Background. Adipose tissue is an important endocrine organ that secretes cytokines, including adiponectin, levels of which are negatively correlated with the severity of the inflammatory process. Aim. To assess the time course of adiponectin levels following open heart surgery with cardiopulmonary bypass and its correlation with early postoperative outcomes. Materials and Methods. Blood samples were obtained from 24 children undergoing cardiac surgery and analyzed for adiponectin, C-reactive protein, and other inflammatory markers. Results. Baseline adiponectin levels were negatively correlated with patients’ preoperative weight and age. Postoperative adiponectin levels decreased compared to baseline () and correlated negatively with duration of cardiopulmonary bypass (, ), length of stay in the pediatric intensive care unit (, ), and the inotropic score (, ). Adiponectin levels were positively correlated with sVCAM 1 levels; however, there was no correlation between adiponectin levels and sP selectin, tPA, MCP1, and sCD40. Conclusions. The inflammatory response after open heart surgery with cardiopulmonary bypass is associated with a reduction in adiponectin levels. Prolonged or more complicated surgery induced a more substantial inflammatory process characterized by a significant reduction in adiponectin levels over time and a delayed return to baseline levels.

Background: Cardiac surgery involving cardiopulmonary bypass (CPB) causes a systemic inflammatory process which can lead to multiple organ failure and postoperative morbidity. Recent animal and human studies suggested a possible involvement of leptin in the systemic inflammatory response. Aim: To characterize the response of leptin to open heart surgery (OHS) and the relationship between the time course of leptin levels and the post-operative clinical course, and to examine the effect of exogenous glucocorticoids. Patients and methods: Forty-seven pediatric patients, undergoing OHS for congenital heart disease were studied. Thirty-four patients (Group 1) received methylprednisolone during CPB while 13 (group 2) did not. Serial blood samples were collected perioperatively and up to 24 h after surgery, and assayed for leptin and cortisol. Results: All patients’ leptin levels decreased significantly during CPB (to 44–48% of baseline, p<0.001); they then increased, peaking at 12 h post-operatively. The levels of groups 1 and 2 were similar up to 8 h post-operatively; thereafter, those of group 1 were significantly higher. Recovery of leptin levels in patients with a more complicated post-operative course was comparatively slower. Cortisol levels of all patients increased significantly during CPB (p<0.001), gradually decreasing afterwards. Cortisol and leptin levels were inversely correlated in both patients’ groups. Conclusions: CPB is associated with acute changes in circulating leptin levels. A complicated postoperative course is associated with lower leptin levels which are inversely correlated with cortisol levels. Leptin may participate in post-CPB inflammatory and hemodynamic responses.

Objective: To determine the effect of acute psychotic stress on adipokine secretion in non-diabetic subjects. Research design and methods: Adiponectin, leptin, and cortisol serum levels were determined in 39 non-diabetic patients with acute psychotic stress reaction admitted to a psychiatric ward. The clinical global impression (CGI) score was used to evaluate the level of psychotic stress. Insulin sensitivity (IS) was determined by the homeostasis model assessment (HOMA). Patients were re-assessed 2 weeks after admission. During hospitalization patients were treated for variable times with either phenothiazines or thiox-anthenes. Results: The mean CGI score decreased significantly with time: 5.3±0.8 and 2.6±0.8 on admission and after 2 weeks respectively (p<0.001). On admission, the mean adiponectin level was significantly lower in patients compared to normal controls: 15.3±8.2 μg/ml and 26±12.8 μg/ml, respectively (p=0.02). It increased significantly after 2 weeks to 18.2±10 μg/ml (p=0.003). By contrast, the leptin and cortisol levels did not change significantly. No correlation was found between the changes in individual CGI scores and adiponectin levels. However, female patients with the highest stress on admission demonstrated the lowest adiponectin levels and insulin sensitivity: p=0.002 and 0.03 respectively. Conclusions: These data suggest a link between acute psychotic stress reaction and decreased serum adiponectin levels. Further studies are recommended to determine the strength of this association.

