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PubMed2003

Evidence that the anorexia induced by lipopolysaccharide is mediated by the 5-HT2C receptor.

Rats consistently reduce their food intake following injections of bacterial lipopolysaccharides (LPS). Because inhibition of serotonergic (5-HT) activity by 8-OH-DPAT (5-HT(1A) activation) attenuates LPS-induced anorexia, we conducted a series of studies to examine whether other 5-HT-receptors are involved in the mediation of peripheral LPS-induced anorexia. In all experiments, rats were injected with LPS (100 microg/kg body weight [BW] ip) at lights out (hour 0). Antagonists were administered peripherally at hour 4, shortly after the onset of anorexia, which presumably follows the enhanced cytokine production after LPS. Food intake was then recorded during the subsequent 2 h or longer. 5-HT receptor antagonists cyanopindolol and SB 224289 (5-HT(1B)), ketanserin (5-HT(2A)), RS-102221 (5-HT(2C)), and metoclopramide (5-HT(3)) failed to attenuate LPS-induced anorexia. In contrast, both ritanserin (5-HT(2A/C)-receptor antagonist) (0.5 mg/kg BW) and SB 242084 (5-HT(2C)) (0.3 mg/kg BW) attenuated LPS-induced anorexia at doses that did not alter food intake in non-LPS-treated rats (all P<.01). Our results suggest that at least part of the anorexia following peripheral LPS administration is mediated through an enhanced 5-HT-ergic activity and the 5-HT(2C) receptor.

Adrenergic beta-Antagonists↗
PubMed2003

Evidence for a role of the 5-HT2C receptor in central lipopolysaccharide-, interleukin-1 beta-, and leptin-induced anorexia.

We examined the role of serotonin (5-HT) and the 5-HT(1A) and 5-HT(2C) receptors in the anorectic effects of centrally administered lipopolysaccharide (LPS), interleukin-1 beta (IL-1 beta), and leptin. Food intake was measured in rats after intracerebroventricular (ICV) injections of LPS (20 ng), IL-1 beta (10 ng), or leptin (1 microg) at lights out, followed by intraperitoneal (IP) injections of either the 5-HT(1A) autoreceptor agonist 8-hydroxy-2-(di-n-propylamino)tetraline (8-OH-DPAT) (125 microg/kg) or the 5-HT(2C) receptor antagonist SB 242084 (0.3 mg/kg) at the onset of anorexia. SB 242084 significantly attenuated the food intake reduction caused by all compounds (all P<.01). IP 8-OH-DPAT attenuated ICV IL-1 beta-induced anorexia (P<.01). We also tested the involvement of the median raphe 5-HT(1A) receptors in peripheral LPS- and IL-1 beta-induced anorexia. Rats were injected intraperitoneally with either LPS (100 microg/kg) or IL-1 beta (2 microg/kg) at lights out, and 8-OH-DPAT (4 nmol) was administered directly into the median raphe nucleus at the onset of anorexia. Median raphe injections of 8-OH-DPAT significantly attenuated both IL-1 beta- and LPS-induced anorexia (both P<.01). These results implicate the 5-HT(2C) receptors in the mediation of central LPS-, IL-1 beta-, and leptin-induced anorexia. Our results also suggest that the midbrain raphe nuclei play a role in mediating the anorectic response to peripheral LPS and IL-1 beta.

Animals↗
PubMedDate not supplied

Anorexia in response to acute illness.

Anorexia associated with acute illness remains one of the most common, challenging, and difficult symptoms to treat. Surprisingly, little attention has been devoted to development of interventions to reverse this form of anorexia. Although incomplete, current understanding of the mechanisms responsible for illness-induced anorexia is sufficient to suggest therapeutic approaches. In this article, the major physiologic mechanisms underlying illness-induced anorexia are described. In addition, potential moderating effects of social, psychologic, and environmental factors are discussed. This information was used to develop recommendations for the treatment of anorexia. A majority of these interventions, however, are not research based. Further advances in the treatment of illness-induced anorexia will require greater understanding of the complex, interactive effects of psychologic, environmental, and biologic factors on eating behavior during illness. Therefore, areas requiring continued investigation are also outlined.

Acute Disease↗
PubMed1990

Ocular manifestations and impression cytology of anorexia nervosa.

