Serum Leptin Concentrations In Patients Research Articles

Association of the Human Leptin Receptor Gene (rs1137101; Gln223Arg) Polymorphism and Circulating Leptin in Patients with Metabolic Syndrome in the Indian Population.

Phenotypic expression of metabolic syndrome is precipitated by environmental variables along with the individual genetic susceptibility to the obesogenic environment and growing body of evidence suggest a paramount role of adipocytokines. Therefore, identifying the genetic influence on circulation leptin levels and clarifying genotype-phenotype correlation of rs1137101 {Leptin receptor gene (LEPR) Gln223Arg (Q223R; A668G)} in metabolic syndrome were the primary objective of this study. A total of 447 adult participants, including 214 metabolic syndrome patients and 233 healthy controls, were genotyped using polymerase chain reaction-restriction fragment length polymorphism method to unravel the effects of genetic risk loci {Leptin receptor gene; Gln223Arg (Q223R; A668G); rs1137101} on the occurrence of metabolic syndrome in consort with circulation leptin levels. Suitable descriptive statistics was used for different variables. The genotype frequencies were found to be in Hardy-Weinberg equilibrium for both cases (p > 0.2722) as well as in controls (p > 0.2331). However, genotype (x2: 11.26, 2 d.f. p = 0.0036) and allele distribution (x2: 10.51, 2 d.f. p: 0.0012) of the LEPR Gln223Arg (Q223R; A668G) differed significantly between cases and controls. Gln/Arg genotype (OR = 1.6099; 95% CI = 1.0847-2.3893; p value = 0.0181), Arg/Arg genotype (OR = 2.8121; 95% CI = 1.4103-5.6074; p value = 0.0033) and R allele (OR = 1.5875; 95% CI = 1.1996-2.1008; p value = 0.0012) were significantly associated with increased risk of metabolic syndrome in univariate analysis. Further a multivariate logistic regression adjusted for potential confounders showed that Arg/Arg genotype (OR = 1.9; 95% CI = 1.271-2.639; p-value < 0.05) and Gln/Arg (OR: 1.3; 95% CI = 0.873-2.034; p value < 0.05) have a significant risk for the occurrence of the metabolic syndrome. A progressive increase in the serum leptin levels from major homozygous alleles to minor homozygous alleles were observed indicating that rs1137101 modify the serum leptin concentrations in patients with metabolic syndrome. These findings provide enough evidence of a significant association of LEPR Gln223Arg (Q223R; A668G) polymorphism in the LepR gene in Indian patients with increased risk of metabolic syndrome for R allele and Arg/Arg homozygote. Thus, rs1137101 might be a pleiotropic locus for metabolic syndrome and its components in studied population.

The Association Between Serum Levels of Leptin and Lipid Profiles in Cardiovascular Patients With Valve Calcification

Adipose tissue-derived hormones known as adipokines, like leptin, have multiple bioactions. Notwithstanding the key roles of leptin in regulating energy homeostasis and metabolism, its cardiovascular functions are complex and not fully understood. This study aimed to investigate the association between serum concentrations of leptin and lipid profiles in patients with valve calcification. Seventy-two patients with valve calcification and 72 healthy individuals participated in this case-control study. The serum levels of biochemical markers and leptin were measured by the standard enzymatic methods and enzyme-linked immunosorbent assay (ELISA) technique, respectively. Significantly increased serum concentrations of FBS (P=0.001), urea (P&lt;0.0001), creatinine (P=0.018), P (P&lt;0.0001), LDL-C (P=0.011) and lower Ca (P=0.006), and HDL-C (P&lt;0.0001) levels were observed in patients compared to controls. There was no significant difference in the serum level of TG and TC of patients than controls. Systolic and diastolic blood pressures were significantly increased in patients relative to controls (P&lt;0.0001). However, a significantly diminished serum level of leptin was observed in patients than controls (P&lt;0.0001). The correlation analysis demonstrated that the serum leptin concentration is negatively correlated with creatinine, but it is positively correlated with systolic blood pressure (P=0.0302, P=0.0362, respectively). There was no statistically significant association between serum levels of leptin and lipid profiles. Our findings indicated dyslipidemia and reduced serum leptin concentrations in patients with valve calcification, suggesting the role of lipid abnormalities and reduced leptin levels in the development and pathogenesis of valve calcification diseases.

