concentrations

plasma leptin concentration

serum leptin concentration

Selected Abstracts

Relationships between plasma leptin levels and body composition parameters measured by different methods in postmenopausal women

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 5 2003
Toivo Jürimäe
The aim of this study was to determine the effects of body composition measured by different methods with different measurement errors on fasting plasma leptin level in normal body mass and obese postmenopausal women. It was hypothesized that the relationship between plasma leptin concentration and body fat is higher using more sophisticated laboratory methods (dual energy X-ray absorptiometry, DXA) in comparison with field methods (bioelectrical impedance analysis, BIA, or skinfold thickness) for body fat measurement because of the greater precision of DXA measurements. Thirty-five postmenopausal (55,83 years of age) healthy Estonian women were divided into two groups: BMI < 27kg/m2 as non obese (n = 18) and BMI> 27kg/m2 as obese (n = 17). Body composition was determined using DXA (total body, arms, legs, and trunk fat percent, fat mass, and LBM) and BIA methods. Body fat percent was significantly higher using the DXA method. Subcutaneous adipose tissue distribution was determined by measuring nine skinfold thicknesses. Body fat distribution was defined as the ratio of waist-to-hip (WHR) and waist-to-thigh (WTR) circumferences. Leptin was determined by means of radioimmunoassays. Leptin concentration was not significantly different between groups (19.0 ± 13.3 and 21.5 ± 21.5ng/ml in non obese and obese groups, respectively). Body fat percent and fat weight measured by DXA or BIA methods and all measured skinfold thickness values, except biceps and abdominal, were higher in obese women. Body height did not correlate significantly with leptin concentrations. The relationships between leptin concentration were highest with body weight (r = 0.67) and BMI (r = 0.73) values in the obese group. All measured body fat parameters using DXA or BIA methods correlated significantly with plasma leptin concentration in the obese group. LBM did not influence the leptin concentration in postmenopausal women. Stepwise multiple regression analysis indicated that the body fat percent measured using the DXA method was highly related to plasma leptin concentration in the obese group (63.2%; R2 × 100). When absolute fat mass parameters were considered, leptin concentration was related to the mass of arms fat tissue in the obese group of women (62.3%). Body fat percent measured by BIA was highly related to plasma leptin concentration in the obese group (63.3%). Only biceps skinfold thickness was related to leptin concentration (22.5% and 58.9%, in the nonobese and obese groups, respectively) from the nine measured skinfold thicknesses. WHR and WTR did not reflect leptin concentration in different groups of postmenopausal women. It was concluded that different methods of body composition estimation generate different correlations with plasma leptin concentration. Body fat percent and especially fat mass measured by DXA are the main predictors relating to plasma leptin concentration in obese, but not in nonobese, postmenopausal women. In addition, fat mass in arms measured by DXA and biceps skinfold thickness were also highly related to leptin concentration. Am. J. Hum. Biol. 15:628,636, 2003. © 2003 Wiley-Liss, Inc. [source]

Adipocytokines are associated with radiographic joint damage in rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 7 2009
Young Hee Rho
Objective Obesity protects against radiographic joint damage in rheumatoid arthritis (RA) through poorly defined mechanisms. Adipocytokines are produced in adipose tissue and modulate inflammatory responses and radiographic joint damage in animal models. The purpose of this study was to examine the hypothesis that adipocytokines modulate inflammation and radiographic joint damage in patients with RA. Methods We compared serum concentrations of leptin, resistin, adiponectin, and visfatin in 167 RA patients and 91 control subjects. The independent association between adipocytokines and body mass index (BMI), measures of inflammation (C-reactive protein [CRP], interleukin-6 [IL-6], and tumor necrosis factor , [TNF,]), and radiographic joint damage (Larsen score; n = 93 patients) was examined in RA patients by multivariable regression analysis first controlling for age, race, and sex, and then for obesity (BMI) and inflammation (TNF,, IL-6, and CRP). Results Concentrations of all adipocytokines were significantly higher in RA patients than in controls; for visfatin and adiponectin, this association remained significant after adjusting for BMI, inflammation, or both. Visfatin concentrations were associated with higher Larsen scores, and this association remained significant after adjustment for age, race, sex, disease duration, BMI, and inflammation (odds ratio [OR] 2.38 [95% confidence interval (95% CI) 1.32,4.29], P = 0.004). Leptin concentrations showed a positive association with the BMI (, = 0.58, P < 0.01) and showed a negative association with the Larsen score after adjustment for inflammation (OR 0.32 [95% CI 0.17,0.61], P < 0.001), but not after adjustment for BMI (OR 0.86 [95% CI 0.42,1.73], P = 0.67). Conclusion Concentrations of adipocytokines are increased in patients with RA and may modulate radiographic joint damage. Visfatin is associated with increased, and leptin with reduced, levels of radiographic joint damage. [source]