A prospective age- and sex-controlled study of seven anorexia nervosa patients and seven normal control patients was conducted to determine the ocular manifestations of anorexia nervosa. Slit-lamp examination of the anorexic patients demonstrated a high incidence (4/7) of multiple episcleral capillary aneurysms and subconjunctival hemorrhages. Two of seven anorexia nervosa patients had bilateral superficial punctate keratopathy. Anesthetized Schirmer tear testing demonstrated a significantly (P less than 0.005) reduced mean tear production in the anorexia nervosa group (11.3 mm) compared with the control group (22.4 mm). Masked interpretation of conjunctival impression cytology demonstrated moderate to severe conjunctival squamous metaplasia in the majority of the anorexia nervosa group (5/7) compared to normal conjunctival epithelium in the majority of the control group (5/7). Absence of nyctalopia, Bitot's spots, and xerosis, and lack of conjunctival goblet cell loss indicate that the anorexia nervosa group did not have vitamin A deficiency.

Adult↗
PubMedDate not supplied

Anorexia in the elderly.

Weight loss and anorexia occur commonly in the elderly. While in many cases the anorexia can be attributed to associated disease processes, it does appear that a true anorexia of aging exists. Animal studies have suggested that older rodents have an excessive satiety effect of cholecystokinin and a decreased opioid feeding drive. Other older persons develop anorexia in association with depression. In these subjects, excess corticotropin-releasing factor may be the neurotransmitter involved in the pathogenesis of the anorexia. In Alzheimer's disease, decreases in norepinephrine and neuropeptide Y may be involved in the anorexia seen in the these patients.

Aged↗
PubMed2002

[Determination of insulin, leptin and neuropeptide y by radioimmunoanalysis in patients with morbid obesity and anorexia nervosa after therapeutic intervention].

The present study was conducted in order to analyze the relationship existing between leptin, insulin and neuropeptide Y (NPY) levels in massive weight loss and weight recovery. Twenty-three patients with severe obesity, 23 patients with anorexia nervosa and 28 healthy control subjects were studied. Patients with severe obesity underwent a vertical banded gastroplasty followed by an 800 kcal/day diet during 16 weeks, with evaluation taking place before (Body mass index, BMI, 52,1 8 Kg/m2) and after the drastic weight loss (BMI 39,2 6,2 Kg/m2). Patients with anorexia nervosa were treated with nutritional therapy exclusively during 16 weeks, and they were evaluated in the low weight situation (BMI 15,3 1,7 Kg/m2) and after weight recovery (BMI 18,9 2,8 Kg/m2). Normal subjects had a normal BMI from 20 to 27 (average 21,8 2 Kg/m2). BMI, percentage of body fat, and serum levels of leptin, insulin, and NPY, were determined in each patient and normal subjects. In severe obese patients serum leptin and insulin decreased significantly after drastic weight reduction (leptin: from 48,8 19,2 to 24,3 9,8 ng/ml; insulin: from 26,2 10,8 to 18 6 U/ml). In patients with anorexia nervosa serum leptin mean levels were significantly higher after weight recovery (3,7 1,9 vs 9,2 5,1 ng/ml). In subjects with morbid obesity NPY levels decreased after weight loss below those of control group (43,5 16,1 vs 57,3 12,8 pmol/l). On the other hand, patients with anorexia nervosa had NPY levels superior to those of control group. In subjects with anorexia, NPY levels decreased after weight recovery (69,1 16,7 a 59,1 20,3 pmol/l). In the whole population, Leptin and NPY plasma levels were correlated with body fat percentage. Leptin was positively correlated with BMI and body fat percentage in obese and anorectic subjects after weight loss or recovery, respectively. NPY was inversely correlated with body fat percentage in controls and obese subjects before treatment. These data reveal that the concentration of serum leptin and NPY correlates significantly with the total adiposity in subjects with a wide weight range and caloric intake. Leptin plasma levels are proportional to fat stores in patients with severe obesity and anorexia nervosa after drastic weight loss or recovery, respectively. NPY serum levels are negatively correlated with de total body fat in normal weight subjects and obese patients in their initial weight.

Adult↗
PubMed1996

The role of tumor necrosis factor-alpha in the pathogenesis of anorexia and bulimia nervosa, cancer cachexia and obesity.

