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 Leptin resistance: unsolved diagnostic issues

2018 ◽  
Vol 64 (1) ◽  
pp. 62-66
Author(s):  
Daria A. Borodkina ◽  
Olga V. Gruzdeva ◽  
Olga E. Akbasheva ◽  
Ekaterina V. Belik ◽  
Elena I. Palicheva ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Skeletal Muscles ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Fatty Tissue ◽  
Leptin Receptors ◽  
Secretion Regulation ◽  
Tissue Sensitivity

Leptin and its receptors are key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity, insulin resistance, dyslipidemia, etc. Currently, the phenomenon of leptin resistance is explained by a number of mechanisms, including impairment of gene structure, leptin transport through the blood-brain barrier, and leptin receptor signaling. However, it is not known, a decrease in the number of receptors of which area leads to the development of leptin resistance. No relationship has been found between the basal leptin level in obesity and expression of leptin receptors in the skeletal muscles. It is also important to investigate the contribution of fatty tissue of different localization to leptin secretion regulation and activity of its receptors. The term «leptin resistence» reflects a complex pathophysiological phenomenon with broad perspectives for study. In this review, we analyze methods of diagnosing leptin resistance.

scholarly journals Leptin resistance: unsolved diagnostic issues

2018 ◽  
Vol 64 (1) ◽  
pp. 62-66
Author(s):  
Daria A. Borodkina ◽  
Olga V. Gruzdeva ◽  
Olga E. Akbasheva ◽  
Ekaterina V. Belik ◽  
Elena I. Palicheva ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Skeletal Muscles ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Fatty Tissue ◽  
Leptin Receptors ◽  
Secretion Regulation ◽  
Tissue Sensitivity

Leptin and its receptors are key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity, insulin resistance, dyslipidemia, etc. Currently, the phenomenon of leptin resistance is explained by a number of mechanisms, including impairment of gene structure, leptin transport through the blood-brain barrier, and leptin receptor signaling. However, it is not known, a decrease in the number of receptors of which area leads to the development of leptin resistance. No relationship has been found between the basal leptin level in obesity and expression of leptin receptors in the skeletal muscles. It is also important to investigate the contribution of fatty tissue of different localization to leptin secretion regulation and activity of its receptors. The term «leptin resistence» reflects a complex pathophysiological phenomenon with broad perspectives for study. In this review, we analyze methods of diagnosing leptin resistance.

scholarly journals Neonatal leptin treatment programmes leptin hypothalamic resistance and intermediary metabolic parameters in adult rat

2006 ◽  
Vol 95 (4) ◽  
pp. 830-837 ◽  
Author(s):  
Fabiane Pereira Toste ◽  
Egberto Gaspar de Moura ◽  
Patrícia Cristina Lisboa ◽  
Aline Teixeira Fagundes ◽  
Elaine de Oliveira ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Leptin Receptor ◽  
The Body ◽  
Leptin Resistance ◽  
Control Group ◽  
Adult Rats ◽  
Leptin Receptors ◽  
Adult Rat ◽  
Anorectic Effect

We previously showed that neonatal leptin treatment programmes higher body weight and food intake in adult rats. Here we investigate whether leptin treatment during lactation affects the anorectic effect of leptin on adult rats and their hypothalamic leptin receptors (OB-Rb) and whether those changes could have consequences on intermediary metabolism. When the offspring were born, pups were divided into two groups: the Lep group, injected daily with leptin (8μg/100g body weight, subcutaneously) for the first 10d of lactation, and the control group, injected daily with saline. After weaning (day 21), body weight and food intake were monitored until the rats were 150d old. Food intake was higher in the Lep group (approximately 14%, p<0·05) from day 133 onwards, and body weight was higher (approximately 10%, p<0·05) from day 69 onwards, compared with the control group. At 150d of age, the rats were tested for food intake in response to either leptin (05mg/kg body weight intraperitoneally; groups CL and LepL) or saline (groups CSal and LepSal). The CL group showed a decrease in food intake, but no response was observed in the LepL group, suggesting leptin resistance. The Lep group demonstrated a decrease in OB-Rb expression (−40% p<0·05), hyperleptinaemia (+78%, p<0·05), hyperinsulinaemia (+100%, p<0·02), hypertriacylglycerolaemia (+17%, p<0·05) and a higher protein content in the body (+16%, p<0·05) without changes in fat mass and glycaemia. We conclude that neonatal leptin treatment programmes both hyperleptinaemia and hyperinsulinaemia in adulthood, which leads to leptin resistance by reducing the expression of the hypothalamic leptin receptor.