Circulating leptin and body composition in chronic obstructive pulmonary disease

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 10 2005
S. Karakas
Summary Nutritional depletion and weight loss are two features of chronic obstructive pulmonary disease (COPD), and the association between low body mass index (BMI) and poor prognosis in patients with COPD is a common clinical observation. Mechanisms of weight loss are still unclear in COPD. Excessive energy expenditure partly due to increased work of breathing was shown, but other mechanisms have been searched for. Leptin is a hormone secreted by adipocytes that plays an important role in energy homeostasis and regulates body weight through control of appetite and energy expenditure. The aim of this study was to evaluate the association of circulating leptin levels and measures of body composition in COPD patients. Thirty male COPD outpatients (mean age 66.3 ± 8.4) and 20 controls (mean age 65.9 ± 10.8) were included in the study. After standard spirometry and body composition measurements, serum leptin concentration was measured by ELISA assay. COPD patients were grouped according to BMI. Mean BMI was 19.01 ± 2.26 kg/m2 in group 1 (COPD patients with low BMI), 26.85 ± 4.51 in group 2 COPD (COPD patients with normal/high BMI) and 27.64 ± 2.75 kg/m2 in healthy controls (group 3). Mean serum leptin concentration was 1.41 ± 1.86 ng/ml in group 1, 2.60 ± 1.38 ng/ml in group 2 and 2.82 ± 1.46 ng/ml in group 3 (p = 0.002). Leptin correlated to not only BMI but also body weight, waist circumference, triceps and biceps skinfold thickness and body fat percent (p < 0.05 for all). Results of this study suggest that the cause of weight loss is not increased circulating leptin in COPD. Instead, leptin remains regulated in COPD and further decreased in patients with low BMI, probably as a compensatory mechanism to preserve body fat content, which should be evaluated in further studies. [source]

Relationship between plasma leptin concentrations and carcass composition in fattening mutton: a comparison with ultrasound results

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 9-10 2005
M. Altmann
Summary Positive relationships between circulating leptin concentrations and body fat content have been established in sheep when covering a rather broad range of age and/or body weight. The usefulness of leptin measurements for predicting carcass fat has yet to be evaluated specifically in fattening lambs. We therefore measured plasma leptin concentrations in 56 male lambs half and half Merino Mutton and Blackheaded Mutton. Subcutaneous fat thickness was measured by ultrasound 1 day before the lambs were slaughtered at 35 or 45 kg live weight. Carcass composition was determined by tissue dissection. The coefficients of correlations between leptin and the different amounts in fat depots ranged from 0.40 to 0.56 within the two live weight groups, and from 0.53 to 0.64 when taking the two groups together. Carcass fat percentage was estimated by leptin concentrations with the same accuracy (R2 = 0.34) as with ultrasound fat thickness. The accuracy was higher for leptin in the 35 kg-group whereas the accuracy was higher for ultrasound fat thickness in the 45 kg-group (R2 = 0.26 vs. 0.31). A combination of leptin and ultrasound fat thickness clearly enhanced the precision of estimation in all groups. Further investigations on the influence of factors such as breed, gender, duration of feed withdrawal or photoperiod on the association between leptin and carcass composition are necessary before the suitability of plasma leptin concentration for practical application can be evaluated. [source]

Impaired Energetic Metabolism After Central Leptin Signaling Leads to Massive Appendicular Bone Loss in Hindlimb-Suspended Rats,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 12 2008
Aline Martin
Abstract We previously showed in rats that the leptin effects on bone were dose dependent. Positive effects were observed when serum leptin concentration was in a physiological range. In contrast, important increases in serum leptin levels led to negative effects on bone formation similar to those reported after intracerebroventricular leptin administration in mice. To clarify whether leptin effects on bone depend on administration route and/or animal model, female rats were hindlimb unloaded or not and treated either with intracerebroventricular infusion of leptin or vehicle for 14 days. By increasing cerebrospinal fluid (CSF) leptin concentration, intracerebroventricular infusion of leptin significantly reduced food intake and consequently body weight, abdominal fat, and lean mass of the animals. Leptin infusion inhibited bone elongation over the 14 days and blunted cortical bone thickening at the femoral diaphysis site. Interestingly, leptin effects were site dependent in the cancellous bone envelopes, because tibia metaphysis BMD was lower and lumbar spine BMD was higher under intracerebroventricular leptin. Treated groups showed reduced bone remodeling independently of hindlimb unloading. Multiple downstream pathways were implicated in the mediation of these negative leptin effects on bone including not only stimulation of the sympathetic nervous system but also a decrease in somatotropic axis activity. Therefore, the intracerebroventricular leptin-induced bone loss could be largely related to the concurrent alteration of energetic and metabolic status. In summary, our study supports the hypothesis of a concentration-dependent balance between peripheral and central control of leptin on bone. [source]

Gingival crevicular fluid and serum leptin: their relationship to periodontal health and disease

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2007
B. V. Karthikeyan
Abstract Background & Aims: Leptin is a pleiotrophic hormone produced by adipose tissue and it plays an important role in protection of the host from inflammation and infection. The purpose of this study is to determine the presence of leptin in gingival crevicular fluid (GCF) and serum samples and to find out their association, if any. Methods: Forty two subjects were selected based on their body mass index and were divided into three groups of 14 each; healthy (Group I), chronic gingivitis (Group II) and chronic periodontitis (Group III). GCF samples (by microcapillary pipettes) and serum samples (by venipuncture) were collected to estimate the levels of leptin using enzyme linked immunosorbent assay kit. Results: The highest mean leptin concentration in GCF was obtained for Group I (2658 pg/ml) and the least for Group III (1312 pg/ml). In contrast, the lowest serum leptin concentration was obtained for the Group I (8783 pg/ml), and the highest for Group III (12082 pg/ml). This suggests a negative correlation of GCF leptin concentration and a positive correlation of serum leptin concentration as the clinical attachment level progresses (p<0.05). Conclusion: These results suggest that greater the periodontal destruction, lesser is the GCF leptin concentration and greater the serum leptin concentration. [source]

