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Leptin induced obesity in mice – Development of high fat diet-induced obesity and leptin resistance in C57Bl/6J mice

However, a previous study suggests that partial leptin deficiency favors diet-induced obesity and related metabolic disorders in mice, arguing that a lower leptin level may indeed promote diet-induced obesity and its associated metabolic disorders. The mice in the first group were fed with high-fat diet HFF and the mice in the second group were fed with low-fat diet LFF.

Ethan Walker
Monday, April 29, 2019
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  • Visual inspections of these regions suggested that the intensity of cellular P-STAT3 staining was also similar in the two leptin-treated groups.

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  • STAT3 signalling is required for leptin regulation of energy balance but not reproduction. Current address: Myriad Genetic, Inc.

Publication types

After an i. Douglas Braymer. We first mapped leptin-responsive cells in brains from DIO mice using phospho-signal transducer and activator of transcription P-STAT3 immunohistochemistry.

There is no convincing evidence to indicate that mutations in the genes encoding either leptin or its receptor are a part of the aetiology of normal human obesity. We tested whether leptin deficiency or leptin resistance due to a high-fat diet HFD can regulate the potent reproductive neuropeptide kisspeptin. Substances Insulin Leptin. Figure 4. However, LFF mice, after i.

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Diet and experimental procedure Mice were obtained from the Animal Resource Centre Western Mive and were fed standard laboratory chow for the first week to allow them to adjust to the new environment. You have full access to this article via your institution. B Effects of i. Blood samples were obtained by puncturing its right ventricle of the heart and plasma leptin was measured using an RIA kit for mouse leptin Linco Inc. Six mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks. Danielle SimsWilliam J.

Int J Obes 24, obestiy The study contains two major experiments. Peripheral and central effects of exogenous leptin on the cumulative energy intake of mice fed either a high-fat or low-fat diet for 1, 8 and 19 weeks. After 19 weeks of high or low-fat diet, two dosages of i. Download PDF.

Introduction

Disruption of leptin induced obesity in mice signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal ih. This difference sixfold was still evident in OM rats that had been fed the HF and LF diets for 7 d, although at this time, the leptin levels of both OM groups had decreased significantly from those observed at 2 d. This study showed that 0. Weight reducing effects of the plasma protein encoded by the OB gene Science : —

The high-fat diet increased body-weight gain and plasma leptin levels. Recombinant mouse leptin was from Dr. This study showed that 0. Acute cold-induced suppression of ob obese gene expression in white adipose tissue of mice: mediation by the sympathetic system. Each lane represents one animal.

Opentanova I. These data suggest that dietary fat acutely increases serum leptin and that this response is normal in OM rats. Indeed, administration of recombinant leptin to obese, hyperleptinemic subjects failed to decrease body weight and food intake 7. Schemmel R.

Six mice for each group were killed after being fed either high induce low-fat diet for 1, 8, 15 and 19 weeks. In contrast, other hypothalamic and extrahypothalamic sites appear leptin responsive, suggesting a state of selective leptin resistance in the brain of DIO mice. As expected, high-fat feeding and attendant obesity were associated with increased leptin levels Figure 2 c. Shillabeer G. Diet composition. Leptin enters the brain by a saturable system independent of insulin.

Introduction

Briefly, animals were deprived of food overnight. George A. Maness L. Stunkard AJ.

Lonnqvist F. Overweight chart mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks. Endocrinology : — Collins S. This is consistent with direct measurements demonstrating reduced whole-brain uptake in obese rodents Neurobehav Toxicol Teratol 8 : —

Similarly, after an i. One of five series from each animal was analyzed. Paxinos GWatson C Leptin induced obesity in mice rat brain in stereotaxic coordinates. The results demonstrate that in addition to an apparent defect in leptin access to the hypothalamus, a signaling defect also exists upstream of STAT3 activation in leptin-responsive hypothalamic neurons in these DIO mice.

Materials and Methods

Food consumption was estimated by subtracting the leptin induced obesity in mice of food left in the plastic dishes and the amount of food spilled from the initial food weight. Identification and expression cloning of a leptin receptor, OB-R Cell 83 : — After removing faeces and woodshavings from the paper, food spillage was collected and weighed. The hormone leptin modulates a diverse range of biological functions, including energy homeostasis and reproduction. A Body weight in mice fed either a high-fat or low-fat diet for 19 weeks; B Energy intake in mice fed either a high-fat or low-fat diet for 19 weeks.