The relationship between BMI, leptin, leptin receptors (LepR) and Foxp3+ Tregs cells in women with asthma

2016 ◽  
Vol 51 (4) ◽  
pp. 277-284
Author(s):  
Łukasz Kraszula ◽  
Makandjou-Ola Eusebio ◽  
Anna Jasińska ◽  
Maciej Kupczyk ◽  
Piotr Kuna ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Leptin Receptor ◽  
Control Group ◽  
Soluble Receptor ◽  
Leptin Receptors ◽  
Global Initiative For Asthma ◽  
Moderate Disease ◽  
Global Initiative ◽  
And Control ◽  
The Relationship

The aim of this study was evaluation whether there is an association between BMI, leptin and its soluble receptor, the expression of FoxP3 in CD4+ pTreg in women with severe asthma. Materials and methods. The study included thirty women with asthma: 17 patients with severe and 13 with mild-moderate disease. The control group comprised of 25 healthy women. Asthma was diagnosed in accordance with the Global Initiative For Asthma guidelines (GINA 2014). The phenotype of CD4+CD25highCD127lowFoxp3+CD152+ cells was evaluated by multicolor flow cytometry. The concentration of leptin and its soluble receptor were determined using an immunoenzymatic method (ELISA). Results. It has been shown significantly increased leptin concentration in the group of women with severe asthma compared with mild-moderate asthma and control group (p <0.05). The concentration of the leptin receptor significantly increased (p <0.05) in women with severe asthma compared with control group. There were no differences in percentage of CD4+FoxP3+ and CD4+CD25highCD127low- FoxP3+CD152+ subsets after leptin stimulation in all tested groups. Conclusions. Our results don’t confirm the direct effect of leptin on the CD4+ pTreg cells and the expression of FoxP3 in these cells, in tested groups.

scholarly journals Suppression of Leptin Receptor Messenger Ribonucleic Acid and Leptin Responsiveness in the Ventromedial Nucleus of the Hypothalamus during Pregnancy in the Rat

Endocrinology ◽  
2005 ◽  
Vol 146 (9) ◽  
pp. 3868-3874 ◽  
Author(s):  
S. R. Ladyman ◽  
D. R. Grattan
Keyword(s):  
Choroid Plexus ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Ventromedial Nucleus ◽  
Mrna Levels ◽  
Pregnant Rats ◽  
Messenger Ribonucleic Acid ◽  
Leptin Receptors ◽  
Receptor Isoforms

Abstract Pregnancy in the rat is a state of leptin resistance associated with impaired leptin signal transduction in the hypothalamus. The aim of this study was to determine whether this leptin-resistant state is mediated by a change in the level of leptin receptors in the hypothalamus. Real-time RT-PCR was used to determine levels of mRNA for the various leptin receptor isoforms in a number of microdissected hypothalamic nuclei and the choroid plexus. To investigate the functional activation of the leptin receptor, immunohistochemistry for phosphorylated signal transducer and activator of transcription 3 (pSTAT3) was examined in the arcuate nucleus and the ventromedial nucleus of the hypothalamus (VMH) of fasted diestrous and d-14 pregnant rats after an intracerebroventricular (i.c.v.) injection of either leptin (4 μg) or vehicle. A significant reduction of Ob-Rb mRNA levels was observed in the VMH during pregnancy compared with the nonpregnant controls. Furthermore, in pregnant rats the number of cells positive for leptin-induced pSTAT3 in the VMH was greatly reduced during pregnancy compared with nonpregnant rats. There were no differences in the level of Ob-Rb mRNA or in the number of leptin-induced pSTAT3-positive cells in the arcuate nucleus of nonpregnant and pregnant rats. These data implicate the VMH as a key hypothalamic site involved in pregnancy-induced leptin resistance. There were also reduced levels of mRNA for Ob-Ra, a proposed leptin transporter molecule, in the choroid plexus on d 7 and 21 of pregnancy. Hence, diminished transport of leptin into the brain may also contribute to pregnancy-induced leptin resistance.