Hypothalamic Expression of Human Growth Hormone Induces Post-Pubertal Hypergonadotrophism in Male Transgenic Growth Retarded Rats

JOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2006
J. S. Davies
Growth hormone (GH) is known to regulate peripheral components of the hypothalamo-pituitary gonadal (HPG) axis, but it remains unclear whether GH exerts a significant influence on the activity of the hypothalamo-pituitary components of the HPG axis. In this study, we investigated the development of HPG axis function in the male transgenic growth retarded (Tgr) rat, a model of moderate systemic GH deficiency caused by hypothalamic expression of human (h)GH. Impaired postnatal somatotroph expansion and moderate GH deficiency in male Tgr rats were accompanied by a two- to three-fold increase in pituitary gonadotrophin content, but without a significant change in the pituitary gonadotroph population. A three- to nine-fold elevation in basal circulating luteinising hormone concentration was seen in postpubertal Tgr rats, with a smaller increase in follicle-stimulating hormone. Despite this hypergonadotrophism, there was no corresponding increase in steroidogenic (circulating testosterone and seminal vesicle weights) or gametogenic (spermatozoa counts in seminiferous tubules) activity in the postpubertal Tgr testis. Following puberty, the plasma leptin concentration also became progressively elevated in Tgr males. Circulating gonadotrophin and leptin levels were normalised in Tgr rats by peripheral physiological replacement of rat GH, but plasma testosterone concentration was unaffected. These results confirm that hGH exerts a positive influence on the central control of gonadotrophin secretion in the Tgr rat, but the absence of a corresponding elevation in the steroidogenic or gametogenic function of the Tgr testis implies that the peripheral GH/insulin-like growth factor I axis may also exert a permissive influence on testicular function. The relative contribution of somatogenic and lactogenic mechanisms and the potential influence of elevated leptin and decreased sensitivity to androgen feedback to the development of postpubertal hypergonadotrophism in Tgr males remain to be determined. [source]

Leptin levels in gingival crevicular fluid in periodontal health and disease

JOURNAL OF PERIODONTAL RESEARCH, Issue 4 2007
B. V. Karthikeyan
Background and Objective:, A high concentration of leptin is associated with healthy gingival tissue, and the concentration of leptin decreases as periodontal disease progresses. However, to date, the leptin concentration in gingival crevicular fluid has not been documented. Hence, the present study was carried out to explore the presence of leptin in gingival crevicular fluid in periodontal health and disease, and to probe further into its possible role in periodontal disease progression. Material and Methods:, A total of 45 adult patients were selected, based on their body mass index, for the study. They were categorized into three groups of 15 patients each, based on their periodontal tissue status, as follows: group I (clinically healthy gingiva with no loss of attachment); group II (chronic gingivitis with no loss of attachment); and group III (chronic periodontitis). Gingival crevicular fluid samples of 1 µL were collected extracrevicularly using white color-coded 1,5 µL calibrated volumetric microcapillary pipettes from one site in each person, and samples were analyzed for leptin using a commercially available enzyme-linked immunosorbent assay kit. Results:, The concentration of leptin in gingival crevicular fluid of patients in group I (2292.69 pg/mL) was statistically higher (p < 0.05) than in those of groups II (1409.95 pg/mL) and III (1071.89 pg/mL). This suggests a negative correlation of gingival crevicular fluid leptin concentration with clinical attachment loss (p < 0.05). Conclusion:, As periodontal tissue destruction increased, there was a substantial decrease in gingival crevicular fluid leptin concentration. This observation extends our knowledge of the protective role of leptin in periodontal health. [source]

Lack of association between leptin G2548A gene polymorphism and Behçet's disease

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 1 2007
F Aydin
Abstract Background, Behçet's disease is a chronic, multisystem, inflammatory disease characterized by the predominance of T-helper 1 cytokines. The disease is also characterized by infiltration of lymphocytes and neutrophils into the affected tissues. Because cytokines are involved in the regulation of lymphocyte and phagocyte functions, they may play an important role in the pathogenesis of Behçet's disease. Leptin, a member of the gp 130 family of cytokines, induces a strong T-helper 1 response and is regarded as a proinflammatory inducer. Recent studies have shown that serum leptin concentration was increased in patients with Behçet's disease and correlated with disease activity. Objectives, We aimed to investigate the role of G2548A polymorphism of leptin gene in patients with Behçet's disease and compare the results with healthy controls. Patients and methods, A total of 93 subjects with Behçet's disease and 125 healthy controls were included in this study. Analyses of G-2548A polymorphism of the LEP gene were performed using the PCR-restriction fragment length polymorphism technique. The genotypes (GG, GA, and AA of leptin G2548A) and alleles (G and A of leptin 2548) were scored and the frequency was estimated. The frequencies of the alleles and genotypes in patients and controls were compared. We analysed the correlation between leptin gene polymorphism and the clinical features of BD. Results, Both genotype and allele frequencies were not significantly different between controls and Behçet's disease patients [OR = 0.67, 95% CI (0.35,1.29), P = 0.197 and OR = 0.77, 95% CI (0.52,1.15), P = 0.184]. We did not find any significant relationship between leptin gene polymorphism and the clinical features of BD (P > 0.05). Conclusion, In the present case-control study, we found no evidence of an association between the G-2548A variant of the leptin gene and BD among Turks. Further studies are needed to investigate serum leptin level to explain the mechanisms behind the lack of association between leptin G2548A gene polymorphism and BD. [source]