Increased Expression of the Leptin Gene in Adipose Tissue of Patients with Chronic Kidney Disease-The Possible Role of an Abnormal Serum Fatty Acid Profile.

Chronic kidney disease (CKD) is associated with an increased level of leptin and an abnormal fatty acid (FA) profile in the serum. However, there are no data on the associations between them, and the reason for increased serum levels in patients with CKD is not well elucidated. Recently, we found that a CKD-related abnormal FA profile caused significant changes in the expression of genes involved in lipid metabolism in hepatocytes. The aim of this study was to examine whether leptin gene expression in subcutaneous adipose tissue (SAT) of patients with CKD may contribute to increased serum levels of this adipokine and whether the abnormal serum FA profile observed in CKD patients has an impact on leptin gene expression in adipocytes. The FA profile was measured in serum samples from patients with CKD and controls by GC–MS. The relative mRNA levels of leptin were measured in SAT by Real-Time PCR. Moreover, the effect of the CKD-related abnormal FA profile on leptin gene expression was studied in in vitro cultured 3T3-L1 adipocytes. Patients with CKD had higher concentrations of serum leptin than controls and higher expression level of the leptin gene in SAT. They also had increased serum monounsaturated FAs and decreased polyunsaturated FAs. The incubation of adipocytes with FAs isolated from CKD patients resulted in an increase of the levels of leptin mRNA. Increased leptin gene expression in SAT may contribute to elevated concentrations of these adipokine in patients with CKD. CKD-related alterations of the FA profile may contribute to elevated serum leptin concentrations in patients with CKD by increasing the gene expression of this adipokine in SAT.

Serum leptin concentration in patients with type 2 diabetes

Abstract With the increasing importance of early type 2 diabetes (DM2) and obesity detection, it is useful to reevaluate leptin role in these conditions. Our study aimed at investigating circulating leptin concentrations in a group of patients with DM2, and at assessing in detail whether leptin concentrations correlate with selected biochemical, clinical parameters and markers of systemic inflammation in patients with DM2 and in healthy volunteers. In our work, we analysed samples and data drawn from 71 patients aged 61.4 ± 11.7 years, who have been diagnosed with type 2 diabetes, as well as from a healthy control group (HC) consisting of 51 healthy subjects with a mean age of 57.8 ± 13.7 years. Therein, the concentration of leptin in the DM2 patients was significantly higher than in the HC (p &lt; 0.01), with median value of 16.59 (IQR 8.58-33.39) ng/ml in the DM2, vs median value of 6.66 (IQR 4.52-21.40) ng/ml in the HC. In the analysis of variance, higher leptin concentrations were revealed in the DM2 group as compared to the HC, and this figure remained significant after adjusting for gender and age (p &lt; 0.001). Moreover, it was independent of HOMA-IR (p = 0.003). However, the differences in leptin levels between the groups disappeared when additional adjustments for anthropometric parameters (BMI, waist circumference) were applied (p = 0.088). Beyond the aforementioned, significant positive correlations were found in the DM 2 group between leptin level and CRP (r=0.256; p &lt; 0.05) and IL-6 (r = 0.345; p &lt; 0.01). Among the selected variables, only gender and BMI were included in the predictive model explaining the variability of leptin, and, in total, were responsible for 72.6% of the original variation of the studied adipocytokine. The results of this study have led to conclusion that leptin may participate in the complex pathogenesis of DM2 and be a predictor of the development of this disease. As higher concentrations of leptin coexist with obesity, and this situation correlates positively with markers of inflammation (CRP, IL-6), leptin level, hence, should be considered in the pathogenesis of DM2.

Polymorphism in LEP and LEPR May Modify Leptin Levels and Represent Risk Factors for Thyroid Cancer.