Introduction of the HF diet increased serum leptin dramatically within 48 h in OM rats, whereas there was no effect in rats fed the LF diet Fig. Kawada T. Zhong Y. We therefore conclude that this analysis is likely an underestimate of the degree of leptin-resistant signaling in the ARC of DIO mice.

New issue alert. Email alerts Article activity alert. York D. The HF diet increased serum leptin significantly by d 2 to levels that were similar in both rat strains. Sipos G. Vitamin mixture AIN As shown in Fig.

MATERIALS AND METHODS

ShihS. Sympathetic activation of leptin via the ventromedial hypothalamus: leptin-induced increase in catecholamine secretion. Fushiki T.

Identification of SOCS-3 as a potential mediator of central leptin resistance. Direct double-labeling studies of brain slices are, ogesity, required to fully determine the chemical nature of all leptin-resistant cells in the ARC of DIO mice. J Biol Chem : — Thus, prolonged high-fat feeding induced profound resistance to peripherally administered leptin as measured by STAT3 signaling in the hypothalamus. Oxford Academic.

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The molecular mechanism for the apparent defect in leptin induced obesity in mice access or transport remains unknown at present. Subject alert. Abstract Objective: Hyperleptinemia per se is sufficient to promote leptin resistance in the obese state. Newman: London pp — We did not detect reduced STAT3 activation by leptin in most brain regions after 4 or 16 wk of DIO, arguing against a global defect in leptin transport. Concannon P.

PelleymounterM. HFD mice had a significantly lfptin caloric intake Fig. Abnormal splicing of the leptin receptor in diabetic mice. Leptin-induced nuclear translocation of STAT3 immunoreactivity in hypothalamic nuclei involved in body weight regulation. Cox N. Further studies will be required to determine whether the protein expression or function of putative leptin transporters at the blood-brain barrier are impaired in DIO.

The mice in the first group were fed mice high-fat diet HFF and the mice in the second group were fed with low-fat diet LFF. A Body weight in mice fed either a high-fat or low-fat diet for 19 weeks; B Energy intake in mice fed either a high-fat or low-fat diet for 19 weeks. CAS Google Scholar. Introduction Obesity is defined as increased adipose mass resulting from a chronic imbalance between energy intake and expenditure. Inhibition of food response to intracerebroventricular injection of leptin is attenuated in rats with diet-induced obesity Diabetes 46 : — Six mice from each group received an i.

Publication types

Rayner D. The HF diet increased serum leptin significantly by d 2 to levels that were similar in both rat strains. Abnormal splicing of the leptin receptor in diabetic mice Nature : — Auwerx J.

However, a previous study suggests that partial leptin deficiency favors diet-induced obesity and related metabolic disorders in mice, arguing that a lower leptin leptin induced obesity in mice may indeed promote diet-induced obesity and its associated metabolic disorders. RESULTS: The results from the first experiment suggested that the development of high fat diet-induced obesity in mice could be divided into early, middle and late stages. Further reading Evaluation of anti-obesity potential of aqueous extract of Achyranthes aspera Linn. However, after an i. Results Experiment 1: measurements of body weight, calorie intake, fat storage and plasma leptin in mice fed a high- or low-fat diet for 1, 8, 15 or 19 weeks A significant increase in body weight gain in mice fed the high-fat diet was evident after only 2 weeks of high-fat feeding, and this trend continued throughout the dietary protocol Figure 1A.

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There is no convincing evidence to indicate that mutations in leptin induced obesity in mice genes encoding either leptin or its receptor are a part of the aetiology of normal human obesity. Serum leptin in obesity is related to gender and body fat topography but dose not predict successful weigh loss Eur J Endocrinol : 61— HFF mice, after an i. Firstly, we fed the mice with a high- or low-fat diet for up to 19 weeks to examine a progressive development of high fat diet-induced obesity. On chow diet, male OBHZ and LepHZ mice showed elevated fat mass and body weight, while their glucose tolerance and insulin sensitivity remained unchanged.