Relationships between plasma leptin levels and body composition parameters measured by different methods in postmenopausal women

Potential association between endogenous leptin and sympatho-vagal activities in young obese Japanese women

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 1 2003
Tamaki Matsumoto
Leptin is an adipocyte-derived hormone that decreases food intake and increases energy expenditure through the activation of the sympathetic nervous system (SNS). Notwithstanding recent intensive research, the underlying physiological mechanism of leptin as well as the etiology of obesity in humans remains elusive. The present study attempted to investigate the potential association between endogenous circulating leptin and sympatho-vagal activities in age- and height-matched obese and nonobese healthy young women. Plasma leptin concentrations were measured by radioimmunoassay. The autonomic nervous system activity was assessed during the resting condition by means of a recently devised power spectral analysis of heart rate variability, which serves to identify three separate frequency components, very low (VLO), low (LO), and high (HI). Plasma leptin concentrations were greater in the obese than in the control group (45.7 ± 5.89 vs. 11.2 ± 1.10 ng · ml,1, P < 0.01). As to the contribution of endogenous leptin to SNS activity, both the ratios of the VLO frequency component reflecting thermoregulatory sympathetic function and the global SNS index [(VLO + LO)/HI] to plasma leptin concentration were markedly reduced in the obese compared to the control group (VLO per leptin: 5.9 ± 1.39 vs. 37.8 ± 8.1 ms2 · ml · ng,1, P < 0.01; SNS index per leptin: 0.04 ± 0.008 vs. 0.33 ± 0.01 ml,,·,ng,1, P < 0.01). Additionally, a nonlinear regression analysis revealed that these ratios exponentially decreased as a function of body fat content (VLO per leptin r2 = 0.57, P < 0.01; SNS index per leptin r2 = 0.53, P < 0.01). Our data suggest that reduced sympathetic responsiveness to endogenous leptin production, implying peripheral leptin resistance, might be a pathophysiological feature of obesity in otherwise healthy young women. The findings regarding the association of leptin, body fat content, and SNS activity further indicate that the 30% of total body fat, which has been used as a criterion of obesity, might be a critical point at which leptin resistance is induced. Am. J. Hum. Biol. 15:8,15, 2003. © 2002 Wiley-Liss, Inc. [source]

Serum leptin in first-trimester Down syndrome pregnancies

PRENATAL DIAGNOSIS, Issue 6 2008
Paula Hedley
Abstract Background Leptin is a key regulator of satiety; and the serum concentration is considered to reflect nutritional status. Expressed predominantly by the adipocytes, leptin is also expressed in placenta, which is a major source of both leptin and the leptin receptor in pregnancy serum. As a placenta protein, leptin serum concentrations may be perturbed in Down syndrome (DS) pregnancies as seen for pregnancy-associated plasma protein-A (PAPP-A) and human chorionic gonadotrophin-, (hCG,). We examined whether leptin is a maternal serum marker for foetal DS in the first trimester. Materials and Methods Serum samples from 44 pregnant women with a DS foetus, and 135 control pregnant women in week 8 to 14 had the leptin concentration determined by immunoassay and the concentrations were converted into multiples of the median (MoM) of controls based on log-regression analysis. The distributions of log10 MoM leptin was compared in DS and control pregnancies. Results Serum leptin increased significantly with gestational age in controls (p = 0.02). The mean log10 MoM in controls was , 0.0486, with a median empirical MoM of 0.89, and , 0.0618, with a median empirical MoM of 0.80, in DS pregnancies. This difference was not significant. The log10 MoM leptin values in DS pregnancies did not change with gestational age (p = 0.32). Conclusion Leptin is not a first-trimester marker for foetal DS. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Maternal serum leptin concentration during the second trimester of pregnancy: association with fetal chromosomal abnormalities

PRENATAL DIAGNOSIS, Issue 3 2002
Demetrios Rizos
Abstract Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8,ng/ml around the 20th week, and then rapidly increase to 28.2,ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16,17 week of gestation to r=0.544 at >22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Leptin exists in tubuli seminiferi and in seminal plasma

ANDROLOGIA, Issue 4 2002
H.-J. Glander
Summary. Leptin is a 167-amino acid protein that stimulates gonadotrophin-releasing hormone secretion and exerts indirect effects on the gonads via neuropeptide Y, NPY. Recent research has suggested that leptin may also have an effect on testosterone secretion. To investigate the role of leptin in reproduction, leptin in testicular tissue and seminal plasma was examined in relation to leptin in serum, semen sample qualities and vasectomy. Seminal plasma and serum of 64 infertility patients, and 15 individuals after vasectomy, were assayed for leptin using a competitive ,in house' radioimmunoassay. The concentration of leptin in seminal plasma was significantly lower in the ,normal' semen sample group than in the ,pathological' group (Mean ± SEM; 1.45 ± 0.18 vs. 3.19 ± 0.57 ng ml,1; P <,0.05), and showed a significantly negative correlation with percentage of motile spermatozoa (r=,0.46; P=0.0005) and with the velocity straight line, VSL, (r=,0.30; P= 0.029). In contrast, leptin concentration in serum did not show any relationship with the spermiogram parameters. In testicular tissue, leptin was preferentially found within the tubuli seminiferi using anti-leptin polyclonal antibody, Ob A-20 Sc 842. The amount of leptin per ejaculate did not significantly change after vasectomy, and was not correlated to fructose, zinc or neutral alpha glucosidase in seminal plasma (P > 0.05). These results suggest that the amount of leptin in the genital tract, including the tubuli seminiferi, may influence the mechanisms involved in the motility development of spermatozoa. [source]

