Serum Leptin Concentration (serum + leptin_concentration)

Distribution by Scientific Domains


Selected Abstracts


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]


Adipocytokines, insulin resistance, and coronary atherosclerosis in rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 5 2010
Young Hee Rho
Objective The prevalence of subclinical coronary atherosclerosis is increased in patients with rheumatoid arthritis (RA), and the increased risk is associated with insulin resistance. Adipocytokines have been linked to obesity, insulin resistance, inflammation, and coronary heart disease in the general population. This study was undertaken to examine the hypothesis that adipocytokines affect insulin resistance and coronary atherosclerosis among patients with RA. Methods The coronary calcium score, homeostatic model assessment for insulin resistance (HOMA-IR) index, and serum adipocytokine (leptin, adiponectin, resistin, and visfatin) concentrations were determined in 169 patients with RA. The independent effect of each adipocytokine on insulin resistance according to the HOMA-IR index and on coronary artery calcification determined by electron beam computed tomography was assessed in models adjusted for age, race, sex, body mass index (BMI), traditional cardiovascular risk factors, and inflammation mediators. In addition, an interaction analysis was performed to evaluate whether the effect of the HOMA-IR index on the coronary calcium score is moderated by adipocytokines. Results Increased concentrations of leptin were associated with a higher HOMA-IR index, even after adjustment for age, race, sex, BMI, traditional cardiovascular risk factors, and inflammation mediators (P < 0.001), but concentrations of visfatin (P = 0.06), adiponectin (P = 0.55), and resistin (P = 0.98) showed no association with the HOMA-IR index. None of the adipocytokines was independently associated with the coronary calcium score (all P > 0.05). Serum leptin concentrations showed a significant interaction with the HOMA-IR index (P for multivariate interaction = 0.02). Increasing leptin concentrations attenuated the increased risk of coronary calcification related to insulin resistance. Serum concentrations of the other adipocytokines showed no significant interactions with the HOMA-IR index (each P > 0.05). Conclusion Leptin is associated with insulin resistance in patients with RA but, paradoxically, attenuates the effects of insulin resistance on coronary calcification. [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]


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]


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]


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 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]


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]


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]


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]


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]


The relationship between breast milk leptin and neonatal weight gain

ACTA PAEDIATRICA, Issue 4 2009
Hakan Doneray
Abstract Aim: To investigate whether change in leptin content of breast milk during lactation acts on neonatal body weight gain. Methods: In total 15 lactating women and their 15 term infants were involved in the study. Breast milk and neonatal serum samples were obtained from the same women and their neonates on the 1st day and any day between the 21st and 30th days after birth. Breast milk and serum leptin concentrations were determined by radioimmunoassay. Anthropometric indexes of the infants were recorded. Results: The study was completed with 15 multiparious mothers aged 19,37 years and their infants. The mean collection time of the first samples after birth was 6.07 ± 1.94 h. The leptin level in the mature milk was significantly higher than in the colostrum (p < 0.001). Neonatal weight and height were significantly increased on 21,30 lactation days compared to 1st day of lactation (p < 0.05 and p < 0.001, respectively). The leptin concentration in the mature milk was negatively correlated with delta BMI (r =,0.53; p < 0.05). The delta breast milk leptin concentration was also found to be inversely correlated with delta BMI (r =,0.529; p < 0.05). Conclusion: The results of this study have suggested that change in the leptin content of breast milk during lactation might play a role in the regulation of weight gain in healthy neonates. [source]