scholarly journals Leptin, soluble leptin receptor, and free leptin index in patients with metabolic syndrome

2017 ◽  
Vol 14 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Elena N. Smirnova ◽  
Sofia G. Shulkina
Keyword(s):  
Metabolic Syndrome ◽  
Leptin Receptor ◽  
Therapy Group ◽  
Objective Evaluation ◽  
Leptin Resistance ◽  
Obesity And Overweight ◽  
Soluble Leptin Receptor ◽  
Average Body Mass ◽  
Group 2 ◽  
Healthy Persons

Aim. To assess the levels of leptin, its soluble receptor, and index of the formation of free leptin in metabolic syndrome (MS). Materials and methods. The study included 110 individuals with obesity and overweight. The group 1 consisted of 70 patients with MS (IDF, 2005), the average body mass index (BMI) 38.4 4.4 kg/m2, aged 48.2 2.4 years, with arterial hypertension (AH) 12 degree, without regular antihypertensive therapy. Group 2 "healthy" obesity accounted for 40 patients aged 38.4 6.2 years, BMI 36.0 5.5 kg/m2 without hypertension and metabolic disorders. Group 3 consisted of 30 healthy persons, BMI 27.1 1.3 kg/m2. All patients were evaluated for insulin, HOMA index, leptin, leptin receptor, leptin free index (calculated as the ratio of leptin (ng/ml) to the leptin receptor (ng/ml), multiplied by 100). Results: In patients with MS as compared to other two groups there were higher levels of HOMA IR index, leptin and free leptin index. Values of leptin receptor in groups 1 and 2 did not differ significantly and were lower than in healthy persons. The free leptin index was significantly higher in MS group relative to the group 2 and 15 times higher than in the healthy individuals. Free leptin index correlated with values of BMI (R = 0.32; p = 0.02), blood pressure (R = 0.3; p = 0.04), uric acid (R = 0.27; p = 0.04), triglycerides (R = 0.42; p = 0.02), index HOMA-IR (R = 0.45; p = 0.02). Conclusions: Reduction of soluble leptin receptor, depending on the degree of abdominal obesity, may cause progression of leptin resistance in patients with MS. The levels of leptin and soluble leptin receptor appears to have dramatical gender differences. Calculation of free leptin index should be used for the objective evaluation of leptin resistance, regardless of gender, degree of obesity, and other metabolic parameters.

scholarly journals Astrocytic leptin-receptor knockout mice show partial rescue of leptin resistance in diet-induced obesity

2013 ◽  
Vol 114 (6) ◽  
pp. 734-741 ◽  
Author(s):  
Bhavaani Jayaram ◽  
Weihong Pan ◽  
Yuping Wang ◽  
Hung Hsuchou ◽  
Aurelien Mace ◽  
...  
Keyword(s):  
Heat Dissipation ◽  
Leptin Receptor ◽  
Uncoupling Protein ◽  
Subcutaneous Fat ◽  
Leptin Resistance ◽  
Blood Concentrations ◽  
Leptin Signaling ◽  
Diet Induced Obesity ◽  
Soluble Leptin Receptor ◽  
Similar Body

To determine how astrocytic leptin signaling regulates the physiological response of mice to diet-induced obesity (DIO), we performed metabolic analyses and hypothalamic leptin signaling assays on astrocytic leptin-receptor knockout (ALKO) mice in which astrocytes lack functional leptin receptor (ObR) signaling. ALKO mice and wild-type (WT) littermate controls were studied at different stages of DIO with measurement of body wt, percent fat, metabolic activity, and biochemical parameters. When fed regular chow, the ALKO mice had similar body wt, percent fat, food intake, heat dissipation, respiratory exchange ratio, and activity as their WT littermates. There was no change in blood concentrations of triglyceride, soluble leptin receptor (sObR), mRNA for leptin and uncoupling protein 1 (UCP1) in adipose tissue, and insulin sensitivity. Unexpectedly, in response to a high-fat diet the ALKO mice had attenuated hyperleptinemia and sObR, a lower level of leptin mRNA in subcutaneous fat, and a paradoxical increase in UCP1 mRNA. Thus, ALKO mice did not show the worsening of obesity that occurs with normal WT mice and the neuronal ObR mutation that results in morbid obesity. The findings are consistent with a competing, counterregulatory model between neuronal and astrocytic leptin signaling.