In this paper a new immunological model of anorexia and bulimia nervosa will be presented in which the inflammatory cytokines are conceived as the fundamental regulators of body metabolism. This conception differs from the conventional view in which the inflammatory cytokines are perceived primarily as peptide molecules utilized by the immune system to control infection, inflammation and tissue or neuronal damage. Given that the inflammatory cytokines are also fundamental regulators of body metabolism, when they become dysregulated they create physiological chaos which results in the development of a number of autoimmune, metabolic and psychiatric disorders. In this proposed immunological model of anorexia and bulimia nervosa, elevated tumor necrosis factor-alpha features as the primary cause of these conditions. Pathophysiological parallels are drawn between anorexia nervosa and cancer cachexia in terms of the causal role the cytokines, neuropeptides and neurotransmitters play in the manifestation of shared symptoms. These shared symptoms include elevated tumour necrosis factor-alpha, down-regulated interleukin-2 and interleukin-4 and depletion of lean body mass. Furthermore, the following neuropeptides are dysregulated in both anorexia nervosa and cancer cachexia: vasoactive intestinal peptide, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, peptide YY and beta-endorphin. In addition, in anorexia and bulimia nervosa, secretion of the neurotransmitter serotonin is inhibited while norepinephrine is enhanced. It will be argued that the causal interplay between the cytokines, neuropeptides and neurotransmitters initiates a cascade of biochemical events which may result in either anorexia or bulimia nervosa, or cancer cachexia. The extent to which these inflammatory cytokines, neuropeptides and neurotransmitters are causally efficacious in the pathogenesis of other autoimmune disorders, such as diabetes mellitus and rheumatoid arthritis, will also be addressed.

Anorexia Nervosa↗
PubMedDate not supplied

How the immune and nervous systems interact during disease-associated anorexia.

Anorexia is one of the most common symptoms associated with illness and constitutes an adaptive strategy in fighting acute infectious diseases. However, prolonged reduction in food intake and an increase in metabolic rate, as seen in the anorexia-cachexia syndrome, lead to depletion of body fat and protein reserves, thus worsening the organism's condition. Because the central nervous system controls many aspects of food intake, soluble factors known as cytokines that are secreted by immune cells might act on the brain to induce anorexia during disease. This review focuses on the communication pathways from the immune system to the brain that might mediate anorexia during disease. The vagus nerve is a rapid route of communication from the immune system to the brain, as subdiaphragmatic vagotomy attenuates the decrease in food-motivated behavior and c-Fos expression in the central nervous system in response to peripheral administration of the proinflammatory cytokine, interleukin-1beta, or bacterial lipopolysaccharide. At later time points after peripheral lipopolysaccharide administration, interleukin-1 itself acts in the brain to mediate anorexia and is found in the arcuate nucleus of the hypothalamus. The mechanisms by which interleukin-1beta gains access to the brain and the potential role of neuropeptide-Y-containing neurons in the arcuate hypothalamus in mediating anorexia during disease are discussed.

Animals↗
PubMed2003

Lack of effects by tricyclic antidepressant and serotonin inhibitors on anorexia in MCG 101 tumor-bearing mice with eicosanoid-related cachexia.

OBJECTIVES: Anorexia is a major clinical problem in large number of patients with advanced cancer disease. Serotonergic mechanisms are assumed to play a role in the process of feeding behavior during normal and pathologic circumstances, which may also involve cancer anorexia according to previous experimental and clinical studies. METHODS: In the present study, we evaluated the effect of the tricyclic antidepressants desipramine (7.5 mg x kg(-1) x d(-1), intraperitoneal) and imipramine (2 to 5 mg. kg(-1) x d(-1), intraperitoneal) the serotonin synthesis inhibitor para-chlorophenylalanine (300 mg x kg(-1) x d(-1), intraperitoneal), the serotonin receptor 5-HT(2C) antagonist cyproheptadine (5 mg x kg(-1) x d(-1), intraperitoneal) and the selective serotonin reuptake inhibitor citalopram (20 mg x kg(-1) x d(-1), intraperitoneal) on anorexia in MCG-101 tumor-bearing mice, a model with significant anorexia and cachexia sensitive to cyclooxygenase inhibition. Also, MCG 101-bearing mice develop well-recognized alterations in brain tryptophan/serotonin metabolism as increased Trp, 5-HPT, and 5-HIAA during tumor progression. RESULTS: Daily provision of desipramine, imipramine, para-chloropheylalanine, cyproheptadine, and citalopram at doses that cause behavioral and metabolic alterations in normal mice did not alter food intake or body weight in tumor-bearing and healthy control mice. Also, the treatments did not decrease elevated plasma concentrations of interleukin-6 and prostaglandin E(2) in the tumor-bearing mice. CONCLUSIONS: Thus, our results do not support previous observations that serotonin metabolism itself is a major factor behind anorexia in tumor-bearing animals in general. Rather, other mechanisms, such as eicosanoid and nitric oxide-dependent pathways, seem to be more important for induction of anorexia along tumor progression in the present model.