OBJECTIVE:Pregnancy is a unique situation characterized by insulin resistance. The role of adiponectin, an insulin-sensitizing hormone, has not been completely clarified during pregnancy. The aim of this cross-sectional study was to evaluate adiponectin levels during pregnancy and postpartum. STUDY DESIGN:Adiponectin and leptin levels were tested in 80 pregnant women, 20 in each trimester (mean gestational age 10.5+/-1.9; 19.3+/-4.9; 39.3+/-0.8 weeks,) as well as 4 days postpartum. RESULTS:Adiponectin levels during first (13.3+/-3.6 micro g/ml), second (12.6+/-4.4 micro g/ml) and third trimester (11.2+/-3.7 micro g/ml) did not differ and were significantly higher than postpartum levels (8.8+/-2.1 micro g/ml; P<0.0001, P<0.004 and P<0.02, respectively). CONCLUSION:Despite increased insulin resistance during pregnancy, no significant alterations in adiponectin levels were observed. This may imply that the regulation of adiponectin during gestation is altered. The elevated gestational adiponectin levels are consistent with increased 'adiponectin resistance' during pregnancy.

BACKGROUND:The hormone ghrelin and the adipocytokines leptin and adiponectin participate in body weight regulation. In response to weight loss, ghrelin and adiponectin levels increase and leptin decreases. Cancer cachexia is a complex metabolic state, characterized by loss of muscle mass and adipose tissue together with anorexia. The authors hypothesized that responses of these hormones may be attenuated in cancer cachexia.METHODS:Fasting plasma ghrelin, adiponectin, and leptin levels, as well as weight loss, were determined in 40 cancer patients: 18 of them suffered from cancer-induced cachexia, and 22 served as a comparison group. Hormone levels were measured before administration of cancer therapy.RESULTS:A similar distribution of age, gender, and diagnosis was observed in both study groups, but the cachectic patients had higher rates of metastatic disease and lower albumin levels. No significant correlation was observed between plasma adiponectin levels and weight loss. Mean plasma ghrelin levels were higher among cachectic compared with noncachectic patients. Notably, the association between ghrelin levels and weight loss was only modest, and in a third of the cachectic patients, ghrelin levels were equal to or lower than those in the noncachectic group. Plasma leptin levels showed gender-dependent associations, and significantly lower levels were found among cachectic women but not among cachectic men.CONCLUSIONS:Results suggested a gender-dependent attenuation of expected physiologic responses to weight loss among cancer cachexia patients. Thus, impaired response of adiponectin, ghrelin, and leptin may play a role in the pathogenesis of cancer cachexia syndrome.

Severely discordant twins are a unique model which enables the investigation of aberrant intrauterine fetal growth. Adiponectin is a novel adipocytokine produced abundantly and exclusively in adipose tissue. In singletons, cord blood adiponectin is positively correlated with birth weight. Thus, it may have a role in intrauterine fetal growth. The aim of this study was to evaluate adiponectin and leptin levels in bichorionic, biamniotic twins with and without growth discordance. Twenty nine couples of twins were included in this study. Of them, 14 were with severe growth discordancy (range 25-52%) - in all of them the smaller twin was severely growth restricted (mean percentage 3.5 ± 0.9) and the co-twin was appropriate for gestational age (AGA) (mean percentage 35.7 ± 18.2). The additional 15 control twins were accordant (range 0.8-13%, both AGA) and matched for gestational age and maternal age, weight, gravity and parity. Adiponectin and leptin were determined in cord blood using RIA kits (Linco Research, Inc., St. Charles, MO). A positive correlation was found between adiponectin and both birth weight and gestational age in all twins (r = 0.4 p < 0.002 and r = 0.3 p < 0.002, respectively). Mean adiponectin was significantly lower in IUGR fetuses of the discordant twins as compared with their co-twin (27.1 vs. 38.2 μg/ml respectively, p < 0.03). Leptin levels were also lower in the IUGR twins but the difference did not reach a statistical significance (2.5 vs. 3.7 ng/ml, p < 0.09). Conversely, in the control group there were no differences in mean adiponectin (29.6 vs. 32.0 μg/ml) and leptin levels (3.1 vs. 3.6 ng/ml). This paradigm of discordance twins may point to a key role of adiponectin in intrauterine fetal growth. Moreover, since adiponectin has profound insulin-sensitizing and anti-atherogenic effects, the low adiponectin levels found in the IUGR twins may provide a link between abnormal growth in utero and the high prevalence of adulthood metabolic syndrome in IUGR newborns (Barker hypothesis).