Leptin and ghrelin concentrations and weight loss in Parkinson's disease

ACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010
U. Fiszer
Fiszer U, Micha,owska M, Baranowska B, Woli,ska-Witort E, Jeske W, Jethon M, Pia,cik-Gromada M, Marcinowska-Suchowierska E. Leptin and ghrelin concentrations and weight loss in Parkinson's disease. Acta Neurol Scand: 2010: 121: 230,236. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, To investigate the role of leptin, ghrelin, GH and IGF-1 in energy balance disturbances in Parkinson's disease (PD). Materials and methods,,, Thirty-nine patients were included: 11 PD patients with unintentional weight loss, 16 PD patients without weight loss and 12 controls. UPDRS, MMSE, MADRS, appetite scale, BMI, adipose tissue content, plasma leptin and active ghrelin concentrations and serum GH, IGF-1, TSH, T3 and T4, concentrations were evaluated. Results,,, A lower plasma leptin concentration and a higher serum IGF-1 concentration were found in PD patients with weight loss. BMI and the content of adipose tissue were positively correlated with leptin concentration in all PD patients. Paradoxically, the lower BMI was, the lower plasma active ghrelin concentration was in PD patients with the weight loss. Conclusion,,, These findings confirm that changes of plasma leptin concentration occur in PD patients with loss of weight. [source]

Leptin and the metabolic syndrome in patients with myotonic dystrophy type 1

ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2010
V. Rakocevic Stojanovic
Rakocevic Stojanovic V, Peric S, Lavrnic D, Popovic S, Ille T, Stevic Z, Basta I, Apostolski S. Leptin and the metabolic syndrome in patients with myotonic dystrophy type 1. Acta Neurol Scand: 2010: 121: 94,98. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, To evaluate serum leptin concentration and its relation to metabolic syndrome (MSy) in non-diabetic patients with myotonic dystrophy type 1 (DM1). Materials and methods,,, This study included 34 DM1 patients, and the same number of healthy subjects matched for age, sex and body mass index (BMI). Results,,, DM1 patients had increased BMI and insulin resistance, and increased leptin and insulin concentrations, but the other features of MSy such as diabetes, glucose intolerance and hypertension were not detected in DM1 patients. Serum leptin levels were higher in patients with DM1 than in healthy controls (8.5 ± 6.6 ng/ml vs 3.6 ± 2.9 ng/ml in men, and 13.9 ± 10.0 ng/ml vs 10.9 ± 6.9 ng/ml in women, respectively). In DM1 patients, leptin levels correlated with BMI, fasting insulin and insulin resistance (HOMA) (P < 0.01). Conclusions,,, The leptin overproduction correlated with insulin resistance in DM1 patients but the significance of this finding remains unclear. [source]

Cord plasma concentrations of adiponectin and leptin in healthy term neonates: positive correlation with birthweight and neonatal adiposity

CLINICAL ENDOCRINOLOGY, Issue 1 2004
Po-Jung Tsai
Summary objective, Adiponectin is negatively associated with leptin, insulin and obesity in children and adults. Whereas increases in fetal insulin and leptin are associated with increased weight and adiposity at birth, the role of adiponectin in fetal growth has not yet been determined. The aims of this study were to examine the relationships between adiponectin and insulin, leptin, weight and adiposity at birth in healthy term infants. design and methods, Anthropometric parameters including weight, length, circumferences and skinfold thickness were measured, and plasma lipid profiles, insulin, leptin and adiponectin concentrations in cord blood samples from 226 singleton infants born at term after uncomplicated pregnancies were assayed. results, Cord plasma adiponectin, leptin and insulin levels correlated significantly and positively with birthweight (P = 0·001, P < 0·001, P < 0·001, respectively) and the sum of skinfold thicknesses (P < 0·001, P < 0·001, P < 0·001, respectively). Mean cord plasma adiponectin and leptin levels, but not insulin level, were significantly higher in large-for-gestational-age (LGA) infants compared with appropriate-for-gestational-age (AGA) infants. Cord plasma leptin concentration, but not adiponectin concentration, was significantly higher in female infants than in male infants (P = 0·003 and P = 0·94, respectively). Cord plasma adiponectin concentration correlated positively with leptin level (P = 0·007) but not with insulin level (P = 0·78). conclusions, High adiponectin levels are present in the cord blood. Cord plasma adiponectin and leptin levels are positively correlated with birthweight and adiposity. This suggests that adiponectin may be involved in regulating fetal growth. [source]

Glucocorticoids contribute to the heritability of leptin in Scottish adult female twins

