Increase In Serum Leptin Concentrations Research Articles

Maternal obesity driven changes in collagen linearity of breast extracellular matrix induces invasive mammary epithelial cell phenotype

Obesity has been linked with numerous health issues as well as an increased risk of breast cancer. Although effects of direct obesity in patient outcomes is widely studied, effects of exposure to obesity-related systemic influences in utero have been overlooked. In this study, we investigated the effect of multigenerational obesity on epithelial cell migration and invasion using decellularized breast tissues explanted from normal female mouse pups from a diet induced multigenerational obesity mouse model. We first studied the effect of multigenerational diet on the mechanical properties, adipocyte size, and collagen structure of these mouse breast tissues, and then, examined the migration and invasion behavior of normal (KTB-21) and cancerous (MDA-MB-231) human mammary epithelial cells on the decellularized matrices from each diet group. Breast tissues of mice whose dams had been fed with high-fat diet exhibited larger adipocytes and thicker and curvier collagen fibers, but only slightly elevated elastic modulus and inflammatory cytokine levels. MDA-MB-231 cancer cell motility and invasion were significantly greater on the decellularized matrices from mice whose dams were fed with high-fat diet. A similar trend was observed with normal KTB-21 cells. Our results showed that the collagen curvature was the dominating factor on this enhanced motility and stretching the matrices to equalize the collagen fiber linearity of the matrices ameliorated the observed increase in cell migration and invasion in the mice that were exposed to a high-fat diet in utero. Previous studies indicated an increase in serum leptin concentration for those children born to an obese mother. We generated extracellular matrices using primary fibroblasts exposed to various concentrations of leptin. This produced curvier ECM and increased breast cancer cell motility for cells seeded on the decellularized ECM generated with increasing leptin concentration. Our study shows that exposure to obesity in utero is influential in determining the extracellular matrix structure, and that the resultant change in collagen curvature is a critical factor in regulating the migration and invasion of breast cancer cells.

Steroid effect on serum leptin in Libyan children with minimal change nephritic syndrome

Few studies have looked at the status of leptin in renal diseases especially nephrotic syndrome. The aim of this study was to investigate the effect of steroid therapy on serum leptin, anthropometric and appetite in patients with minimal change nephrotic syndrome (MCNS). Twenty children were recruited for this prospective study. Group I included ten children aged between 2 - 12 years with MCNS without any associated complications as impaired renal functions, hematuria, hypertension and others. Group II included ten healthy children with matching age, sex and BMI as a control group. Body weight, height, nutritional history including appetite, quantity of food, clinical examination, blood pressure and blood for kidney function parameter and serum leptin were taken before and after 3 days and after 2 weeks following prednisolone dose of 2 mg/kg/day. The same parameters were also performed for group II. Serum leptin was higher in group II than group I (1.575 ± 1.07 vs 0.575 ± 0.76 ng/ml p < 0.01). After 3 days and after 2 weeks of 2 mg/kg of prednisolone, serum leptin increased significantly in group II (t = 4.65, p < 0.014) without significant difference as it compared with group I (t = 1.65, p = 0.08). A highly significant increase in serum leptin concentration was detected in 2 weeks after prednisone therapy compared to the base line levels before therapy, compared to 3 days after therapy and to the control group (t = 5.69, p < 0.001, t = 3.95, p < 0.001 and t = 8.96, p < 0.001, respectively). In group I, serum leptin was higher in females than males (4.8 ± 2.8, p < 0.001). BMI was also higher in females compared to males. Patients' appetite improved after prednisolone for food quantity as recorded by the recall methods. Blood urea and serum creatinine in groups I and II did change significant within group II after steroid and even the changes were not significantly different from the control. Serum albumin, total serum protein, serum cholesterol concentrations and proteinuria revealed a significant difference between the two groups (t = 5.9, 8.9, 8.98 & 16.33, respectively, p < 0.01, for all). Weight, BMI in group I before and 2 weeks after intake of prednisone did not revealed any significant differences in weight, BMI before and after 2 weeks of prednisone (t = 0.99 and 0.88.8, respectively) in spite of the increase in appetite. Blood pressure had not changed significantly after the steroid therapy in MCNS patients’ group. Thus, serum leptin concentration and appetite were significantly higher especially in females without significant change in anthropometric, blood pressure and renal function indices after steroid therapy in minimal change nephropathy.