scholarly journals Soluble Leptin Receptor and Soluble Receptor-Bound Fraction of Leptin in the Metabolic Syndrome

2003 ◽  
Vol 11 (6) ◽  
pp. 760-768 ◽  
Author(s):  
Anton Sandhofer ◽  
Markus Laimer ◽  
Christoph F. Ebenbichler ◽  
Susanne Kaser ◽  
Bernhard Paulweber ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Leptin Receptor ◽  
Soluble Receptor ◽  
The Metabolic Syndrome ◽  
Soluble Leptin Receptor

scholarly journals Decreased soluble leptin receptor levels in women with polycystic ovary syndrome

2006 ◽  
Vol 154 (2) ◽  
pp. 287-294 ◽  
Author(s):  
Susanne Hahn ◽  
Uwe Haselhorst ◽  
Beate Quadbeck ◽  
Susanne Tan ◽  
Rainer Kimmig ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Body Fat ◽  
Leptin Receptor ◽  
Polycystic Ovary ◽  
Biologically Active ◽  
Leptin Resistance ◽  
Ovary Syndrome ◽  
Soluble Leptin Receptor ◽  
Endocrine Parameters

Objective: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and a high incidence of obesity. Leptin, the product of the ob gene, is involved in the regulation of energy balance and obesity and circulates in both free and bound forms. The soluble leptin receptor (sOB-R) is the most important leptin-binding protein, thus influencing the biologically active free leptin level. Design: We assessed the correlation of metabolic and endocrine parameters with leptin and sOB-R levels in 122 PCOS women (aged 27 ± 5.7 years) and 81 healthy controls (aged 25 ± 4.0 years). Methods: Leptin and sOB-R levels were measured using ELISA kits. In addition, anthropometric variables, body fat and endocrine parameters were evaluated and a glucose tolerance test performed to assess indices of insulin resistance and glucose metabolism. Results: In PCOS patients, no correlation was found between leptin or sOB-R and parameters of hyper-androgenism. However, as expected, body mass index (BMI), body fat, waist circumference and indices of insulin resistance were significantly correlated with leptin in PCOS subjects and controls. In a subgroup analysis of lean, overweight and obese PCOS patients, significant differences were found in leptin (29.7 ± 20.7 vs 45.4 ± 25.0 vs 67.7 ± 28.8 ng/ml, P < 0.0001) and sOB-R (8.0 ± 3.4 vs 6.4 ± 2.5 vs 5.7 ± 2.3 ng/ml, P < 0.05). Compared with BMI-matched controls, lean PCOS patients had lower sOB-R levels (8.0 ± 3.4 vs 12.7 ± 4.7 ng/ml, P < 0.0001) and higher free leptin indices (4.5 ± 3.9 vs 2.8 ± 2.2, P = 0.0285). Conclusion: Taking into account that low sOB-R levels supposedly compensate diminished leptin action, PCOS per se might cause leptin resistance.

scholarly journals FRUCTOSE ALTERS THE EXPRESSION OF TYPE B LEPTIN RECEPTOR IN HYPHOTALAMUS AND INTESTINUM OF Rattus Novergicus

2018 ◽  
Vol 2 (2) ◽  
pp. 26
Author(s):  
Ermin Rachmawati ◽  
Risma Aprinda Kristanti ◽  
Nurlaili Susanti
Keyword(s):  
Insulin Resistance ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Intestinal Cell ◽  
Control Group ◽  
Type B ◽  
Leptin Receptors ◽  
Induce Insulin Resistance ◽  
Group 2 ◽  
Levene Test