Reprints and Permissions. Evidence against either a premature stop codon or the absence of leptin induced obesity in mice gene mRNA in human obesoty J Clin Invest 95 : — The HFD model was used to determine the effects of diet-induced obesity and central leptin resistance on kisspeptin cell number and gene expression. In mice with normalized levels of estradiol, leptin deficiency markedly reduced kisspeptin gene expression, particularly in the arcuate nucleus ARCand kisspeptin immunoreactive cell numbers in the rostral periventricular region of the third ventricle RP3V. Plasma leptin concentration were significantly elevated in the HFF mice compared with LFF mice when measured at 8, 15 and 19 weeks of feeding Figure 2D. Correspondence to XF Huang. Adipose tissue leptin production and plasma leptin kinetics in humans Diabetes 45 : —

Clinical Phytoscience Blood samples were obtained by puncturing its right ventricle of the heart and plasma leptin was measured using an Leptin induced obesity in mice kit for mouse leptin Linco Inc. Discussion The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. Abnormal splicing of the leptin receptor in diabetic mice Nature : —

Mice were subsequently randomly assigned to obeity leptin induced obesity in mice two groups: a high-fat diet fed group or a low-fat diet fed group. Alphacel nonnutritive bulk Diabetes 52 : — Close mobile search navigation Article Navigation. Firstly, we fed the mice with a high- or low-fat diet for up to 19 weeks to examine a progressive development of high fat diet-induced obesity.

Phenotype of fatty due to GlnPro mutation in the leptin receptor Lepr. Receive exclusive offers and updates from Oxford Academic. The effect of leptin on food intake is mediated in part via leptin receptors present in the hypothalamus. Rayner D.

Fan H. Importantly, a strong reduction of adipose tissue inflammation is observed along with improvements in insulin sensitivity and enhanced glucose tolerance. We did not directly assess leptin resistance by evaluating the effects of leptin administration on food intake and body weight at 4 weeks in the current study. Petro A. However, at this point, the energy intake of HFF mice began to decrease, and by the fifth week of feeding, it had fallen significantly below that of the LFF mice.

  • Cox N. However, most cases of obesity in rodents 6 and humans 7 are associated with high circulating leptin levels; the resistance to leptin that characterizes these states has not yet been explained.

  • You have full access to this article via your institution. Blood samples were obtained by puncturing its right ventricle of the heart and plasma leptin was measured using an RIA kit for mouse leptin Linco Inc.

  • Each guide was fitted with a gauge obdurator that extended 0.

  • Abnormal splicing of the leptin receptor in diabetic mice Nature : —

  • Baum H. Issue Date : 01 May

Clinical Phytoscience This study showed that 0. Download references. However, after an i. Issue Date : 01 May The composition of the respective diets is the same as used previously.

However, there were interesting divergences in the patterns of response of leptin mRNA levels and serum mice concentrations. Download references. Discussion The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. CampfieldL. Sign In or Create an Account. Consistent with these results, immunohistochemical IHC studies demonstrate rapid activation of STAT3 by leptin in hypothalamic and extrahypothalamic brain regions of rats and mice.

  • Rentsch J. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks Science : —

  • Scientific Reports

  • This study again confirmed this observation.

  • Mantzoros C.

  • The composition of the respective diets is the same as used previously. Leptin levels in human and rodent: measurement of plasma leptin and ob mRNA in obese and weight-reduced subjects Nat Med 1 : —

In their studies, they also mice that the mice that became obese consuming the HF diet lost their responsiveness to peripheral leptin. Six mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks. Fat feeding causes widespread in vivo insulin resistance, decreased energy expenditure, and obesity in rats Am J Physiol : E—E D Effects of i.

Six mice from each group received an i. Skip to main content Thank you for visiting nature. After an i. Needle placement was confirmed by visual examination of the lateral ventricle in the tissue sections.

There was no significant difference in tibia bone length between the two groups Figure 2E. Lin, S. Obesity is defined as increased adipose mass resulting from a chronic imbalance between energy intake and expenditure. In the first experiment, 48 mice were used to compare body weight, food intake, fat storage and serum leptin concentration between the mice fed a high and low-fat diet.

Published : 31 May Laboratory Investigation Amount of fat storage in mice fed either a high-fat or low-fat diet for 1, 8, 15 and 19 weeks. From 8 weeks, however, the energy intake of the HFF group began a gradual increase; then, at approximately 15 weeks, it increased dramatically, surpassing that of the LFF mice, and after 19 weeks of feeding, was In the first experiment, 48 mice were used to compare body weight, food intake, fat storage and serum leptin concentration between the mice fed a high and low-fat diet. View author publications.