Purpose. To understand the role of polymorphisms in the LEP (rs7799039 and rs2167270) and LEPR (rs1137101 and rs1137100) genes in DTC susceptibility and their effect on leptin levels. Methods. We studied 153 patients with DTC and 234 controls through TaqMan SNP Genotyping and ELISA, comparing these data to the clinicopathological data of patients with DTC. Results. Patients with AA genotype of rs7799039 had higher levels of serum leptin (9.22 ± 0.98 ng/mL) than those with AG genotype (10.07 ± 0.60 ng/mL; P = 0.005). Individuals with AG genotype of rs2167270 also produced higher serum leptin levels (10.05 ± 0.59 ng/mL) than the subjects with GG genotype (9.52 ± 0.79 ng/mL; P < 0.05). A multivariate logistic regression adjusted for gender, age, and BMI showed that the AG genotype of rs7799039 was an independent risk for DTC (OR, 11.689; P = 0.0183; 95% CI, 1.516–90.119). Similarly, AG and GG genotypes of rs1137101 increased the susceptibility to DTC (OR, 3.747; P = 0.027; 95% CI, 1.161–12.092 and OR, 5.437; P = 0.013; 95% CI, 1.426–20.729). Conclusions. We demonstrated that rs7799039 and rs2167270 polymorphisms modify the serum leptin concentrations in patients with DTC. Furthermore, polymorphisms rs7799039 and rs1137101 increase the risk of DTC development, although they do not correlate with tumor aggressiveness.

Serum Leptin and Adiponectin Levels in Korean Patients with Psoriasis

Psoriasis is a disorder caused by genetic and immunological factors. Leptin, a peptide hormone secreted predominantly from adipose tissue, regulates energy intake and expenditure, as well as the T-helper response. There have been conflicting reports regarding serum levels of leptin and adiponectin in patients with psoriasis. In the present study, we measured serum levels of leptin and adiponectin in Korean patients with psoriasis. Twenty-four patients with psoriasis and fifteen control subjects were included in the study. Serum leptin and adiponectin levels were determined by an immunometric sandwich enzyme-linked immunosorbent assay (ELISA). The mean serum leptin concentration in patients with psoriasis was higher than in controls, and the difference was statistically significant. In contrast, serum adiponectin levels in patients with psoriasis were significantly decreased compared with healthy controls. Leptin levels in vitamin D-deficient patients were statistically significantly higher than in vitamin D-sufficient patients. Serum adiponectin concentrations showed a negative correlation with body mass index (BMI) and psoriasis area and severity index (PASI) in patients with psoriasis. In conclusion, the present study demonstrated that leptin and adiponectin may play a role in the immunopathogenesis of psoriasis and may be useful biomarkers indicating severity of psoriasis in Korean patients.

Leptin receptor (Ob-R) mRNA expression and serum leptin concentration in patients with colorectal and metastatic colorectal cancer

The objective of the present study was to investigate the effect of leptin on the progression of colorectal carcinoma to metastatic disease by analyzing the serum leptin concentration and Ob-R gene expression in colon cancer tissues. Tissue samples were obtained from 31 patients who underwent surgical resection for colon (18 cases) and metastatic colon (13 cases) cancer. Serum leptin concentration was determined by an enzyme-linked immunosorbent assay (ELISA) and Ob-R mRNA expression by real-time polymerase chain reaction (RT-PCR) for both groups. ELISA data were analyzed by the Student t-test and RT-PCR data were analyzed by the Mann-Whitney U-test. RT-PCR results demonstrated that mRNA expression of Ob-R in human metastatic colorectal cancer was higher than in local colorectal cancer tissues. On the other hand, mean serum leptin concentration was significantly higher in local colorectal cancer patients compared to patients with metastatic colorectal cancer. The results of the present study suggest a role for leptin in the progression of colon cancer to metastatic disease without weight loss. In other words, significantly increased Ob-R mRNA expression and decreased serum leptin concentration in patients with metastatic colon cancer indicate that sensitization to leptin activity may be a major indicator of metastasis to the colon tissue and the determination of leptin concentration and leptin gene expression may be used to aid the diagnosis.