An Evaluation and Correlation of Leptin in Gingival Crevicular Fluid and Serum in Health, Gingivitis and Periodontitis

ABSTRACT Background and objective Plasma leptin is associated in patients with inflammatory diseases. A high concentration of leptin is associated with healthy gingival tissue. The purpose of this study was to assess the concentration of human leptin in gingival crevicular fluid (GCF) and serum within healthy and diseased gingiva, further to explore the possibility of using the levels of leptin in GCF and serum as a biochemical marker of periodontal disease progression. Materials and methods Ninety subjects were selected with age (30-39 years) and sex (15 males and 15 females) matched, to eliminate age and sex as confounders. The subjects were divided into three groups consisting of 30 subjects in each group based on the clinical and radiological parameters; healthy (group I), gingivitis (group II), periodontitis (group III), from whom the GCF samples were collected with Periopaper GCF collection strips (Proflow, Amityville, NY, USA) for 30 seconds and blood samples with 20-gauge needle syringe respectively. Leptin concentration was determined from individual GCF and serum samples by enzyme-linked immunosorbent assay (ELISA). Results The highest mean leptin concentration in GCF was observed in group I (2,664.30 pg/ml ± 324.73) and least mean leptin concentration was obtained in group III (1,309.43 pg/ml ± 202.45). The mean concentration of group II (1,639.43 pg/ml ± 344.46) was intermediate between the highest and lowest values. In contrast, the highest mean leptin concentration in serum was obtained for group III (12,086.57 pg/ml ± 1,698.23) and least mean leptin concentration was obtained for group I (8,715.09 pg/ml ± 1,649.19). The mean concentration of the group II (10,694.01 pg/ml ± 1,777.72) were intermediate between the highest and lowest values. Conclusion The results indicated a statistically significant decrease in the GCF leptin concentration and increase in serum leptin concentration as the periodontal disease progressed. How to cite this article Vadvadgi VH, Saini R, Padmawar N. An Evaluation and Correlation of Leptin in Gingival Crevicular Fluid and Serum in Health, Gingivitis and Periodontitis. Int J Experiment Dent Sci 2012;1(2):93-97.

Refeeding after prolonged food restriction differentially affects hypothalamic and adipose tissue leptin gene expression

Rat adipose tissue is the principal site of leptin synthesis, however, leptin gene expression has been demonstrated in many rat tissues. Some data indicate that leptin produced by human brain and adipose tissue could cooperate in the regulation of food intake. In this case the regulation of leptin gene expression in hypothalamus and in adipose tissue should be coordinately regulated. Food restriction is often undertaken by many humans trying to lose body weight. Thus, the current study was aimed to analyze whether leptin gene expression in rat hypothalamus and in adipose tissue is regulated synchronously by prolonged food restriction and prolonged food restriction/refeeding. We demonstrate here that although leptin gene is expressed at very low level in rat hypothalamus, its expression in hypothalamus was down-regulated by prolonged food restriction similarly as in the white adipose tissue. Refeeding after prolonged food restriction caused both an increase of leptin gene expression in white adipose tissue and the increase in serum leptin concentration. In contrast, no significant effect of prolonged food restriction/refeeding on hypothalamic leptin gene expression was observed. The reduction of leptin gene expression in both hypothalamus and white adipose tissue by prolonged food restriction was associated with a significant increase of NPY gene (a target of leptin signaling) expression in hypothalamus. Refeeding after prolonged food restriction caused the decrease of NPY gene expression in hypothalamus, however NPY mRNA level remained higher than in controls. The results presented in this paper indicate that prolonged food restriction/refeeding differentially affects leptin gene expression in adipose tissue and in hypothalamus. Moreover, obtained data suggest that in rats leptin synthesized in hypothalamus exerts marginal effect on NPY gene expression and on serum leptin concentration.