Article Google Scholar. Lin S, Huang XF. Leptin promotes GnRH function via an indirect action on forebrain neurons. There was no significant difference in tibia bone length between the two groups Figure 2E.

Laboratory Investigation About this article Cite this article Lin, S. Food consumption measurement Food consumption was estimated by subtracting the amount of food left in the plastic dishes and the amount of food spilled from the initial food weight. Reprints and Permissions. Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity J Clin Invest 95 : —

Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks. Bray G. This suggests that leptin resistance may be associated with access of leptin to central sites of action.

Mice were fed using small plastic dishes mice before the beginning of the dark cycle. These data provide evidence that leptin's effects on reproductive function are regulated by kisspeptin neurons in both the ARC and RP3V, although in the latter site the effects are likely to be indirect. Food spillage was determined as follows: any food that spilled was collected on absorbent paper placed beneath the cages in which the mice were kept. CAS Google Scholar. Serum leptin in obesity is related to gender and body fat topography but dose not predict successful weigh loss Eur J Endocrinol : 61—

  • Recent Prog Horm Res 59 : — Forced expression of SOCS-3 in mammalian cells antagonizes proximal leptin signaling, probably by binding to and antagonizing JAK activity

  • Histology of adipose tissue and liver tissue allowed insights into adipose tissue inflammation and hepatic triglyceride content. This is consistent with other work showing that central leptin sensitivity was still intact after 10 weeks of HFF diet.

  • Published June 15, - More info.

On obeesity diet, male OBHZ and LepHZ mice showed elevated fat mass and body weight, while their glucose tolerance and insulin sensitivity remained unchanged. A Body weight in mice fed either a high-fat or low-fat diet for 19 weeks; B Energy intake in mice fed either a high-fat or low-fat diet for 19 weeks. Scientific Reports Lin S, Huang XF. Additionally, partial leptin deficiency protects the mice from fatty liver and liver fibrosis.

Ranganathan S. Email the journal. Mce activation of phosphatidylinositol 3-kinase in the hypothalamic arcuate nucleus: a key mediator of insulin-induced anorexia. Obese gene expression: reduction by fasting and stimulation by insulin and glucose in lean mice, and persistent elevation in acquired diet-induced and genetic yellow agouti obesity. However, there were interesting divergences in the patterns of response of leptin mRNA levels and serum leptin concentrations.

Discussion The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. RESULTS: The results from the first experiment suggested that the development of high fat diet-induced obesity in mice could be divided into early, middle and late stages. Reprints and Permissions. Mice were fed using small plastic dishes just before the beginning of the dark cycle.

Adipose tissue leptin production and plasma leptin kinetics in humans Diabetes 45 : — In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. E Effects of i. ShihS. Importantly, a strong reduction of adipose tissue inflammation is observed along with improvements in insulin sensitivity and enhanced glucose tolerance.

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Leptin induced obesity in mice example, it has been shown that microinjection of small doses of leptin directly into the ARC result in reduced energy intake Food intake and body weight were measured daily after which the rats were given fresh quantities of their individual diets. The alphabet of weight control. Permissions Icon Permissions. Peptides 17

Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Open in new tab Download slide. Although the obese Zucker rat appears to retain some sensitivity to central leptin Cusin et al. View author publications. The apparent discrepancy between this finding and our earlier study where total hypothalamic leptin-dependent signaling was nearly ablated in DIO mice is likely because of the superior sensitivity of the IHC assay compared with the earlier gel-shift assay that was performed using whole hypothalamic extracts. Table 2. Nat Genet 14 : 95 —

Figure 2. By some 4 months of high-fat feeding, the energy intake of the HFF mice increased dramatically, and by 19 weeks their energy obesity mice was jice Food consumption measurement Food consumption was estimated by subtracting the amount of food left in the plastic dishes and the amount of food spilled from the initial food weight. These data provide evidence that leptin's effects on reproductive function are regulated by kisspeptin neurons in both the ARC and RP3V, although in the latter site the effects are likely to be indirect.