Association between leptin gene promoter methylation and type 2 diabetes mellitus

To assess the association between leptin gene promoter methylation and serum leptin concentrations in patients with impaired glucose regulation (IGR) and type 2 diabetes mellitus (T2DM). Methylation status of leptin gene promoter was determined with methylation-specific polymerase chain reaction. Serum leptin concentrations were determined using enzyme-linked immunosorbent assay. Among three groups of individuals with different levels of glucose, the methylation rates of leptin gene in IGR and T2DM groups were 43.6 % and 31.5 %, respectively, which were significantly lower than that of healthy subjects (59.2%; Chi-square=22.499 and 5.109, respectively, P<0.05). A lower methylation rate was also observed in T2DM group compared with IGR group (Chi-square=3.962, P<0.05). Leptin levels in both T2DM and IGR groups were elevated compared with normoglycemic subjects, but only T2DM group was significantly higher (q=6.81, P<0.01). Linear regression analysis indicated that serum leptin concentrations has increased along with declining of DNA methylation rate (r=-0.95, P<0.01). Lower levels of leptin gene promoter DNA methylation and serum leptin concentrations are associated with the development of diabetes. Measurement of the methylation status of leptin gene promoter and expression can facilitate early intervention of the disease.

Decreased Serum Leptin Concentration in Patients With Chronic Pancreatitis

Previously reported data suggest that serum leptin concentration changes in some acute and chronic inflammatory diseases. The aim of the present study was to assess serum leptin concentration in patients with chronic pancreatitis. Forty-four male patients with chronic pancreatitis and 16 healthy (male) subjects were examined. Fasting blood samples were collected from patients and healthy controls. Serum leptin and insulin concentrations were determined by radioimmunoassay method. Significantly lower serum leptin concentration in patients with chronic pancreatitis than in healthy subjects was found. No significant difference in serum leptin concentration between patients without and with exacerbation of chronic pancreatitis on admission was observed. Moreover, patients with chronic pancreatitis had (a) lower serum insulin concentration, (b) higher serum glucose concentration, and (c) lower body mass index than healthy subjects. The results presented in this article indicate that chronic pancreatitis in humans is associated with the decrease in serum leptin concentration. One can suppose that the decrease in serum insulin concentration, maldigestion, and fat loss all contribute to the decrease of serum leptin concentration in chronic pancreatitis.

Increased Serum Leptin Concentrations in Patients with Chronic Stable Angina Pectoris and ST-Elevated Myocardial Infarction

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 +/-1.34 vs 6.37 +/-1.85 ng/mL, p=0.021 and 8.22 +/-3.13 vs 6.37 +/-1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 +/-5.96 vs 11.40 +/-2.11 micromol/L, p=0.025) and patients with STEMI (15.90 +/-5.02 vs 11.40 +/-2.11 micromol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 +/-1.39 vs 3.45 +/-1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.

Serum leptin concentration in patients after heart transplantation

Leptin is primarily produced by adipocytes but its receptors are expressed in a variety of tissues including the heart. Elevated plasma leptin levels predict acute myocardial infarction and it has been shown as acute phase reactant and a risk factor for coronary heart disease. The present study was undertaken to answer the question whether there exists a relationship or not, between serum leptin levels and grades of acute cellular rejection confirmed by elective endomyocardial biopsies in stable patients after orthotopic heart transplantation. We observed higher serum leptin levels compared with reference values, regardless of histopathologic biopsy findings studied. There was a positive correlation between serum leptin concentrations and body mass index, diastolic blood pressure, total cholesterol and low-density lipoprotein. The elevated leptin levels found in heart transplant recipients could be due to the result of steroid therapy. These results point the need for further studies to explain the leptin role in heart transplant recipients.

Effect of cyproheptadine on serum leptin levels

Leptin is a 167 amino acid protein encoded by the obesity gene that is synthesized in adipose tissue and interacts with receptors in the hypothalamus linked to the regulation of appetite and metabolism. It is known to suppress appetite and increase energy expenditure. Cyproheptadine is a piperidine antihistamine that increases appetite through its antiserotonergic effect on 5-HT2 receptors in the brain. Although both leptin and cyproheptadine are effective in controlling appetite, their interaction has not been addressed in clinical studies. This study evaluated serum leptin concentrations in patients who received cyproheptadine to treat a variety of disorders. Sixteen patients aged 7 to 71 years (mean, 26.25 years) were given cyproheptadine 2 to 6 mg/day for a minimum of 7 days. Body weight was measured and blood samples were obtained at baseline and after 1 week of treatment. Serum leptin levels were determined by leptin radioimmunoassay. The mean body weight at baseline (52.59 kg) did not differ significantly from that at 1 week after treatment (52.84 kg; P > .05), but the mean leptin level after 1 week of treatment with cyproheptadine (3.14 ng/mL) was 14.2% higher than that at baseline (2.75 ng/mL; P < .05). This increase may suggest that both leptin and cyproheptadine may affect appetite via similar receptors and that cyproheptadine does not impair leptin activity through these receptors. Further study will be necessary to clarify this relationship.