Hypercaloric diets differing in fat composition have similar effects on serum leptin and weight gain in female subjects with anorexia nervosa

Weight regain in subjects with anorexia nervosa is associated with an increase in serum leptin concentrations that is hypothesized to impair full weight restoration. As diets rich in n-3 polyunsaturated fatty acids (PUFA) have been described to lower serum leptin concentrations, we tested the hypothesis that consumption of a hypercaloric diet rich in n-3 PUFA is associated with an attenuated increase in serum leptin and a higher efficiency of body weight gain in subjects with anorexia nervosa. Twenty-five female subjects with anorexia nervosa were enrolled into this controlled dietary intervention study. Four subjects discontinued therapy or participation in the study prematurely, and six were excluded. 15 subjects completed the study. Subjects consumed hypercaloric diets rich in either saturated fatty acids (SFA, n = 8) or n-3 PUFA (n = 7) for 5 weeks. Primary endpoints were the change in serum leptin concentrations and body weight gain relative to energy consumed. Serum leptin concentrations increased distinctly throughout the study (P < .001), and to a similar extend in both groups [+2.9 (SD 2.4) vs. +2.8 (SD 3.4) ng/mL in the SFA- and n-3 PUFA group, respectively; P = .487]. The efficiency of body weight gain also did not differ significantly between groups, with a body weight gain of 63.1 (SD 12.4) vs. 79.2 (SD 26.0) g per 4.2 MJ (1000 kcal) consumed in the SFA- and n-3 PUFA group, respectively (P = .132). Hypercaloric diets rich in either SFA or n-3 PUFA do not differ in their effects on serum leptin concentrations and the efficiency of body weight gain in female subjects with anorexia nervosa.

Body Mass Index, percent body fat, and regional body fat distribution in relation to leptin concentrations in healthy, non-smoking postmenopausal women in a feeding study

BackgroundThe relationship between BMI and leptin has been studied extensively in the past, but previous reports in postmenopausal women have not been conducted under carefully controlled dietary conditions of weight maintenance using precise measures of body fat distribution. The aim of the present study was to examine the association between serum leptin concentration and adiposity as estimated by BMI and dual energy x-ray absorptiometry (DEXA) measures (percent body fat, central and peripheral fat, and lean mass) in postmenopausal women.MethodsThis study was conducted as a cross-sectional analysis within the control segment of a randomized, crossover trial in which postmenopausal women (n = 51) consumed 0 (control), 15 (one drink), and 30 (two drinks) g alcohol (ethanol)/d for 8 weeks as part of a controlled diet. BMIs were determined and DEXA scans were administered to the women during the 0 g alcohol treatment, and a blood sample was collected at baseline and week 8 of each study period for leptin analysis.Results and discussionIn multivariate analysis, women who were overweight (BMI > 25 to ≤ 30 kg/m2) had a 2-fold increase, and obese women (BMI > 30 kg/m2) had more than a 3-fold increase in serum leptin concentrations compared to normal weight (BMI ≤25 kg/m2) women. When the models for the different measures of adiposity were assessed by multiple R2, models which included percent body fat explained the highest proportion (approximately 80%) of the serum leptin variance.ConclusionUnder carefully controlled dietary conditions, we confirm that higher levels of adiposity were associated with higher concentrations of serum leptin. It appears that percent body fat in postmenopausal women may be the best adiposity-related predictor of serum leptin.

Effects of cocaine–amphetamine regulated transcript (CART) on hormone release

Objective: Cocaine- and amphetamine-regulated transcript (CART) is a recently described neuropeptide widely expressed in the rat brain. CART is abundant in hypothalamus nuclei controlling anterior pituitary function. In the paraventricular nucleus CART mRNA is colocalized with vasopressin and corticotrophin-releasing factor containing neurons. The data may suggest that CART plays a role in hypothalamic regulation of neuroenocrine functions. Material and methods: Male Wistar–Kyoto rats were investigated. Experiment I: CART was administered intracerebroventricularly (i.c.v.) in a dose of 0.5 μg dissolved in 5 μl vehicle. At 60, 120 min after the infusion of CART or vehicle animals were decapitated and trunk blood was collected until hormonal estimations. Experiment II: CART in a dose of 10 μg was injected intravenously (i.v.). At 60, 120, 240 min the rats were decapitated and the trunk blood was collected. Serum rLH, rFSH, rPRL, rTSH, rGH and plasma leptin, NPY concentrations were measured by RIA methods. Results: CART administered centrally (i.c.v.) simulated significantly GH release after 60 min ( p<0.05) and after 120 min ( p<0.01). CART increased also PRL after 60 min ( p<0.05). A marked increase of corticosterone level was observed at 60 and 120 min ( p<0.01, p<0.01). We did not observe significant changes in LH, FSH and TSH. We found an increase of serum leptin concentrations at 60 min after CART administration ( p<0.01). However, serum NPY levels did not change. After intravenous injection (i.v.) of CART an increase of GH was observed at 120, 240 min ( p<0.01, p<0.01, respectively). A rise in serum PRL was found at 240 min ( p<0.05). Corticosterone concentrations were enhanced at 60, 120, 240 min ( p<0.01, p<0.01, p<0.01, respectively). We did not observe significant changes in LH, FSH and TSH. Conclusions: CART may play a modulating role in the mechanism of pituitary hormone release.