scholarly journals CHARACTERISTICS OF METABOLIC PROCESSES IN THE FORMATION OF MENSTRUAL FUNCTION DISORDERS IN ADOLESCENT GIRLS WITH OBESITY

2021 ◽  
Vol 11 (4(42)) ◽  
pp. 28-33
Author(s):  
A. Borshuliak ◽  
O. Andriets ◽  
A. Andriets ◽  
A. Semeniak
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Body Weight ◽  
Menstrual Cycle ◽  
Body Mass ◽  
Adolescent Girls ◽  
Main Group ◽  
Leptin Resistance ◽  
Control Group ◽  
Menstrual Dysfunction

Іntroduction. Today, a quarter of the population of economically developed countries has a body weight that is 15% larger than the norm. According to various authors, the timely onset of menarche in women with various forms of obesity and reproductive dysfunction is observed in 31% of cases only. Obesity results in insulin resistance, which in its turn results in hyperinsulinemia. The main reason of the connection of insulin resistance with reproductive function disorders consists in the specific influence of insulin on ovaries. Insulin suppresses apoptosis, binding to receptors of various growth factors that promotes long existence of atresizing follicles. In the pathogenesis of the metabolic syndrome, along with the development of hyperinsulinemia and insulin resistance, a significant role belongs to the imbalance of adipocytokines, one of which is adiponectin. The aim is to analyze metabolic processes in the formation of menstrual dysfunction in adolescent girls with obesity to improve diagnostic methods of menstrual disorders. Material and methods. Clinical and laboratory examination of adolescent girls aged 12-18 years was held, among which 79 had obesity and complaints about menstrual dysfunction (the main group); 31 with normal body weight and regular menstrual cycle (the control group). Research methods: general clinical, biochemical (indicators of lipid and carbohydrate metabolism were determined), instrumental (ultrasound), statistical. Results. It was found that 53.3% of the girls from the main group had the beginning of the first menstruation after 14 years, delayed menstruation from 42 days to 6 days, duration 2.1 ± 0.05 days, which was significantly shorter, the volume of 10.2 ± 0.05; 0.4 points (average 1-2 pads per day) was significantly lower (p <0.05). Ultrasound showed uterine hypoplasia in almost every second girl in the main group - 36 (45.46%). Hyperleptinemia and leptin resistance was found in obesity of the first degree 34.8 ± 1.75, in obesity of the second degree 37.15 ± 2.12, in obesity of the third degree 40.64 ± 2.0. It was 14.35 ng / ml in the control group, p<0,01. Hyperleptinemia in the main group was accompanied by hyperinsulinemia in 26% of cases and insulin resistance. The relationship between low values of adiponectin and elevated body mass index in patients of the main group was established, which was confirmed by the results of correlation analysis (adiponectin & body mass index: ρ = -0.74). Analysis of the results revealed a decrease of A/L level in the main group by 4.3 times. Based on our own results, the A/L and HOMA-AD models can be considered more accurate for determining insulin resistance. Conclusions. 1. Changes of the menstrual cycle in overweight girls were found. The association of adipokines secretion disorders is characterized by hyperleptinemia, leptin resistance, decreased Adiponectin / Leptin index and hypoadiponectinemia, which, in combination with insulin resistance, indicates the participation of adipokines in the genesis of oligomenorrhea. The algorithm of adolescents’ treatment with menstrual dysfunction on the background of obesity must include the calculation of Adiponectin/Leptin and HOMA-AD, which will make it possible to avoid overdiagnosis of insulin resistance.