Objective: The purpose of this study was to disclose the relationship between adiponectin and birth weight in a large group of newborns with normal and aberrant growth ("overweight").Study design: Eighty-one healthy, term newborns were divided into 2 groups: 20 in the large-for-gestational age (LGA; 4297 +/- 207 g), and 61 newborns in the appropriate-for-gestational age (AGA; 3384 +/- 368 g). Cord blood was analyzed for adiponectin, leptin, and insulin levels.Results: Mean adiponectin level was significantly lower in LGA newborns (29.4 +/- 13.8 vs 35.0 +/- 9.9 mu g/mL, P <.04). Both leptin and insulin levels were higher in LGA than AGA newborns, and leptin levels positively correlated with birth weight in both groups. Insulin levels positively correlated with birth weight in AGA newborns.Conclusion: The results of this study imply that adiponectin may have a role in fetal growth and support the notion of negative feedback exerted by adipose tissue on adiponectin levels, as previously shown in adults. (C) 2005 Mosby, Inc. All rights reserved.

8113 Background: The hormone ghrelin and the adipocytokines leptin and adiponectin participate in body weight regulation. In response to severe weight loss, ghrelin and adiponectin levels increase and leptin decreases. Here we studied the association between plasma levels of these mediators and cancer cachexia. Methods: Study population included breast (n=14) and colon (n=26) cancer patients. The mean age was 65±14. Fasting plasma ghrelin, adiponectin and leptin levels, as well as weight loss, were determined prior to administration of cancer therapy. Patients who had other acute or chronic cachectic states were excluded. Results: Patients were classified as either cachectics (defined as ≥5% loss of body mass index, n=18) or non-cachectics (n=22). Similar distribution of age, gender and diagnosis was observed in both study groups, but the cachectic patients had higher rates of metastatic disease and lower albumin levels (p<0.02 for both variables). Mean plasma ghrelin levels (pg/ml) were higher among cachectic compared to non-cachectic patients, for all categories examined (table). Yet, statistical significance was not reached for the differences between cachectic and non-cachectic men and colon cancer patients (table). Notably, the association between ghrelin levels and weight loss was only modest (r=-0.49) and in a third of the cachectic patients, ghrelin levels were equal or lower than the mean levels of the non-cachectic group. Mean plasma adiponectin levels were higher among cachectic patients compared to the control (12.3±5.2 ng/ml vs. 9.6±3.6 ng/ml respectively, p=0.06). Mean leptin levels were similar in both study groups. No correlation was found between ghrelin, adiponectin and leptin levels. Conclusions: Baseline plasma ghrelin and adiponectin levels are high among cancer cachexia patients. Yet, these expected physiologic responses are absent in a significant proportion of these patients and seem be gender and tumor type dependent. No significant financial relationships to disclose.

Adiponectin is a novel adipocytokine produced abundantly and exclusively in adipose tissue. This hormone has profound insulin-sensitizing properties. Pregnancy is a unique situation in which there is a physiological increase in insulin resistance. Despite the importance of adiponectin in regulation of insulin sensitivity, little is known about the role of this hormone during pregnancy. The aim of this study is to evaluate adiponectin levels during the pregnancy and immediate postpartum period. Twenty healthy pregnant women in first trimester (mean gestational age 10.5 ± 1.9 weeks) 20 patients in second trimester (19.3 ± 4.9 weeks) and 20 patients in third trimester (39.3 ± 0.8 weeks) were included in the study. In addition, 20 patients 4 days postpartum were included in the study. Patients were matched for age, pre conceptional BMI, gravity and parity. Blood sample were tested for adiponectin and leptin levels using RIA kits (Linco Research, Inc., St. Charles, MO). There were no significant differences between adiponectin levels in first (13.3 ± 4.2 μg/ml) second (12.6 ± 4.4 μg/ml) and third trimester (11.2 ± 3.7 μg/ml). However, postpartum adiponectin levels (8.8 ± 2.1 μg/ml) were significantly lower as compared with first (p < 0.0001) second (p < 0.004) and third trimester (p < 0.02). Leptin levels in second (23.6 ± 11.7 ng/ml) and third trimester (30.2 ± 13.4 μg/ml) were higher (p < 0.02 and p < 0.0001 respectively) as compared with postpartum levels(16.0 ± 13.2 μg/ml). Leptin levels in first trimester (21.2 ± 12.2 ng/ml) were significantly lower as compared with third trimester (p < 0.01). The significantly higher levels of adiponectin during pregnancy as compared with postpartum may imply that adiponectin has a role in the regulation of insulin resistance along pregnancy. The gradual decrease (although not statistically significant) in adiponectin levels throughout the pregnancy support this hypothesis, as the negative correlation between adiponectin and insulin resistance is well established.