Serum leptin concentrations in patients with severe ovarian hyperstimulation syndrome during in vitro fertilization–embryo transfer treatment

To investigate the changes in serum leptin concentration in the conception cycle of severe ovarian hyperstimulation syndrome (OHSS). Prospective longitudinal study of 66 IVF-ET cycles between May 2000 and June 2002. Infertility outpatient clinic at a Japanese medical school. Infertile patients undergoing IVF-ET cycles at the infertility outpatient clinic were divided into three groups consisting of group 1 (conception-cycle patients with severe OHSS, n = 9), and group 2 (conception cycle, non-OHSS, n = 28), and group 3 (nonconception cycle, non-OHSS, n = 29). Blood samples were collected at five different periods. Period I, on the first day of ovarian stimulation with FSH; period II, at hCG administration before oocyte retrieval; period III, 7 days after oocyte retrieval; period IV, 14 days after oocyte retrieval; and period V, 21 days after oocyte retrieval. Serum leptin concentration. The serum leptin concentration was low in the OHSS group compared with that of the non-OHSS groups in all serum samples, with significant levels at periods III (vs. groups 2 and 3; P<.05) and IV (vs. group 3; P<.01). A twofold increase of leptin concentration from period I to period II (P<.05) was observed in all groups. The change pattern in serum leptin concentration might provide a great contribution to the pathophysiology development of OHSS patients during assisted reproductive treatment.

Serum leptin concentration and advanced gastrointestinal cancers: a case controlled study.

BackgroundSerum leptin level is associated with appetite and energy expenditure in healthy individuals. We aimed to evaluate the serum leptin concentration and the other factors which may be associated with weight loss in patients with advanced gastrointestinal cancer.MethodsForty-four patients with advanced gastrointestinal cancer (25 gastric and 19 colorectal cancer) and 25 healthy controls were enrolled. Serum leptin levels were measured as ng/ml via enzyme linked immuno-sorbent assay (ELISA) method in all subjects. The difference in serum leptin concentration between cancer and control group, the factor associated with its serum level and the relationship between serum leptin concentration and weight loss was evaluated.ResultsSerum leptin concentration of cancer group was significantly lower than controls (p = 0.002). Female subjects had significantly higher serum leptin concentration than male subjects in control group (p = 0.01), while not in cancer group (p > 0.05). Serum leptin concentration was significantly related with gender in controls (p = 0.023, β = 0.479), while no gender difference was observed in cancer group (p > 0.05). No relationship was found between serum leptin concentration and weight loss percentage in cancer group in linear regression analysis (p > 0.05). No significant difference was observed in serum leptin concentrations between colon and gastric cancer sub-groups (p > 0.05).ConclusionIndependently from the site of gastrointestinal tract, serum leptin concentration in advanced gastrointestinal cancer is lower than controls and it is not a determinant factor in weight loss. In contrast to healthy subjects, gender does not effect the serum leptin concentration in patients with advanced gastrointestinal cancer.

408 The serum leptin concentration in patients with congestive heart failure

408 The serum leptin concentration in patients with congestive heart failure

Serum leptin concentration is increased in patients with Behçet's syndrome and is correlated with disease activity.