After obesit mice were killed at week 1, 8, 15 and 19, adipose tissues epididymal, perirenal and inguinal fat masses and tibial length were measured. The early stage of high leptin induced diet-induced obesity in mice is characterized by relatively normal food intake but elevated body weight and fat gain. Positional cloning of the mouse obese gene and its human homologue Nature : — However, at this point, the energy intake of HFF mice began to decrease, and by the fifth week of feeding, it had fallen significantly below that of the LFF mice. After 8, 15 and 19 weeks feeding, body weight gain of the HFF group was

A Epididymal fat mass; B perirenal fat mass; C inguinal fat mass; D plasma leptin concentration in mice fed a high-fat or low-fat diet for 1, 8, 15 and 19 weeks; E the length of tibia in mice fed either a high-fat or low-fat diet for 1, 8, 15 and 19 weeks. Revised : 08 November JohnstonShayna M. Fushiki T. Congenital leptin deficiency is associated with severe early-onset obesity in humans. The latter data point to downstream signaling defects as possible primary causes of leptin resistance.

Evidence is accumulating to suggest that this pathway is involved in mediating leptin effects on energy intake and body weight. E Effects of i. Accepted : 16 December Download citation. Full size image.

Laboratory Investigation Food spillage was determined as follows: any food that spilled was collected on absorbent paper placed beneath the cages in which the mice were kept. Int J Obes 24, — Diet and experimental procedure Mice were obtained from the Animal Resource Centre Western Australia and were fed standard laboratory chow for the first week to allow them to adjust to the new environment. In support of this hypothesis, leptin resistance has recently been described in a rodent model of obesity that may more closely reflect the human condition, namely, diet-induced obese mice.

O -GlcNAcylation is essential for rapid Pomc expression and cell proliferation in corticotropic tumor cells. However, from d 2 to 7, the amount of LF diet consumed was greater than that of HF diet; thus, there was little difference in energy ingested between the groups. For example, the high levels of leptin in obese mice do not result in suppression of appetite as would be expected in lean mice given the same level of circulating leptin. Address correspondence to: Jeffrey S. The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. Increased expression in adipocytes of ob RNA in mice with lesions of the hypothalamus and with mutations at the db locus.

Download PDF. Discussion The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. Figure 2. The pharmacologic approach to the treatment of obesity J Clin Pharmac 37 : —

However, our data are similar to those of Van Heek et al. This finding was confirmed in an independent experiment with five mice in each group data not shown. J Neurosci 22 : — Six mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks. B, Food intake during wk 12 of diets. Frederich R.

  • Oxford University Press is a department of the University of Oxford.

  • Mice were subsequently randomly assigned to one of two groups: a high-fat diet fed group or a low-fat diet fed group. Upregulation of leptin receptor mRNA expression in obese mouse brain Neuroreport 8 : —

  • Nat Med 10 : —

  • Leptin was administered by either the ip or icv route, after which leptin signaling to activate STAT3 in the hypothalamus was assessed.

STAT3 signalling obesity mice required for leptin regulation of energy balance but not reproduction. About this article Cite this article Lin, S. Rohner-Jeanrenaud F. The recent identification of the leptin-signaling system and the demonstration that defects in either the production of leptin or the response to leptin will cause obesity prompted the current experiments. Objective: Hyperleptinemia per se is sufficient to promote leptin resistance in the obese state.

These data suggest that leptin action in the ARC, but not in other hypothalamic or extrahypothalamic leptin-responsive brain regions, is specifically impaired in DIO mice. Although the specific function s of each nucleus in leptin action is yet largely unknown, injection of small doses of the hormone into the VMH, but not into the ARC, PVN, or DMH, stimulates the sympathetic nervous system Chomczynski P. Alternatively, the different results could relate to the fact that different models were used. Abstract Obesity in humans and in rodents is usually associated with high circulating leptin levels and leptin resistance. J Biol Chem : —

Leptin promotes GnRH function via an indirect action on forebrain neurons. However, LFF mice, after i. Additionally, partial leptin deficiency protects the mice from fatty liver and liver fibrosis. Peripheral and central effects of exogenous leptin on the body weight change of mice fed either a high-fat or low-fat diet for 1, 8, 19 weeks. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • The compositions of these diets are given in Table 1. The composition of the respective diets is the same as used previously.

  • The early stage of high fat diet-induced obesity in mice is characterized by relatively normal food intake but elevated body weight and fat gain. Mice were fed using small plastic dishes just before the beginning of the dark cycle.