Adiponectin, an adipocyte-derived plasma protein, with insulin-sensitizing properties, is negatively correlated with obesity and insulin resistance in adults. Adiponectin in plasma is found in distinct forms: trimer, hexamer and a high molecular weight (HMW) species. The aim of this study was to evaluate adiponectin levels in appropriate for gestational age (AGA) and intrauterine growth restricted (IUGR) newborns and to characterize the alterations of fetal adiponectin isoforms throughout pregnancy and in the two groups. Adiponectin, leptin and insulin levels, were measured (by RIA) in cord blood samples obtained from 80 newborns at delivery between 25 and 42 weeks of gestation. Of this group, 45 AGA (mean percentile 55.0 ± 26.3) and 21 IUGR (5.4 ± 2.4) newborns, were compared for their adiponectin and leptin and insulin concentrations. In addition, cord blood samples were analyzed for adiponectin isoforms by SDS-PAGE under nondenaturing conditions. Adiponectin was found in cord blood of all newborns in levels ranging from 1-118 μg/mL and positively correlated with the gestational age (r = 0.65, P < .01). Adiponectin levels in the AGA group were significantly higher compared with the IUGR group (68.2 ± 14.5 μg/mL and 48.5 ± 2 0.9 μg/mL, respectively, P < .0001). Similarly, leptin levels were significantly lower in the IUGR group (10.6 ± 7.7 vs. 5.6 ± 5.6 ng/mL; P < .006). The trimer and hexamer isoforms of adiponectin were the prevalent species in serum samples from 25-35 weeks of gestation, and in IUGR group, while in later gestational weeks and in AGA group, the HMW form predominated. These findings indicate that adiponectin is produced in the fetus as early as 25 weeks of gestation, and increases with gestational age, potentially reflecting the development of adipose tissue. The quantitative and qualitative (isoforms) changes in adiponectin throughout pregnancy and between IUGR and AGA groups may suggest a putative role of adiponectin in physiological and pathological fetal growth.

Adiponectin, an adipocyte-derived plasma protein, with insulin-sensitizing properties, is negatively correlated with insulin resistance (IR) in adults. It has an important role in the regulation of glucose homoeostasis and IR. Pregnancy is a unique situation associated with physiological transient increase in IR. The aim of this study is to evaluate whether the changes in IR before and after delivery are correlated with adiponectin levels. Forty five healthy pregnant women scheduled for elective cesarean section at term were included in the study. Two blood samples (after overnight fasting) were taken from each woman: 1. several hours before the operation; 2. on the fourth day postpartum. Adiponectin, leptin, glucose, insulin and prolactin were measured. Antepartum and postpartum homeostasis model assessment for IR index (HOMA) was calculated. Mean antepartum adiponectin concentration (16.8 ± 7.8 μg/mL) was significantly higher than postpartum concentration (13.2 ± 6.9 μg/mL P < .01). In consistence with the postpartum normalization of IR, fasting glucose and insulin concentration declined from 81.5 ± 13.9 mg/dL to 72.9 ± 5.3 mg/dL (P < .04) and from 7.3 ± 4.0 mIU/L to 4.0 ± 3.7 mIU/L (P < .001), respectively. HOMA studies revealed significant postpartum increase in insulin sensitivity (129.6 ± 90.8% vs. 269.5 ± 122.0%, P = .001). There was no correlation between adiponection and insulin sensitivity, leptin, prolactin, neonatal birth weight, maternal BMI, glucose and insulin. In contrast to the reported inverse relationship between adiponectin concentration and IR in adults, we found relatively high maternal serum adiponectin concentration in the third trimester and significant decrease in adiponectin concentration postpartum. The allegedly paradoxical postpartum decrease in adiponectin levels can be explained by a number of hypotheses e.g. transport from the fetus, specific hormonal regulation and compensatory reaction. Nevertheless, these data implies that pregnancy is a unique condition in which the linkage between adiponectin and IR is disrupted.

Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and anti-atherosclerotic properties found abundantly in cord blood. The aim of this study was to examine maternal adiponectin levels and to establish a possible connection between these levels and placental or fetal production. The study was comprised of three studies. Study 1 - blood was obtained from 23 women one day prior to and four days after delivery. Study 2–seventeen blood samples were obtained from mothers and their newborns at delivery. Blood samples were tested for adiponectin and leptin. Study 3–human placental tissues were tested for adiponectin mRNA by RT-PCR. Study 1- Maternal adiponectin levels before and after delivery were 22.2±7.0 and 17.5±6.8 g/ml respectively (P<0.03). A similar decline was measured for leptin, known to be expressed in the placenta, (27.9±13.4 and 13.2±8.0 ng/ml, respectively, P<0.001). No correlation was found between adiponectin levels and maternal characteristics. Study 2–Cord blood adiponectin levels were significantly higher when compared with maternal adiponectin levels (61.1±19.0 vs. 22.7±6.8 g/ml, P<0.001). No correlation was found between cord blood and maternal adiponectin (r = 0.3, P<0.2). Study 3−there was no expression of adiponectin mRNA in human placental tissues. Our findings demonstrate that adiponectin levels are relatively high in the serum of women in the third trimester and decline after delivery. These findings can not be explained either by placental production or by transport from fetal compartments.

Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and antiatherosclerotic properties. The aim of this study was to examine whether adiponectin is present in human fetal blood, to define its association with fetal birth weight, and to evaluate whether dynamic changes in adiponectin levels occur during the early neonatal period. Cord blood adiponectin levels were extremely high (71.0 +/- 21.0 microg/ml; n = 51) compared with serum levels in children and adults and positively correlated with fetal birth weights (r = 0.4; P < 0.01). No significant differences in adiponectin levels were found between female and male neonates. In addition, there was no correlation between cord adiponectin levels and maternal body mass index, cord leptin, or insulin levels. Cord adiponectin levels were significantly higher compared with maternal levels at birth (61.1 +/- 19.0 vs. 17.6 +/- 4.9 microg/ml; P < 0.001; n = 17), and no correlation was found between cord and maternal adiponectin levels. There were no significant differences between adiponectin levels at birth and 4 d postpartum (61.1 +/- 19.0 vs. 63.8 +/- 22.0 microg/ml; n = 17). These findings indicate that adiponectin in cord blood is derived from fetal and not from placental or maternal tissues. The high adiponectin levels in newborns compared with adults may be due to lack of negative feedback on adiponectin production resulting from lack of adipocyte hypertrophy, low percentage of body fat, or a different distribution of fat depots in the newborns.

A unique 16-year old female patient presented after acute Epstein-Barr virus (EBV) infection with severe primary hypothyroidism. Her thyroid test results were thyrotropin level (TSH) of 198 mU/L (normal, 0.4-4 mU/L), free thyroxine [FT4], 2.5 pmol/L (normal, 10-25 pmol/L), total triiodothyronine (TT3) > 19.5 nmol/L (normal, 1.3-2.7 nmol/L), and free triiodothyronine (FT3), 0.77 pmol/L (normal, 3.3-6.3 pmol/L). She had high titers of thyroglobulin and thyroid peroxidase autoantibodies. In vitro triiodothyronine (T-3)-binding measured by radioimmunoprecipitation was 86% (normal, up to 8.5%) and thyroxine (T-4)-binding 8.2% (normal, 6.4%). Serum immunoglobulin G (IgG) absorption, achieved by protein-G Sepharose beads, decreased TT3 toward normal. Levothyroxine treatment normalized the low baseline FT4 and FT3 values, and suppressed TSH to normal. However, TT3 remained highly elevated and returned to normal after 20 months, while T-3 binding gradually decreased. Thus, her severe hypothyroidism was masked by this unusual phenomenon. Thirty-four patients with EBV infection (15 with acute disease and 19 with previous infection) were tested for thyroid hormone levels. EBV antibodies (early antigen immunoglobulin M [IgM] and IgG and anti-Epstein-Barr virus nuclear antigen [EBNA] IgG) were measured by enzyme-linked immunosorbent assay (ELISA). In 15 patients with acute EBV the mean TT3 level was 2.47 +/- 0.39 nmol/L (5 had TT3 values above normal) compared to a mean TT3 of 1.70 +/- 0.53 nmol/L in 19 subjects with previous infection (p < 0.0005; only 1 had a TT3 result above normal), with no differences in FT4 and TSH concentrations between the two groups. Acute EBV infection may be associated with transient mild to severe TT3 elevation as a result of assay interference by anti-T-3 autoantibodies.