Background Behçet's syndrome is a systemic, relapsing immuno-inflammatory disease with a generalized vasculitis of the microvasculature endothelial dysfunction. Leptin, a recently discovered neuroendocrine hormone, is a metabolic peptide that appears to be involved. Serum proinflammatory cytokines upregulate leptin levels and leptin itself directly induces nitric oxide production from endothelial cells with its specific receptors. To detect changes of serum leptin concentrations in patients with Behçet's syndrome compared with age- and sex-matched healthy volunteers by using enzyme-linked immunosorbent assay. We also investigated whether disease activity or the duration of Behçet's syndrome correlates with leptin concentration. Thirty-five consecutive patients with Behçet's syndrome (41.2 +/- 8.4 years, 16 male, 19 female) and 20 age- and sex-matched healthy control subjects (40.4 +/- 10.91 years, nine male, 11 female) were included in this study. The body mass index (BMI) [weight (kg) height(-1) (m(2))] was calculated for subjects at study enrollment. We measured serum leptin with a leptin enzyme immunoassay kit, and acute-phase reactants, including erythrocyte sedimentation rate, alpha1-antitrypsin, alpha 2-macroglobulin and neutrophil count. The Mann-Whitney U-test was used for statistical analysis and P < 0.05 was considered significant. Values were expressed as mean +/- SD. The gender ratio, age and BMI were not substantially different among Behçet's patients and controls. The mean serum leptin concentrations in patients with Behçet's syndrome (16.8 +/- 7.49 ng mL(-1)) were significantly (P < 0.001) higher than in healthy control volunteers (7.5 +/- 2.77 ng mL(-1)). Active Behçet's patients had significantly (P = 0.001) higher leptin concentrations (20.5 +/- 7.99 ng mL(-1)) when compared with patients in inactive periods (12.8 +/- 4.43 ng mL(-1)). In addition, patients with longer disease duration (mean, 20.1 +/- 5.15 years) had also significantly (P = 0.013) higher leptin concentrations (20.2 +/- 8.52 ng mL(-1)) than those with shorter disease duration (13.4 +/- 4.52 ng mL(-1)) (mean, 7.4 +/- 3.29 years). All acute-phase reaction parameters were found to be significantly (for each, P < 0.01) increased in active disease. Leptin may have a role in modulating endothelial function and may be involved in mechanisms for vessel endothelium repair, during an exacerbation as well as in chronic disease.

Serum leptin concentrations in patients with short-bowel syndrome

Background: Short-bowel syndrome is a state of severe malabsorption resulting from absence or removal of the small bowel for several causes. A number of short-bowel patients develop hyperphagia. Leptin, a protein secreted from adipose tissue, signals the amount of energy stores to the brain. Objective: To study body composition and leptin regulation in short-bowel patients and to determine whether or not leptin concentrations are linked with hyperphagia.Design : We studied 25 short-bowel patients (remnant bowel less than 150 cm) and 31 controls and 10 oral nutrition. Fifteen patients received total parenteral nutrition and 10 oral nutrition. Anthropometric measurements, body composition (by bioelectrical impedance), and cholesterol, triacylglycerol and leptin concentrations were studied in all subjects. Results: There were no differences between short-bowel patients and controls in anthropometric variables, body composition, or leptin concentrations. Leptin concentrations were higher in short-bowel women than men (9.21±8.54 vs. 3.22±1.86 ng/ml,P =0.01). Leptin concentrations correlated positively with age (r=0.4, P=0.045), body mass index (r=0.52, P=0.007), fat mass (r=0.67, P=0.001) and body fat (r=0.68,P =0.0001); there were no correlations with other body composition parameters. We found no correlations between parenteral or oral nutrition and body composition parameters, or between leptin concentrations and the presence of hyperphagia. Logistic regression analysis showed that body fat correctly identified leptin concentrations in 60% of patients.Conclusions : Body composition, leptin concentrations and leptin regulation in patients with short-bowel syndrome are similar to those of controls. Leptin concentrations do not correlate with hyperphagia in short bowel-patients.

Leptin concentration in non-obese and obese children with type 1 diabetes mellitus

Leptin, the product of the ob gene, is an adipocyte-derived hormone that positively correlates with body fat percantage and body mass index (BMI). There are many data which demonstrate a significant relationship between leptin and insulin, but the mechanism underlying the changes of leptin induced by insulin and vice versa remains to be studied in more detail. In this review, we analysed the data on the behaviour of serum leptin levels in non-obese and obese children with type 1 diabetes mellitus. It has been shown that the diminished serum leptin concentrations in patients with newly discovered insulin-dependent diabetes mellitus (IDDM) could be caused by insulin deficiency and/or increased lipolysis. Moreover, while in some studies in diabetic children with good metabolic control the serum leptin levels are similar to those of healthy children, in other studies children with IDDM have leptin levels higher than non diabetic children; it is possible that in some diabetic children intensified insulin therapy could cause chronic hyperinsulinemia with high leptin levels. The mean serum leptin concentrations in the obese diabetic subjects were significantly higher when compared with non-obese diabetics. Obese diabetic patients showed no significant differences in leptin concentrations in comparison to the non diabetic obese group matched by age, sex and BMI. In obese diabetics, during weight loss, independent of the quality of metabolic control, serum leptin concentration declines. The changes of leptin in diabetes seem to be similar to those observed in healthy obese subjects.