Animals↗
PubMed1996

Cracking the riddle of cancer anorexia.

During tumor growth, anorexia and reduced food intake are among the major causes leading to malnutrition and eventually cachexia, which negatively affect patients' outcome. Consistent evidence from our laboratories in rats and humans indicates a key role for ventromedial hypothalamic (VMH) serotonergic system in the development of cancer anorexia. Thus, we postulated that during cancer, increased plasma tryptophan levels (the precursor of serotonin) lead to increased cerebrospinal fluid tryptophan concentrations and increased VMH serotonin synthesis, which then mediates the occurrence of anorexia. However, recent data strongly suggest that factors other than tryptophan supplied to the central nervous system might be involved in the pathogenesis of reduced food intake during tumor growth. Particularly, a significant role appears to be played by interleukin-1 (IL-1). We recently showed that IL-1 infusion in normal rats causes changes in food intake and its determinants, meal number and meal size, similar to those characterizing cancer anorexia, thus supporting the involvement of this cytokine in the development of anorexia. Interestingly, IL-1 and the VMH serotonergic system appear to be closely linked: peripherally infused IL-1 increases brain tryptophan and serotonin concentrations, while intracerebrally infused IL-1 increases neuronal firing rate and serotonin release. We therefore hypothesize that during tumor growth, increased production/secretion of IL-1 occurs, which facilitates the tryptophan supply to the brain. IL-1 can then also act on the VHM itself, where IL-1 receptors exist, to increase its neuronal activity and serotonin release. In other words, we believe that centrally acting IL-1 increases hypothalamic neuronal firing rate and serotonin release, while peripherally acting IL-1 is critical in supplying the hypothalamus with the precursor, tryptophan, in order to maintain the high rate of serotonin synthesis. Also, additional factors recently proposed as mediators of anorexia (including neuropeptide Y and nitric oxide) appear to be part of the hypothesized pathogenic mechanism.

Animals↗
PubMed1997

Is there a specific trauma precipitating anorexia nervosa?

BACKGROUND: The aims of this study were to explore the role of life events and difficulties in the onset of anorexia nervosa and bulimia nervosa and to find out whether events and difficulties with a specific meaning, i.e. those of a certain sexual nature, are important in the onset of anorexia nervosa. METHODS: Seventy-two patients with anorexia nervosa (AN) and 29 with bulimia nervosa (BN) were assessed with the life events and difficulties schedule (Brown & Harris, 1978), the year before onset was studied. A new dimension to measure specific meaning of life events and difficulties called 'pudicity' was developed. Subjects from two community cohorts were used as comparison groups (Brown & Harris, 1978; Andrews et al. 1990). RESULTS: Anorexic patients, bulimic patients and community controls did not differ in proportion of patients with at least one severe event; however, significantly more AN and BN patients than community controls had experienced a major difficulty. Sixty-seven per cent of anorexics and 76% of bulimia nervosa patients had either a severe event or a marked difficulty during the year before onset. In AN and BN the most common serious life stresses before onset concerned close relationships with family and friends with BN patients being significantly more often than AN patients directly involved in the problem (interpersonal events). Patients with anorexia nervosa had significantly more pudicity events before onset than BN patients or community controls. CONCLUSION: While serious life stresses commonly precede the onset of anorexia nervosa and bulimia nervosa, problems with sexuality seem to be specific in triggering the onset of anorexia nervosa.

Adolescent↗
PubMed1998

Implicit and explicit memory for shape, body weight, and food-related words in patients with anorexia nervosa and nondieting controls.

Twelve patients with anorexia nervosa and 12 control participants watched a series of 64 words. There were 4 word types: anorexia related, positive, negative, and neutral. The last 3 types were anorexia unrelated. Anorexia-related words had the same affective valence as the neutral control words. Next, the participants completed an explicit memory test (cued recall) and an implicit memory test (word stem completion). Results showed a strong explicit memory bias for anorexia-related words for patients with anorexia nervosa but not for nondieting controls. There was no evidence for a similar bias in implicit memory. Results are discussed in the context of cognitive biases in psychopathology.

Adolescent↗
PubMed2003

Bone resorption in anorexia nervosa and rehabilitated patients.