Insulin-like growth factor-1 (IGF-1) and its binding proteins (IGFBPs) are produced by many tissues and are present in serum and other biological fluids. Alterations in sera of IGF-1 and 2 and IGFBPs were demonstrated in patients with malignancy, infection and other diseases causing pleural effusion. In this study the IGF-1 and IGFBP-2 content and the specific electrophoretic patterns of IGFBPs in samples of sera and pleural effusions of 25 patients with malignancy, infection and congestive heart failure were investigated. IGF-1 levels in exudative effusions of malignant solid tumors were significantly higher [(mean+/-SD), 20.9+/-7.5 nmol/L, n = 9] than in lymphoma (11.0 +/- 5.2 nmol/L, n = 5; p < 0.05), infection (11.4 +/- 6.5 nmol/L, n = 6; p < 0.05) and transudative effusion of congestive heart failure (4.3 +/- 3.3 nmol/L, n = 5; p < 0.02). IGFBP-2 was markedly increased in effusions of malignant solid tumors (2.14 +/- 0.82 mg/L, n = 9) compared with exudates of lymphoma, infection and transudates (1.10 +/- 0.70, 1.22 +/- 0.32 and 0.93 +/- 0.52 nmol/L, respectively, p < 0.05). Moreover, in effusion of solid tumors, IGFBP- 2 levels were higher than those in corresponding sera, which suggests local production of this binding protein. The demonstration of IGFBP- 2 in solid tumor cells by immunohistochemistry further supports this possibility. This work demonstrates the existence of the IGF-1/IGFBP system in pleural fluids from different etiologies and implies possible use of IGF-1 and IGFBP-2 as a potential marker of malignant effusions.

OBJECTIVE:To characterize the dynamics of circulating leptin in children after cardiac surgery with cardiopulmonary bypass (CPB), which is known to induce a systemic inflammatory response.DESIGN:Investigative study.SETTING:University-affiliated tertiary care hospital.PARTICIPANTS:Eight children (age range, 3 months to 13 years) undergoing CPB to correct congenital heart disease.INTERVENTIONS:The time courses of leptin and cortisol levels were determined. Serial blood samples were collected from the arterial catheter or from the CPB circuit preoperatively; on termination of CPB; and at 2, 4, 8, 12, 18, and 24 hours postoperatively. Plasma was recovered immediately, divided into aliquots, and frozen at -70 degrees C until use. Leptin was measured by a human leptin radioimmunoassay kit.MEASUREMENTS AND MAIN RESULTS:Leptin levels during CPB decreased to 50% of pre-CPB levels (p < 0.01). After termination of CPB, levels increased gradually and peaked at 12 hours postoperatively (10 P.M. to 1 A.M.). Cortisol levels were inversely correlated to leptin levels (p = 0.016).CONCLUSION:CPB is associated with acute changes in circulating leptin levels. These changes parallel those in cortisol, showing an inverse relationship between leptin and cortisol, suggesting a relationship between the neurobiology of these systems that could be important for the neuroendocrine response to CPB. A prognostic role of leptin and its relationship to cortisol after CPB warrant further study.

Leptin is secreted into the circulation and communicates the peripheral nutritional status to specific hypothalamic centers. Recent studies suggest that leptin may be involved in the acute response to stress, and that its interaction with the hypothalamo-pituitary-adrenal axis and the inflammatory cytokine system may be of clinical importance. Since these systems are activated during acute myocardial infarction (AMI), we studied leptin and cortisol levels during hospitalization in 30 consecutive patients admitted for AMI. The results show that leptin reached its peak on the second day of hospitalization, with a 2-fold increase from its baseline level on admission (p < 0.02). On day 3, leptin levels declined, and were 46%, 9%, and 6% above baseline on days 3, 4 and 5, respectively. The mean cortisol level was elevated on day 1 and decreased toward normal levels thereafter (p < 0.001). The cortisol level did not correlate with leptin concentration throughout the study. These findings suggest that leptin may have a role in the metabolic changes taking place during the first days after an AMI.