Leptin in CAPD patients: serum concentrations and peritoneal loss.

To determine whether serum leptin concentrations in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) are influenced by peritoneal loss of leptin and to compare serum leptin levels of normal subjects with those of patients receiving renal replacement therapy such as haemodialysis (HD), CAPD, or kidney transplantation. Eighty-four individuals were investigated: six females and 14 males on standard CAPD; 13 females and 13 males on chronic HD; 10 female and eight male kidney transplant recipients, and 10 female and 10 male subjects as controls. Morning serum, 8-h and 24-h samples of peritoneal fluid concentrated to 6-20-fold by Centricon 3 (cutoff 3000 daltons), and 24-h urinary concentrations of leptin were measured with commercial RIA (Linco Research, Inc., USA). Venous blood and peritoneal fluid samples of albumin, beta2-microglobulin, glucose, urea, and creatinine were determined by standard laboratory techniques. Serum insulin levels were measured by radioimmunoassay. Patients (men and women) on CAPD and after kidney transplantation exhibited significantly higher serum concentrations of leptin and leptin/BMI ratios than control subjects. These increased values did not reach statistical significance in HD patients. Serum leptin concentrations were correlated very significantly with BMI in all cases (r=0.380, P<0.001). Moreover, in CAPD patients (r=0.630, P<0.007) and in HD patients (r=0.668, P<0.005), but not in kidney transplant recipients or control subjects, significant correlations were observed between serum leptin and insulin concentrations. Residual renal function (RRF) in the range 0-12.8 ml/min and serum beta2-microglobulin levels in the range 7.9-47.1 mg/l did not influence serum leptin levels in CAPD and HD patients. As expected, leptin was detected in the peritoneal fluid of CAPD patients. Twenty-four-hour peritoneal loss (30.95+/-21.05 ng/min) and 24-h peritoneal clearance (0.01+/-0.01 ml/kg/min) of leptin account for only 3.9% of estimated whole-body leptin production rate and 0.7% of leptin clearance from plasma respectively. Twenty-four-hour urinary losses of leptin in CAPD patients were negligible, accounting for 5.6+/-1.8% (range 0.3-15.2%) of total (peritoneal and urinary) loss of this hormone. These findings suggest that serum leptin levels are not affected by continuous peritoneal loss of leptin during CAPD and that insulin resistance and hyperinsulinaemia contribute to elevated serum leptin concentrations in CAPD and HD patients. The aetiology of increased serum leptin levels in kidney transplant recipients is probably different from that in dialysis patients.

Serum Leptin Concentrations in Patients on Hemodialysis

Serum leptin concentrations in normal humans have been reported to correlate with the body mass index (BMI) as well as with the body fat mass. In this study, we measured serum leptin concentrations in 107 patients on hemodialysis, 30 of whom had diabetes mellitus as the cause, and examined the clinical significance. Furthermore, we evaluated the effects of high-flux dialysis membranes on serum leptin levels. Serum leptin concentrations had a linear correlation with BMI as well as with the percentage of body fat in patients on hemodialysis. The serum leptin concentrations showed a positive correlation with the serum concentrations of total cholesterol, low-density lipoprotein cholesterol, and triglyceride, the body weight, the BMI, and the percentage of body fat. The serum leptin levels were not different between the diabetic and the nondiabetic groups. The serum leptin levels in the nondiabetic group were nearly fourfold higher in women than in men. We investigated the differences in the rate of reduction in serum leptin after dialysis with polysulfone membrane dialyzers (PS-N and PS-UW) in comparison with a cellulose membrane dialyzer (AM-SD), and as a result, we found that the polysulfone membrane dialyzers removed serum leptin, while the cellulose membrane dialyzer did not. We conclude that in patients on hemodialysis, the serum leptin concentration is a valuable clinical marker of the body fat content and may also contribute to the evaluation of hyperlipidemia.