<p><strong>Background</strong>: Several epidemiological data’s reported significant correlation between fructose consumption and diabetes mellitus type 2 by inducing insulin resistance. Leptin resistance induced by fructose was proposed as one novel mechanism that induce insulin resistance but the exact mechanism remains unclear.  We hypothesize that fructose diminish the type b leptin receptors in hypothalamus and intestine.</p><p><strong>Aim</strong>: This study was aimed to elucidate fructose effect on the expression of leptin receptor type b in hypothalamus and intestine of Rattus novergicus.</p><p><strong>Method</strong>: twenty eight rats were used and divided into 4 groups: Group 1 was control, group 2 was given fructose 10%, group 3 was given fructose 30% and group 4 was given fructose 55% for 2 months. At the end of treatment, the animal were sacrificed and then the hypothalamus and intestine were collected. The expression of type b leptin receptor were measured by immunohistochemistry technique with primary antibody from <em>Bioss antibodies type</em> <em>Leptin receptor polyclonal antibody bs-0109R using </em>Staining kit <em>Skytec Laboratories and DAB chromogen. </em>A positive expression can be seen as a brown colour in cell cytoplasm and counted in 100 cell. The expression then analysed using SPSS 18 with anova one way tes (p&lt;0,05) followed by post hoc test after the data showed normality and homogeneity using Saphiro wilk and Levene test (p&gt;0,05).</p><p><strong>Result</strong>: There was significant differences in type b leptin receptors found in hypothalamus between each group (p&lt;0.05). The significant differences also could be seen in the expression between control and group fructose 30 and 50% in intestinal cell (p&lt;0.05).</p><p><strong>Conclusion</strong>: the consumption of Fructose 55% for 2 months attenuates the expression of type b leptin receptors in hypothalamus and intestine of <em>R</em><em>at novergicus</em>.</p><p> </p>

scholarly journals CB1R regulates soluble leptin receptor levels via CHOP, contributing to hepatic leptin resistance

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Adi Drori ◽  
Asaad Gammal ◽  
Shahar Azar ◽  
Liad Hinden ◽  
Rivka Hadar ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Leptin Resistance ◽  
Dependent Manner ◽  
Molecular Aspect ◽  
Wild Type ◽  
Homologous Protein ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Soluble Leptin Receptor ◽  
Direct Regulation

The soluble isoform of leptin receptor (sOb-R), secreted by the liver, regulates leptin bioavailability and bioactivity. Its reduced levels in diet-induced obesity (DIO) contribute to hyperleptinemia and leptin resistance, effects that are regulated by the endocannabinoid (eCB)/CB1R system. Here we show that pharmacological activation/blockade and genetic overexpression/deletion of hepatic CB1R modulates sOb-R levels and hepatic leptin resistance. Interestingly, peripheral CB1R blockade failed to reverse DIO-induced reduction of sOb-R levels, increased fat mass and dyslipidemia, and hepatic steatosis in mice lacking C/EBP homologous protein (CHOP), whereas direct activation of CB1R in wild-type hepatocytes reduced sOb-R levels in a CHOP-dependent manner. Moreover, CHOP stimulation increased sOb-R expression and release via a direct regulation of its promoter, while CHOP deletion reduced leptin sensitivity. Our findings highlight a novel molecular aspect by which the hepatic eCB/CB1R system is involved in the development of hepatic leptin resistance and in the regulation of sOb-R levels via CHOP.

scholarly journals CB1R Regulates Soluble Leptin Receptor Levels via CHOP, Contributing to Hepatic Leptin Resistance

2020 ◽  
Author(s):  
Adi Drori ◽  
Asaad Gammal ◽  
Shahar Azar ◽  
Liad Hinden ◽  
Rivka Hadar ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Dependent Manner ◽  
Molecular Aspect ◽  
Homologous Protein ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Soluble Leptin Receptor ◽  
Direct Regulation