CLINICAL ENDOCRINOLOGY, Issue 1 2004
A. M. Wallace
Summary objective, The precise interactions between glucocorticoids and leptin are complex and poorly understood. The aim of the study was to investigate whether the glucocorticoid/leptin interaction is influenced by shared environmental or genetic factors. design, We investigated the heritability of body mass index (BMI), circulating leptin and urinary glucocorticoid metabolites [tetrahydrocortisol (THF), alloTHF and tetrahydrocortisone (THE)] in 54 monozygotic (MZ) and 39 dizygotic (DZ) female twins. Analysis was performed using a structural equation modelling package Mx, developed by Neale. results, Leptin and BMI showed substantial heritability (68·3% and 71·3%, respectively). Bivariate analysis indicated that the genetic determinants of BMI and leptin are partly shared. Total cortisol metabolites (THF + alloTHF + THE), the (THE + alloTHF)/THE ratio [a marker of 11,-hydroxysteroid dehydrogenase (11HSD) activity] and the alloTHF/THF ratio (marker for 5,-reductase activity) followed an environmental pattern. The heritability of leptin was significantly lowered to 63·8% (P = 0·012) when values were corrected for the influence of total cortisol metabolites but unaffected by markers of 11HSD and 5,-reductase activity. conclusions, We confirm that the genetic influence on both BMI and the circulating leptin concentration is substantial and show that these genetic determinants are highly correlated. These genetic factors, which are more likely to be dominant than additive, can be modestly but significantly modified by urinary total cortisol metabolites implying an adrenal influence. [source]

Changes in serum leptin concentration after corticosteroid treatment in preterm infants

ACTA PAEDIATRICA, Issue 6 2002
PC Ng
The aim of this study was to investigate the effect of postnatal systemic dexamethasone on serum leptin, insulin and hormones of the hypothalamic-pituitary-adrenal (HPA) axis in preterm, very low birthweight (VLBW) infants. Nineteen VLBW infants who received a 3 wk dose tapering course of dexamethasone for treatment of bronchopulmonary dysplasia were prospectively enrolled. Blood for hormone assays was collected immediately before the start of the dexamethasone course (Td-pre), 3 wk after commencement of the drug (Td-end) and 2 wk after dexamethasone treatment had been stopped (Td-post). In addition, 28 VLBW infants who participated in a concurrent longitudinal leptin study within the same period but did not receive corticosteroid had their serum leptin and insulin concentrations serially monitored. Blood specimens for the latter group of infants were obtained at 2 (Twk,2), 5 (Twk,5) and 7 (Twk,7) wk of postnatal age. Serum leptin and insulin at Td,end were significantly increased, whereas plasma ACTH and serum cortisol were significantly suppressed compared with the pretreatment (Td,pre) levels in the corticosteroid group (p > 0.0001 for leptin and insulin; p > 0.05 and p > 0.001 for ACTH and cortisol, respectively). In contrast, serum leptin and insulin at weeks 5 (Twk,5) and 7 (Twk,7) did not differ significantly from their respective levels at week 2 (Twk,2) in the non-treatment group. Conclusion: The administration of systemic corticosteroid resulted in significant increases in serum leptin and insulin, but marked suppression of hormones of the HPA axis. The effect of dexamethasone on the "adipoinsular" and HPA axes was transient and reversible. The adipoinsular axis in preterm infants is likely to be functional and active at an early stage of human development, and leptin may regulate energy balance in VLBW infants in the early postnatal period. Corticosteroids may, through the adipoinsular axis or its associated pathways, mediate in the regulation of body weight in preterm neonates. [source]

Changes in serum leptin concentrations in overweight Japanese men after exercise

DIABETES OBESITY & METABOLISM, Issue 5 2004
N. Miyatake
Aim:, To investigate the link between serum leptin concentrations and exercise. Design:, Cross-sectional and longitudinal studies of an exercise intervention. Subjects:, 110 Japanese overweight men aged 32,59 years were recruited. At baseline, the average body mass index (BMI) was 28.5 ± 2.5 kg/m2. From this group, we used data of 36 overweight men (BMI, 28.9 ± 2.3) for a 1-year exercise programme. Measurements:, Leptin was measured at baseline and after 1 year. Fat distribution was evaluated by visceral fat (V) and subcutaneous fat (S) areas measured with computed tomography (CT) scanning at umbilical levels. Anthropometric parameters, aerobic exercise level, muscle strength and flexibility were also investigated at baseline and after 1 year. Results:, In the first analysis, using cross-sectional data, leptin was significantly correlated with total body fat (r = 0.760, p < 0.01), V (r = 0.383, p < 0.01) and S (r = 0.617, p < 0.01) areas. In the second analysis, using longitudinal data, leptin was significantly reduced after 1 year (pre 6.7 ± 4.0 ng/ml vs. post 5.1 ± 3.1 ng/ml, p < 0.01). Results showed that steps per day were increased, and aerobic exercise level, weight-bearing index (WBI) and insulin resistance were significantly improved. Although, there was a positive correlation between , leptin(positive changes in leptin after 1 year) and anthropometric measurements such as , body weight, , BMI and , body fat, leptin/body weight, leptin/BMI and leptin/body fat ratios were significantly reduced during exercise intervention. Conclusion:, The present study indicated exercise significantly lowers serum leptin concentrations, and thus it may improve the leptin resistance observed in overweight Japanese men. [source]

Circulating adipocytokines in non-diabetic and Type 1 diabetic children: relationship to insulin therapy, glycaemic control and pubertal development