Potential role of high serum leptin concentration in age-related decrease of fatty acid synthase gene expression in rat white adipose tissue

Ageing in rats is associated with significant reduction of lipogenic enzymes genes expression and the rate of fatty acids synthesis in white adipose tissue. Since resistance to insulin and/or triiodothyronine is not directly related to reduction in lipogenic enzymes activity in white adipose tissue of old rats, we have proposed recently that the age-related increase in leptin gene expression and high serum leptin concentration could, at least partly, account for the down regulation of lipogenic enzymes gene expression. To test this hypothesis, in this paper we experimentally (by single intraperitoneal injection of recombinant leptin) increased plasma leptin concentration in young rats to the level observed in old animals, and we examined its effect on fatty acids synthase (FAS) gene expression in white adipose tissue. The results presented in this paper indicate that leptin administration to young rats, in amount that cause the increase in serum leptin concentration to that found in old rats, significantly decreased the white adipose tissue FAS gene expression. We propose, therefore, that leptin could play a causative role in the down-regulation of lipogenic enzyme gene expression observed with ageing.

Leptin secretion from the epididymal fat pad is increased by the sexual maturation of the male rat.

Although leptin has been implicated as an important factor in triggering the onset of puberty in females, much less is known about the role of this adipose tissue hormone in the sexual maturation of males. Previous work in the rat has suggested that the peripubertal rise in testosterone precedes an increase in leptin secretion, and it has been suggested that the testosterone rise induces the leptin increase. These studies examined some of the interactions between leptin secretion and the peripubertal testosterone rise in male rats. Serum leptin concentrations were significantly elevated in young adult male rats compared with immature rats. Cultured epididymal fat pads obtained from adult animals secreted significantly more leptin than did those obtained from immature rats. Castration of immature rats with or without testosterone replacement for 1 week did not result in a significant change in either the serum leptin concentrations or the ability of the epididymal fat pad to secrete leptin. Exposure of epididymal fat to 5 ng/mL of testosterone in vitro resulted in a significantly enhanced secretion of leptin into the media compared with plain media controls. These results confirmed that there is an increase in serum leptin concentrations with sexual maturation in the male rat. They also suggest that this increase is due to an enhanced ability of adipose tissue to secrete leptin. Within a normal physiologic range, testosterone may play a role in inducing this increased ability to secrete leptin.

Neuropeptide Y counteracts the anorectic and weight reducing effects of ciliary neurotropic factor.

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 microg/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 microg/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 microg/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 microg/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.

Increase in serum leptin concentrations among women with endometriosis during danazol and leuprolide depot treatments

Objective: This study was undertaken to evaluate serum leptin concentrations in women with endometriosis during treatment with danazol and with leuprolide depot. Study Design: Twenty patients aged 18 to 42 years with regular menses and documented pelvic endometriosis were recruited from a university hospital setting. Treatment was 200 mg danazol 3 times daily for 6 months or 3.75 mg leuprolide depot every 28 days for 6 months. Serum leptin concentrations were measured before, during, and after treatment. A single blood sample was taken from each of 10 control women without endometriosis for comparison. Serum leptin level was measured with a radioimmunoassay kit with human leptin, and analysis of variance and paired t tests were used for statistical analysis. Results: Serum leptin levels were almost the same among women with endometriosis as in the control group. Leptin levels were higher among women with endometriosis during treatment with danazol and leuprolide(P <.001). Three months after treatment, leptin values remained moderately higher than before treatment. Conclusion: Danazol and leuprolide increased serum leptin levels. The mechanism of leptin increase is unclear. Further studies are needed to determine whether an adipogonadal axis exists. (Am J Obstet Gynecol 2000;183:58-62.)