AbstractThe soluble isoform of leptin receptor (sOb-R), secreted by the liver, regulates leptin bioavailability and bioactivity. Its reduced levels in diet-induced obesity (DIO) contributes to hyperleptinemia and leptin resistance, effects that are known to be regulated by the endocannabinoid (eCB)/CB1R system. Here we show that pharmacological activation/blockade as well as genetic overexpression/deletion of hepatic CB1R modulates sOb-R levels and consequently hepatic leptin resistance. Interestingly, peripheral CB1R blockade failed to reverse DIO-induced reduction of sOb-R levels, fat mass, dyslipidemia, and hepatic steatosis in mice lacking C/EBP homologous protein (CHOP), whereas direct activation of CB1R in hepatocytes reduced sOb-R levels in a CHOP-dependent manner. Moreover, CHOP stimulation increased sOb-R expression and release via a direct regulation of its promoter, while CHOP deletion reduced leptin sensitivity. Our findings highlight a novel molecular aspect by which the hepatic eCB/CB1R system involves in the development of hepatic leptin resistance by regulating sOb-R levels via CHOP.SummaryHere we describe a novel molecular aspect by which the hepatic endocannabinoid/CB1R system contributes to hepatic leptin resistance by regulating soluble leptin receptor levels via CHOP.

scholarly journals Author response: CB1R regulates soluble leptin receptor levels via CHOP, contributing to hepatic leptin resistance

2020 ◽  
Author(s):  
Adi Drori ◽  
Asaad Gammal ◽  
Shahar Azar ◽  
Liad Hinden ◽  
Rivka Hadar ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Author Response ◽  
Leptin Resistance ◽  
Soluble Leptin Receptor

Metabolic syndrome in occupational respiratory diseases

2019 ◽  
pp. 8-13
Author(s):  
Lyudmila P. Kuzmina ◽  
Anastasia G. Khotuleva
Keyword(s):  
Metabolic Syndrome ◽  
Respiratory Diseases ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Fold Increase ◽  
Medical Problem ◽  
Individual Characteristics ◽  
Leptin Resistance ◽  
Study Results ◽  
The Individual

Introduction.Metabolic syndrome (MS) is currently considered as aninterdisciplinary medical problem, which is due to its wide prevalence and interrelation with the development of cardiovascular diseases and type 2 diabetes. It is of interest to study the combination of MS and respiratory diseases due to their common pathogenetic mechanisms.Objectiveis to assess an importance of studying MS in patients with occupational respiratory diseases and a possibility of using laboratory parameters as risk markers for developing occupational respiratory diseases and metabolic syndrome combination.Materials and methods.The results of examination of 257 patients with occupational bronchopulmonary pathology were analyzed. Additional tests in patients with occupational asthma (OA) included levels of serum leptin and polymorphisms of inflammatory process regulation genes (interleukins–4, 6, 10, tumor necrosis factor-α, C-reactive protein (CRP), leptin receptor).Study results and discussion.MS was detected in 58.7% of patients with occupational bronchial asthma (OA), in 44.1% of patients with occupational chronic bronchitis, in 48.6% of patients with occupational COPD, and in 38.7% of patients with pneumoconiosis. MS components appeared to be associated with respiratory function parameters. Role of Gln223Arg polymorphisms of leptin receptor gene and C3872T of CRP gene in development of leptin resistance has been confirmed. Findings are that genotype CC (C174G) of IL–6 gene gets 2.5-fold increase of MS development risk (OR=2.507, 95% CI=1.045–6.017), the presence of three or more cytokine gene polymorphisms 2.4 times increases the need to use systemic steroids to control OA (OR=2.449, 95% CI=1.127–5.324).Conclusion.Measures aimed to prevent the development of metabolic disorders in workers exposed to industrial aerosol are at the same time measures to reduce the risk of developing respiratory diseases and to prevent progression of existing diseases. Using informative laboratory markers can optimize treatment and preventive measures, taking into account the individual characteristics of the organism.

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