DIABETIC MEDICINE, Issue 6 2006
F. Celi
Abstract Aim To determine the influence of Type 1 diabetes mellitus on circulating adipocytokines in children. Methods The circulating concentrations of leptin, adiponectin, resistin and tumour necrosis factor (TNF)-, were measured in 91 children, aged 11.1 ± 2.7 years, with Type 1 diabetes mellitus (T1DM). Ninety-one healthy children were selected as control subjects. Results Body mass index-adjusted leptin concentrations were higher in the pubertal diabetic children compared with the control children. There was a significant positive correlation between leptin and daily insulin dose in the diabetic group. Circulating adiponectin concentrations were higher in the prepubertal diabetic children and were positively associated with HbA1c. Resistin concentrations were lower in the prepubertal non-diabetic subjects compared with the pubertal non-diabetic children, whose values were higher than those of the diabetic children. TNF-, concentrations were similar in non-diabetic and diabetic children. Conclusions Circulating concentrations of adipocytokines are abnormal in Type 1 diabetic children, although the direction of change differs by cytokine. Pubertal development, in addition to insulin treatment and glycaemic control, also influences the concentrations. [source]

Neuropeptides and appetite control

DIABETIC MEDICINE, Issue 8 2002
J. P. H. Wilding
Abstract Obesity is important in the aetiology of type 2 diabetes, and presents a major barrier to its successful prevention and management. Obesity develops when energy intake exceeds energy expenditure over time. A complex system has evolved to maintain energy homeostasis, but this is biased towards weight gain. Meal size is controlled by a series of short-term hormonal and neural signals that derive from the gastrointestinal tract, such as cholecystokinin whereas others may initiate meals, such as the recently discovered hormone, ghrelin. Other hormones such as insulin and leptin, together with circulating nutrients, indicate long-term energy stores. All these signals act at several central nervous system (CNS) sites but the pathways converge on the hypothalamus, which contains a large number of peptide and other neurotransmitters that influence food intake. As energy deficit is most likely to compromise survival, it is not surprising that the most powerful of these pathways are those that increase food intake and decrease energy expenditure when stores are depleted. When energy stores are low, production of leptin from adipose tissue, and thus circulating leptin concentrations fall, leading to increased production of hypothalamic neurotransmitters that strongly increase food intake, such as neuropeptide Y (NPY), galanin and agouti-related protein (AGRP) and decreased levels of ,-melanocyte-stimulating hormone (,-MSH), cocaine and amphetamine-regulated transcript (CART) and neurotensin that reduce food intake and increase energy expenditure. The finding that mutations in leptin and POMC lead to severe early onset obesity in bumans has highlighted the importance of these peptides in humans. This new understanding may eventually lead to new treatments for obesity that will be of particular benefit in the prevention and treatment of type 2 diabetes. Diabet. Med. 19, 619,627 (2002) [source]

Adiponectin and visfatin concentrations in children treated with valproic acid

EPILEPSIA, Issue 2 2008
Markus Rauchenzauner
Summary Chronic antiepileptic therapy with valproic acid (VPA) is associated with increased body weight and insulin resistance in adults and children. Attempts to determine the underlying pathophysiologic mechanisms have failed. Adipocytokines have recently been defined as a link between glucose and fat metabolism. We herein demonstrate that VPA-associated overweight is accompanied by lower adiponectin and higher leptin concentrations in children. The absence of any relationship with visfatin concentration does not suggest a role of this novel insulin-mimetic hormone in VPA-associated metabolic alterations. Therefore, adiponectin and leptin but not visfatin may be considered as potential regulators of glucose and fat metabolism during VPA-therapy. [source]

Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies

EQUINE VETERINARY JOURNAL, Issue 2 2009
R. A. CARTER
Summary Reasons for performing study: The ability to predict ponies at increased risk of laminitic episodes, when exposed to nutrient dense pasture, would facilitate management to avoid disease. Objectives: To identify variables and clinically useful cut-off values with reproducible diagnostic accuracy for the prediction of ponies that subsequently developed laminitis when exposed to nutrient dense pasture. Methods: A cohort of predominantly Welsh and Dartmoor ponies from a closed herd was evaluated in March 2006 (n = 74) and March 2007 (n = 57). Ponies were categorised as never laminitic or previously laminitic according to reported laminitic history and as clinically laminitic (CL) if laminitis was observed within 3 months following evaluation. Body condition score (BCS), cresty neck score (CNS), girth and neck circumferences (NC), withers height, blood pressure and hoof surface temperature, and plasma insulin, glucose, triglyceride, leptin, cortisol, ACTH, uric acid and TNF-, concentrations were measured. Analysis of sensitivity, specificity and receiver operating characteristic curves was used to evaluate the diagnostic accuracy for a variable to predict CL ponies. Results: Variables with diagnostic accuracy for the prediction of CL ponies included insulin, leptin, BCS, CNS, and NC:height ratio. Specific cut-off values of insulin (>32 mu/l), leptin (>7.3 ng/ml), BCS (,7), CNS (,4) and NC:height ratio (>0.71) had reproducible diagnostic accuracy for the prediction of laminitis. Combining tests did not result in higher diagnostic accuracy than individual tests of insulin or leptin during either evaluation. Conclusions: Tests of insulin and leptin concentrations and measures of generalised (BCS) and localised (CNS or NC:height ratio) obesity were beneficial in the prediction of laminitic episodes. Potential relevance: These results highlight the importance of monitoring and reducing insulin concentration, and generalised and regional obesity in ponies to reduce risk of laminitis. [source]

Relationship between plasma leptin concentrations and carcass composition in fattening mutton: a comparison with ultrasound results

Neuropeptide Y Counteracts the Anorectic and Weight Reducing Effects of Ciliary Neurotropic Factor

JOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2000
S. Pu
Abstract Ciliary neurotrophic factor (CNTF), a cytokine of the interleukin-6 superfamily, has been shown to induce hypophagia and weight loss. Neuropeptide Y (NPY) and orexin are potent orexigenic signals in the hypothalamus. Anorexia, normally seen in response to infection, injury and inflammation, may result from diminished hypothalamic orexigenic signalling caused by persistently elevated cytokines, including CNTF. To test this hypothesis, we first examined the effects of chronic intracerebroventricular (i.c.v.) infusion of CNTF for 6,7 days on food intake and body weight as well as hypothalamic NPY and orexin gene expression in male rats. Subsequently, the effectiveness of NPY replacement to counteract the effects of CNTF by coinfusion of NPY and CNTF was evaluated. Chronic i.c.v. infusion of CNTF (2.5 µg/day) reduced body weight (14.3% vs control) at the end of 7 days. Food intake remained suppressed for 5 days postinfusion and subsequently gradually returned to the control range by day 7. Serum leptin concentrations in these rats were in the same range seen in control rats. Chronic i.c.v. infusion of higher doses of CNTF (5.0 µg/day) produced sustained anorexia and body weight loss (29% vs controls) through the entire duration of the experiment. This severe anorexia was accompanied by markedly suppressed serum leptin concentrations. Furthermore, CNTF infusion alone significantly reduced hypothalamic NPY gene expression (P < 0.05) without affecting orexin gene expression. As expected, in fusion of NPY alone (18 µg/day) augmented food intake (191.6% over the initial control, P < 0.05) and produced a 25.1% weight gain in conjunction with a 10-fold increase in serum leptin concentrations at the end of the 7-day period. Interestingly, coinfusion of this regimen of NPY with the highly effective anorectic and body reducing effects of CNTF (5.0 µg/day) not only prevented the CNTF-induced anorexia and weight loss, but also normalized serum leptin concentrations and hypothalamic NPY gene expression. These results demonstrate that chronic central infusion to produce a persistent elevation of the cytokine at pathophysiological levels (a situation that may normally manifest during infection, injury and inflammation) produced severe anorexia and weight loss in conjunction with reduction in both serum leptin concentrations and hypothalamic NPY gene expression. Reinstatement of hypothalamic NPY signalling by coinfusion of NPY counteracted these CNTF-induced responses. [source]

The Role of Leptin in the Control of Body Weight

NUTRITION REVIEWS, Issue 2002
Rudolph L. Leibel M.D.
Physiologic responses to high and low leptin concentrations are strikingly asymmetrical. High concentrations often produce minimal effects, whereas low concentrations provoke strong counterregulatory responses. A model and rationale for the physiology is presented. [source]

Relationship between serum leptin and thyroid hormones in children

PEDIATRICS INTERNATIONAL, Issue 3 2000
MAKOTO UCHIYAMA, Tadashi Asami TATIANA CIOMARTEN
Abstract Background: Because leptin decreases food intake and increases energy expenditure, the possible influence of thyroid status on the leptin system has been investigated mainly in adults and animals. However, the data available at present are very confusing. The aim of the present study was to assess the possible interaction of thyroid hormones with the leptin system. Methods: Serum free thyroxine (FT4), a biologically active thyroid hormone, and thyroid stimulating hormone (TSH), a sensitive and reliable index of thyroid status, were examined in 51 children (19 males, 32 females) with mass screening-detected congenital hypothyroidism on continuous L -thyroxine (L-T4) substitution therapy. The subjects were divided into younger (n=35, aged 1 month , 5 years) and older (n=16, 6 years , 11 years) children groups. Serum levels of leptin and thyroid hormones were measured in the subjects. Body mass index (BMI) was estimated by the formula bodyweight (kg)/height`height (m 2), which is known as the Kaup index in younger children and BMI in older children and adults. Results: In the younger children group, serum leptin levels showed no correlation with serum TSH, FT4 or T4. In the older children group, serum leptin concentrations significantly correlated with T4 (r=0.510, P<0.05) and BMI (n=16, r=0.647, P<0.01), but not with TSH or FT4. Conclusion: The role of thyroid hormones in modulating leptin synthesis and secretion seems to have little, if any, clinical or biological relevance. [source]

Developmental changes in the relationship between leptin and adiposity among Tsimané children and adolescents

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2008
Katherine C. B. Sharrock
Leptin is thought to signal energy stores, thus helping the body balance energy intake and expenditure. However, the strong relationship between leptin and adiposity in populations with adequate nutrition or common obesity is not universal across ecologic contexts, and leptin often correlates only weakly, or not at all, with adiposity in populations of lean or marginally-nourished males. To clarify whether the relationship between adiposity and leptin changes during development, this study examines leptin and body fat among children and adolescents of lowland Bolivia. Anthropometric measures of body composition and dried blood spot samples were collected from 487 Tsimane' ranging from 2 to 15 years of age. Leptin was assayed using an enzyme immunoassay protocol validated for use with blood spot samples. In this population, leptin concentrations were among the lowest reported in a human population (mean ± SD: 1.26 ± 0.5 and 0.57 ± 0.3 in females and males). In addition, the relationship between leptin and adiposity follows distinct developmental trajectories in males and females. In males, leptin is weakly correlated with most measures of body composition at all ages investigated. However, in females, the level of body fat and the strength of the correlation between body fat and leptin (a measure of its strength as a signal of energy stores) both increase markedly with age. These findings suggest a more important role of leptin as a signal of energy stores among females as they approach reproductive maturity, while raising questions about the function of this hormone in lean males. Am. J. Hum. Biol., 2008. © 2008 Wiley-Liss, Inc. [source]