Increase in serum leptin concentrations among women with endometriosis during danazol and leuprolide depot treatments

Objective: This study was undertaken to evaluate serum leptin concentrations in women with endometriosis during treatment with danazol and with leuprolide depot. Study Design: Twenty patients aged 18 to 42 years with regular menses and documented pelvic endometriosis were recruited from a university hospital setting. Treatment was 200 mg danazol 3 times daily for 6 months or 3.75 mg leuprolide depot every 28 days for 6 months. Serum leptin concentrations were measured before, during, and after treatment. A single blood sample was taken from each of 10 control women without endometriosis for comparison. Serum leptin level was measured with a radioimmunoassay kit with human leptin, and analysis of variance and paired t tests were used for statistical analysis. Results: Serum leptin levels were almost the same among women with endometriosis as in the control group. Leptin levels were higher among women with endometriosis during treatment with danazol and leuprolide(P <.001). Three months after treatment, leptin values remained moderately higher than before treatment. Conclusion: Danazol and leuprolide increased serum leptin levels. The mechanism of leptin increase is unclear. Further studies are needed to determine whether an adipogonadal axis exists. (Am J Obstet Gynecol 2000;183:58-62.)

Influence of surgical stress and parenteral nutrition on serum leptin concentration

Experimental studies suggest that leptin may be an important metabolic signal for energy regulation.Aim: To assess whether surgical stress produces changes in serum leptin concentration and to investigate and compare the effect of total parenteral nutrition and hypocaloric parenteral nutrition on serum leptin levels.Patients and methods: Twenty-two surgical patients (11 male and 11 female) in need of parenteral nutrition were recruited. Parenteral nutrition was always initiated 24 h after surgical procedure. Group I (n=15) received total parenteral nutrition, while Group II (n=7) were treated with hypocaloric parenteral nutrition. Serum leptin concentration was determined before surgical procedure (day −1), after surgery and before parenteral nutrition was started (day +1), and after 5 days of treatment with parenteral nutrition (day +6).Results: A tendency to increase serum leptin levels was observed after surgical procedure (6.0±1.9 vs 9.9±2.7 ng/ml;P= 0.07). After starting parenteral nutrition no significant changes on serum leptin concentrations were found in both groups, but a trend to raise serum leptin was observed in Group I (6.2±1.7 vs 8.3±2.7 ng/ml) whereas a trend to decrease serum leptin was detected in Group II (4.6±2.5 vs 1.6±0.5 ng/ml). On day +6 an increase of serum leptin and insulin levels was observed in Group I in comparison with Group II (8.3±2.7 vs 1.6±0.5 ng/ml;P⪡ 0.05 and 58±41 vs 12±15 μU/l;P⪡ 0.05 respectively). Finally, a positive correlation at day +6 between insulin and serum leptin levels was observed (r= 0.66;P⪡ 0.01).Conclusions: a) Surgical stress is associated to an increase of serum leptin concentrations; b) Total and hypocaloric parenteral nutrition produces quite different effects on serum leptin levels that could be related to distinct insulin response.

Serum and follicular fluid leptin during in vitro fertilization: relationship among leptin increase, body fat mass, and reduced ovarian response.

The satiety factor leptin is expressed in several reproductive tissues, but its role in the control of reproductive physiology is not well understood. We studied leptin concentrations in the sera and follicle fluids of 52 women [body fat mass percentage (BFM%) range, 19.6-38.8%] undergoing pituitary down-regulation and ovarian hyperstimulation for in vitro fertilization (IVF) treatment. Fasting serum samples were collected 1) at maximal suppression before the initiation of gonadotropin treatment, 2) at maximal ovarian hyperstimulation, 3) at the time of oocyte retrieval, and 4) 16 days later when all subjects were under exogenous luteal support using 600 mg progesterone daily. Follicular fluid (FF) was obtained at oocyte retrieval from two representative preovulatory follicles in both ovaries. During ovarian hyperstimulation there was a significant 60% increase in serum leptin concentrations from 10.9 +/- 1.1 (SEM) to 15.7 +/- 1.5 ng/mL (P < 0.01) between suppression and maximal hyperstimulation, demonstrating that the ovarian functional state can affect serum leptin concentrations. A serum leptin increase of 22-198% during ovarian hyperstimulation was evident in 43 subjects, whereas in 9, leptin concentrations remained unchanged. A positive correlation between leptin change and BFM% (r = 0.55; P < 0.0005) was observed in the 43 leptin responders. The follicular fluid leptin level was similar to that in serum. In separate linear regression analysis, BFM% contributed to 59-64%, body mass index to 46-56%, and weight to 46-55% (all P < 0.001) of the variability in leptin concentrations at the 4 time points. The 20-fold increase in serum estradiol concentrations during IVF was not significantly correlated with changes in leptin concentrations. On the contrary, the relative serum leptin increase was negatively associated with the ovarian response to hyperstimulation, as revealed by the numbers of follicles (b = -0.28; r2 = 8.1%; P < 0.05) and oocytes retrieved (b = -0.39; r2 = 15.2%; P < 0.01). This relationship was further reflected in a positive correlation between the percent increases in leptin and FSH concentrations (r = 0.39; P < 0.01). The significant relationship of high leptin and reduced ovarian response was also maintained when the cumulative dose of FSH was used as a covariable. Reduced ovarian response was not a function of body mass index, BFM%, basal leptin levels, or insulin concentrations. Fasting serum insulin concentrations remained unchanged in response to IVF, but were positively correlated to serum leptin concentrations at all four time points. Our data suggest that leptin production may be influenced by the ovarian functional state. During IVF a high relative leptin increase is associated with adiposity and a reduced ovarian response. These observations support the possibility that high leptin concentrations might reduce ovarian responsiveness to gonadotropins. Hence, leptin might explain in part why obese individuals require higher amounts of gonadotropins than lean subjects to achieve ovarian hyperstimulation.