OBJECTIVE: To assess the impact of anorexia nervosa and that of nutritional rehabilitation on bone resorption. DESIGN: Cross-sectional, observational study. SETTING: Rome, Italy SUBJECTS: Twenty-eight female patients affected by anorexia nervosa (AN, BMI or=18.5 kg/m(2)) and 34 age- and sex-matched healthy controls (CO, BMI >or=18.5 kg/m(2)). Among AN patients, 16 were affected by the 'restrictive' (ANr) and 12 by the 'purging' type (ANp) of anorexia nervosa. METHOD: Body weight, height and skeletal diameters were measured on each individual. The skeletal mass (SKM) was predicted from the skeletal diameters of the elbow, wrist, knee and ankle, using the equation of Martin. Twenty-four-hour urinary excretion of pyridinium crosslinks of collagen (pyridinoline (Pyd) and deoxypyridinoline (Dpd)) and creatinine was assessed by reversed-phase HPLC with fluorimetric detection after solid-phase extraction and by the Jaffé-method with deproteinization, respectively. RESULTS: Twenty-four-hour urinary output of Pyd and Dpd was not significantly different between AN and CO when expressed in absolute values, but AN showed higher bone resorption than CO when Pyd and Dpd excretion was adjusted by either creatinine (P<0.0000) or the SKM (P<0.05). Within the AN group, urinary excretion of both cross-links was significantly and consistently higher in ANp compared with ANr (P<0.05). However, these differences disappeared when crosslink output was adjusted either by urinary creatinine or SKM. RE subjects showed no differences in bone resorption with the AN group despite weight gain, being crosslink excretion consistently elevated compared to controls (Pyd: P<0.01 by creatinine and P<0.05 by SKM; Dpd: P<0.01 by creatinine and P<0.05 by SKM). CONCLUSION: Bone resorption is elevated in anorexia nervosa and different strategies for low-weight maintenance do not seem to have a differential impact. Increased bone resorption persists in subjects with past diagnosis of anorexia nervosa despite rehabilitation lasting more than 6 months. This finding indicates that bone mass and turnover should be monitored in anorexia nervosa patients and ex-patients well beyond recovery of normal body mass. Further investigation is warranted to examine the long-term effect of such prolonged increase in bone turnover at a young age.

Adolescent↗
PubMed2007

Brain activation in uremic anorexia.

This article reviews current knowledge about mechanisms responsible for uremic events, especially those that involve the central nervous system (CNS). Anorexia is a frequent complication of the uremic syndrome that contributes to malnutrition in patients on dialysis. Uremic anorexia has been associated with many factors. Traditionally, anorexia in dialysis patients has been regarded as a sign of uremic toxicity; therefore, 2 hypotheses have been proposed: the "middle molecule" and "peak concentration" hypotheses; both of these remain unproved. Recently, our group has proposed the tryptophan-serotonin hypothesis, which is based on a disorder in the amino acid profile that may be acquired when the patient is in uremic status. It is characterized by low concentrations of large neutral and branched chain amino acids in the cerebrospinal fluid. This situation permits a high level of tryptophan transport across the blood-brain barrier and enhances the synthesis of serotonin (the final target responsible for inhibiting appetite). The role of inflammation in the genesis of anorexia-malnutrition is also emphasized. In summary, in the CNS, factors associated with uremic anorexia include high levels within the cerebrospinal fluid of proinflammatory cytokines, leptin, and free tryptophan and serotonin (hyperserotoninergic-like syndrome), along with deficiency of neural nitric oxide (nNO) and disorders in various receptors such as melanocortin receptor-4 (MC4-R). Uremic anorexia is a complex complication associated with malnutrition and high levels of morbidity and mortality. Several uremia-acquired disorders in the CNS such as high cerebrospinal fluid levels of anorexigen substances and disorders in appetite regulator receptors may explain the lack of appetite.

Amino Acids↗
PubMed1998

Serum leptin and body weight in females with anorexia and bulimia nervosa.

In this study we hypothesized that there is a correlation between serum leptin levels and body mass indices within patients with anorexia nervosa or bulimia nervosa during a twelve weeks' course of in-patient treatment. We evaluated leptin levels weekly in female in-patients with anorexia (n = 17) or bulimia nervosa (n = 18). Only patients with anorexia nervosa were therapeutically encouraged to gain weight throughout the treatment episode. For the whole cohort, body mass indices and serum leptin levels were highly correlated upon admission (r = 0.89, p < 0.001). The median intra-individual correlation in the anorexia group was higher than in the bulimia group (0.63 and 0.39, respectively). The intra-individual correlations were higher in those anorexia nervosa patients who showed increments of their body mass index within the observation span. This dynamic aspect is important specifically in patients with anorexia nervosa during therapeutically induced weight gain.