  • If such factor s are not easily transported across the BBB this might explain why other brain regions remain leptin sensitive in DIO mice. JohnstonShayna M.

  • Thus, one component of the leptin resistance in mice with 15 weeks of DIO can be attributed to a failure to deliver leptin to its sites of action in the hypothalamus, presumably by a defect in the blood-brain-barrier transport system.

  • Thus, the mechanism underlying what appears to be reduced leptin transport across the blood-brain barrier does not involve reduced expression of the mRNA encoding a putative leptin transporter within the blood-brain barrier.

Although fasting and weight loss reduce leptin gene expression Trayhurn et al. The efficacy of such murine monogenic models of obesity in determining the mechanisms underlying human obesity remains to be seen. Email the journal. Moreover, leptin resistance in brain regions located outside the hypothalamus was not examined. Barone M.

Diabetes 37 : — In the first experiment, 48 mice were used to compare body weight, food indiced, fat storage and serum leptin concentration between the mice fed a high and low-fat broker notes overweight chart. Results Experiment 1: measurements of body weight, calorie intake, fat storage and plasma leptin in mice fed a high- or low-fat diet for 1, 8, 15 or 19 weeks A significant increase in body weight gain in mice fed the high-fat diet was evident after only 2 weeks of high-fat feeding, and this trend continued throughout the dietary protocol Figure 1A. The composition of the respective diets is the same as used previously. These data provide evidence that leptin's effects on reproductive function are regulated by kisspeptin neurons in both the ARC and RP3V, although in the latter site the effects are likely to be indirect.

Show results from All leptih This journal. A Effects of intraperitoneal injection i. Substances Insulin Leptin. Figure 1. The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity. Thus, in an obesogenic environment, maintaining lower leptin levels is highly beneficial for both obesity and diabetes management. Newman: London pp —

Male and female mice were included in the study to account for leptin induced obesity in mice differences. Six mice from each group received an i. However, at this point, the energy intake of HFF mice began to decrease, and by the fifth week of feeding, it had fallen significantly below that of the LFF mice. Experiment 2. Discussion The results presented here show that mice exposed to a high-fat diet for 19 weeks develop obesity and, progressively, peripheral and then central leptin insensitivity.

  • Email alerts Article activity alert. Concannon P.

  • Stunkard AJ. C Effects of intracerebroventricular injection i.

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  • Lin, S.

In the first experiment, 48 mice were used to compare body weight, food intake, fat storage and serum leptin concentration between the mice fed a high and low-fat diet. Advanced Search. Mark R. Neurosci Lett : — The ability of leptin to induce STAT3 signaling was first studied after 4 weeks on the diets. Am J Physiol Endocrinol Metab.

Johnston leptin induced obesity in mice, Shayna M. We tested whether leptin deficiency or leptin resistance due to a high-fat diet HFD can regulate the potent reproductive neuropeptide kisspeptin. After 8, 15 and 19 weeks feeding, body weight gain of the HFF group was Download PDF. Flatt JP. There was no significant difference in tibia bone length between the two groups Figure 2E. The body weight and energy intake were measured every week for the week feeding period.

Download citation. Pratley R. Neuroreport 8 : — The current experiments were designed to explore the possibilities that the susceptibility to HF diet induced obesity was related either to the failure to adequately increase leptin synthesis and secretion or to a diminished sensitivity to the effects of central leptin.

Nat Genet 14 : 95 — The catabolic action of insulin in the brain insuced mediated by mice. Obesity is defined as increased adipose mass resulting from a chronic imbalance between energy intake and expenditure. Membranes were then washed and incubated with secondary antibodies antirabbit-horseradish peroxidase coupled, ,; Bio-Radwashed and developed by enhanced chemiluminescence ECLplus, Amersham, Piscataway, NJ and x-ray films Amersham.

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Diabetes 45 a Visual inspections of these regions suggested that the intensity of cellular P-STAT3 staining was also similar in the two leptin-treated groups. However, all values were significantly greater iduced those of OM rats that were fed the nonpurified diet. Prabakaran D. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Alternatively, because there are clearly neurons in the brain that are protected by the BBB but also have terminal segments located in the ME, it is possible that segments of neurons in the ARC that extend into the ME have specific properties that makes them uniquely sensitive to certain circulating factors. Plasma leptin levels were determined by radioimmunoassay Linco Research Inc.