Increase in serum leptin concentrations in women undergoing controlled ovarian hyper stimulation for assisted reproduction

The ob gene product might influence the hypothalamo-pituitary axis and ovarian Junction directly via specific ovarian receptors. Premenopausal women have higher leptin concentrations compared to postmenopausal controls. In this study, we determined changes in leptin serum concentrations under the influence of supraphysio-logical estradiol levels during controlled ovarian hyper-stimulation. In a prospective study of 20 patients undergoing in vitro fertilization (IVF) or intracyto-plasmic sperm injection (ICSI), morning blood samples were collected to determine leptin and estradiol concentrations on day 3 and day 9 of the stimulation cycle and on alternate days until ovulation induction. There was a significant increase in serum leptin concentrations from day 3 to day 9 (9.87 ± 1.5 ng/ml on day 3 and 13.8 ± 2.1 ng/ml on day 9 respectively). No further increase in leptin was observed until the day of ovulation induction. These data further underline the role of leptin as a hormone of reproduction.

Serum leptin concentrations in relation to pubertal development

OBJECTIVESThe amount of adipose tissue influences pubertal development and fertility in girls. A candidate for mediating this is the hormone leptin, derived from adipocytes. This work was carried out to...

Interleukin 1 alpha increases serum leptin concentrations in humans.

Leptin, the protein product of the ob gene, regulates appetite and body weight in animals. Endotoxin and cytokines, induced by endotoxin, interleukin (IL) 1 and tumor necrosis factor, increase expression of leptin in mice and hamsters. We measured serum leptin concentrations in patients with cancer before and after administration of recombinant human IL-1 alpha. Fourteen patients received IL-1 alpha at one of three dose levels (0.03, 0.1, or 0.3 microgram/kg.day) for 5 days. Serum leptin concentrations increased in all but two patients within 24 h after the first dose. The increase in leptin was correlated directly with IL-1 alpha dose (P = 0.0030). Despite continued administration of IL-1 alpha, serum leptin concentrations returned to pretreatment levels by day 5 of therapy. An increase in serum leptin concentrations may be one mechanism by which anorexia is induced by IL-1 alpha. However, tachyphylaxis of the leptin response suggests that other mechanisms also are involved.

R-197. Increase of serum leptin concentrations in women undergoing ovarian stimulation for assisted reproduction

R-197. Increase of serum leptin concentrations in women undergoing ovarian stimulation for assisted reproduction

The expression of leptin and its receptors in pre-ovulatory human follicles.

The expression of leptin and its receptors was examined by reverse transcriptase-polymerase chain reaction and immunofluorescence in granulosa and cumulus cells of pre-ovulatory follicles and in meiotically mature oocytes obtained from women undergoing in-vitro fertilization. Leptin concentrations were measured in newly aspirated follicular fluids and in maternal serum before and after the administration of an ovulatory dose of human chorionic gonadotrophin. The findings demonstrate leptin expression at the mRNA and protein levels by granulosa and cumulus cells, and the presence of leptin in mature human oocytes. While an association between follicular leptin concentration and embryo development was not observed, a post-ovulatory increase in serum leptin concentration was associated with implantation potential. The results are discussed with respect to possible roles of leptin in early human development.