Adolescent↗
PubMed1997

Anorexia of aging: physiologic and pathologic.

Despite the increase in body fat and obesity that occurs with aging, there is a linear decrease in food intake over the life span. This conundrum is explained by decreased physical activity and altered metabolism with aging. Thus, older persons fail to adequately regulate food intake and develop a physiologic anorexia of aging. This physiologic anorexia depends not only on decreased hedonic qualities of feeding with aging (an area that remains controversial) but also on altered hormonal and neurotransmitter regulation of food intake. Findings in older animals and humans have provided clues to the causes of the anorexia of aging. An increase in circulating concentrations of the satiating hormone, cholecystokinin, occurs with aging in humans. In addition, animal studies suggest a decrease in the opioid (dynorphin) feeding drive and possibly in neuropeptide Y and nitric oxide. The physiologic anorexia of aging puts older persons at high risk for developing protein-energy malnutrition when they develop either psychologic or physical disease processes. Despite its high prevalence, however, protein-energy malnutrition in older persons is rarely recognized and even more rarely treated appropriately. Screening tools for the early detection of protein-energy malnutrition in older persons have been developed. Multiple treatable causes of pathologic anorexia have been identified. There is increasing awareness of the importance of depression as a cause of severe weight loss in older persons. Approaches to the management of anorexia and weight loss in older persons are reviewed. Although many drugs exist that can enhance appetite, none of these are ideal for use in older persons currently.

Aged↗
PubMed1988

Biochemical abnormalities of the serum in anorexia nervosa.

Biochemical analyses of sera from 27 patients with anorexia nervosa were performed and compared with those of normal female volunteers and other anorectic groups including patients who had undergone digestive tract surgery and patients with malignancies. There were significant increases in gamma-glutamyltranspeptidase, lactate dehydrogenase, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase, cholesterol, and amylase activity and significant decreases in total serum protein, blood sugar, albumin, globulins, and cholinesterase in anorexia nervosa patients compared with normal control subjects. At discharge, these values slightly improved. Similar alterations were also observed in two other anorectic groups. Compared with anorexia nervosa patients, the two other anorectic groups showed a severe reduction in the albumin level and increase in the globulin level. In two other anorectic groups cholesterol levels were lower, and in the malignancy group cholinesterase level was lower than in the anorexia nervosa patients. In anorexia nervosa patients, biochemical abnormalities in the serum were more frequent in total serum protein (93%), blood sugar (85%), and globulins (78%) than in other serum factors, such as blood urea nitrogen (15%), uric acid (15%), and alkaline phosphatase (7%). These results suggest that detection of biochemical abnormalities in the above-mentioned serum factors in routine analyses would be valuable in making an early diagnosis of anorexia nervosa from various anorectic disorders.

Adolescent↗
PubMed2004

Single nucleotide polymorphisms in the leptin receptor gene: studies in anorexia nervosa.

Anorexia nervosa is an eating disorder of unknown aetiology. There is significant evidence for a genetic component in the pathogenesis of this disorder. A region on chromosome 1 has been identified as a susceptibility locus. The leptin receptor has been mapped to a similar region, further upstream of this susceptibility locus. Leptin and its receptor are known to be important factors in the control and regulation of body weight. Single nucleotide polymorphisms (SNPs) in the leptin receptor are associated with measures of body weight. In the present study, SNPs in the coding region of the leptin receptor were analysed and their possible association with anorexia nervosa was investigated. Two cohorts of young women, 176 Caucasian anorexia nervosa patients and 152 normal Caucasian females, were genotyped for three SNPs in the leptin receptor. There was no significant difference in allele or genotype frequency, for any SNP, between the normal controls and the cohort of anorexia subjects. There were no significant associations with any genotype and body mass index in either the control or anorexic cohorts. When the anorexic cohort was subdivided into restricting and bingeing/purging behaviours, we found no significant association with any genotype. Analysis of haplotypes showed no significant evidence of association with anorexia. In summary, leptin receptor SNPs do not appear to be important factors in the regulation of body weight in young, pre-menopausal women or have any significant association with anorexia nervosa.

Adult↗