Role of leptin in neuroendocrine response to fasting Nature : — Serum leptin in obesity obesihy related to gender and body fat topography but dose not predict successful weigh loss Eur J Endocrinol : 61— Consistent with this hypothesis, icv leptin given at a much lower dose than was given intraperitoneally 0. Experiment 1.

Lau D. Guerre-Millo M. Characterization of short isoforms of the leptin receptor in rat cerebral microvessels and of brain uptake of leptin in mouse models of obesity. Six mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks.

  • View author publications.

  • Publication types Research Support, N. Evidence is accumulating to suggest that this pathway is involved in mediating leptin effects on energy intake and body weight.

  • Taken together, the study suggests that abnormalities in postreceptor leptin signaling, specifically in the ARC, may play a role in the pathogenesis of DIO in mice.

  • We hypothesize that factor s present in the circulation of HFD-fed mice may gain access to the ARC via the ME and negatively influence leptin signaling in cells located in this nucleus. Microvessel isolation.

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Revised : 08 November View author publications. Adipose tissue leptin production and plasma leptin kinetics in humans Diabetes 45 : — You are using a browser version with limited support for CSS.

  • Mutations in either the leptin gene or the leptin receptor gene are not a common cause of human obesity Considine et al. Kuhn C.

  • Published : 31 May Chronic leptin reduction represents a viable preventive strategy whose efficacy awaits clinical testing.

  • Rats were killed by decapitation to allow collection of trunk blood and preparation of serum.

  • Mice were fed using small plastic dishes just before the beginning of the dark cycle. Hatch G.

Importantly, a strong reduction of adipose tissue inflammation is observed along with improvements in insulin sensitivity and enhanced glucose tolerance. Neuroreport 8 : — Download references. Abnormal splicing of the leptin receptor in diabetic mice Nature : — Danielle SimsWilliam J. Next we demonstrated that leptin does not signal via signal transducer and activator of transcription 3 or 5, or mammalian target of rapamycin directly on kisspeptin-expressing neurons in the RP3V. Full size image.

The early stage of high fat diet-induced obesity in mice is characterized by relatively normal food intake but elevated body weight and obesit gain. Leptin induced obesity in mice promotes GnRH function via an indirect action on forebrain neurons. Adipose tissue leptin production and plasma leptin kinetics in humans Diabetes 45 : — Evidence is accumulating to suggest that this pathway is involved in mediating leptin effects on energy intake and body weight. Upregulation of leptin receptor mRNA expression in obese mouse brain Neuroreport 8 : — The efficacy of such murine monogenic models of obesity in determining the mechanisms underlying human obesity remains to be seen.

Microvessel isolation was performed as described earlier This study again confirmed this observation. Positional cloning of the mouse obese gene and its human homologue. When mice were 4 weeks of age, they were divided into two groups.

Flatt JP. Male and female mice were included in the study to account for sex-specific differences. Upregulation of leptin receptor mRNA expression in obese mouse brain Neuroreport 8 : — Search Search articles by subject, keyword or author.

  • Statistical analysis.

  • Stunkard AJ. Reprints and Permissions.

  • This is consistent with other work showing that central leptin sensitivity was still intact after 10 weeks of HFF diet.

  • Advanced search. Food spillage was determined as follows: any food that spilled was collected on absorbent paper placed beneath the cages in which the mice were kept.

The pharmacologic approach to the treatment of obesity J Clin Pharmac 37 : — Six mice for each group were killed after being fed either high or low-fat diet for 1, 8, 15 and 19 weeks. Newman: London pp — Clinical Phytoscience Download PDF. However, a previous study suggests that partial leptin deficiency favors diet-induced obesity and related metabolic disorders in mice, arguing that a lower leptin level may indeed promote diet-induced obesity and its associated metabolic disorders. The middle phase is perhaps the most fascinating.

Thirty minutes after icv or ip administration of leptin or buffer, the animals were anesthetized and then decapitated. The compositions of these obeskty are given in Table 1. To explore whether the defective signaling in the ARC seen after 16 wk of DIO might be detectable earlier during development of obesity, therefore supporting a possible primary defect, we measured responses to leptin in mice after 4 wk and 6 d on the HFD. Phone: ; Fax: ; E-mail: jflier caregroup. David A. Select Format Select format.

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