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 Decreased leptin uptake in hypothalamic nuclei with ageing in Wistar rats

2001 ◽  
Vol 171 (1) ◽  
pp. 23-32 ◽  
Author(s):  
C Fernandez-Galaz ◽  
T Fernandez-Agullo ◽  
F Campoy ◽  
C Arribas ◽  
N Gallardo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Leptin Receptor ◽  
Wistar Rat ◽  
Insulin Dependent Diabetes Mellitus ◽  
Lower Amount ◽  
Dependent Diabetes Mellitus ◽  
Aged Rats ◽  
Leptin Receptors ◽  
Peripheral Insulin Resistance ◽  
Hypothalamic Nuclei

Leptin interacts with specific receptors in hypothalamic nuclei and modulates energy balance. Growing evidence has shown the association of obesity and hyperleptinaemia with non-insulin-dependent diabetes mellitus and insulin resistance. The aged Wistar rat shows peripheral insulin resistance in the absence of obesity and alterations of glucose homeostasis. However, it is not known whether, in these animals, the leptin action is altered. Here we studied the effect of ageing on plasma leptin concentration and the ability of hypothalamic nuclei to capture i.c.v.-injected digoxigenin-labelled leptin. Our data indicate that 24-month-old animals are hyperleptinaemic. However, daily food intake was greater in old animals, suggesting that they are leptin resistant. Leptin uptake in the hypothalamus was reduced in old rats. This uptake was a receptor-mediated process as demonstrated by displacement. Leptin accumulation in hypothalamic nuclei was partially colocalized with neuropeptide Y fibres. Immunohistochemical and western blot analyses showed a lower amount of the long form of leptin receptors in the hypothalamus of aged rats. Analysis by RT-PCR also demonstrated a decreased expression of leptin receptor mRNA in old animals. We conclude that the lower leptin uptake may be explained, at least in part, by a decreased amount of receptors in hypothalamic neurones of the aged rats.

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 Role of neonatal hyperleptinaemia on serum adiponectin and suppressor of cytokine signalling-3 expression in young rats

2008 ◽  
Vol 101 (2) ◽  
pp. 250-256 ◽  
Author(s):  
Magna Cottini Fonseca Passos ◽  
Fabiane Pereira Toste ◽  
Sheila Cristina Potente Dutra ◽  
Paula Affonso Trotta ◽  
Fernanda Pereira Toste ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Food Intake ◽  
Leptin Receptor ◽  
Serum Insulin ◽  
Leptin Resistance ◽  
Serum Adiponectin ◽  
Lower Serum ◽  
Serum Adiponectin Concentration

Previously we had shown that neonatal leptin treatment programmes for both hyperleptinaemia and hyperinsulinaemia, which lead to leptin resistance and low expression of the hypothalamic leptin receptor (OB-Rb) of rats aged 150 d. Here we investigated in young post-weaned rats (age 30 d) if leptin treatment during lactation induces leptin and insulin resistance and if those changes are accompanied by changes in the suppressor of cytokine signalling-3 (SOCS-3) expression and serum adiponectin concentration. After delivery, the pups were divided into two groups: (1) a leptin group (Lep) that were injected with leptin daily (8 μg/100 g body weight subcutaneously) for the first 10 d of lactation; (2) a control (C) group, receiving saline. After weaning (day 21), body weight was monitored until the animals were age 30 d. They were tested for food intake in response to either leptin (0·5 mg/kg body weight intraperitoneally) (CL, LepL) or saline (CSal, LepSal) when they were aged 30 d. The CL group showed lower food intake, but no response was observed in the LepL group, suggesting leptin resistance. The Lep group had hyperleptinaemia (five-fold), hyperinsulinaemia (+42·5 %) and lower levels of serum adiponectin ( − 43·2 %). The hypothalamic expression of OB-Rb was lower ( − 22 %) and SOCS-3 was higher (+52·8 %) in the Lep group. We conclude that neonatal leptin treatment programmes for leptin resistance as soon as 30 d and suggests that SOCS-3 appears to be of particular importance in this event. In the Lep group, the lower serum adiponectin levels were accompanied by higher serum insulin, indicating a probable insulin resistance.

Sign in / Sign up

Export Citation Format

Share Document