Immunology of Eating Disorders

2018 ◽  
pp. 241-250
Author(s):  
Adaliene Versiani Matos Ferreira ◽  
Laís Bhering Martins ◽  
Nayara Mussi Monteze ◽  
Geneviève Marcelin ◽  
Karine Clément
Keyword(s):  
Eating Disorders ◽  
Body Weight ◽  
Anorexia Nervosa ◽  
Immune Cells ◽  
Eating Behaviors ◽  
Viral Infections ◽  
Low Grade ◽  
Obese People ◽  
Obese Subjects ◽  
Low Grade Inflammation

Eating disorders (EDs) are characterized by dysregulation in eating behavior leading to extreme increase or decrease in food intake that, in turn, changes body weight, adiposity, and physical health. Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) are the three major eating disorders. Peculiar immune abnormalities occur in these conditions. Previous studies have reported a higher number of CD4+ T lymphocytes in patients with AN, which are related to a relative resistance to viral infections, even in the presence of leukopenia. It has also been proposed that a cluster of cytokines is altered in these patients. A chronic low-grade inflammation has been observed in obese people with BED and in patients with AN, but with a different profile in each condition. In this context, antagonist drugs of specific cytokines, such as anti-TNF, showed improvement of AN-related symptoms, but increased weight gain in obese subjects. The identification of specific molecules and/or immune cells that impair neuronal circuits implicated in eating behaviors may contribute to the development of pharmacological strategies for eating disorders.

Leptin Functioning in Eating Disorders

CNS Spectrums ◽  
2004 ◽  
Vol 9 (7) ◽  
pp. 523-529 ◽  
Author(s):  
Palmiero Monteleone ◽  
Antonio DiLieto ◽  
Eloisa Castaldo ◽  
Mario Maj
Keyword(s):  
Physical Activity ◽  
Eating Disorders ◽  
Body Weight ◽  
Eating Behaviors ◽  
Clinical Manifestations ◽  
Immune Functions ◽  
Abnormal Eating ◽  
The Brain

AbstractLeptin is an adipocyte-derived hormone, which is involved predominantly in the long-term regulation of body weight and energy balance by acting as a hunger suppressant signal to the brain. Leptin is also involved in the modulation of reproduction, immune function, physical activity, and some endogenous endocrine axes. Since anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by abnormal eating behaviors, dysregulation of endogenous endocrine axes, alterations of reproductive and immune functions, and increased physical activity, extensive research has been carried out in the last decade in order to ascertain a role of this hormone in the pathophysiology of these syndromes. In this article, we review the available data on leptin physiology in patients with eating disorders. These data support the idea that leptin is not directly involved in the etiology of AN or BN. However, malnutrition-induced alterations in its physiology may contribute to the genesis and/or the maintenance of some clinical manifestations of AN and BN and may have an impact on the prognosis of AN.

Association and Familial Coaggregation of Type 1 Diabetes and Eating Disorders: A Register-Based Cohort Study in Denmark and Sweden

2021 ◽  
Author(s):  
Ashley E. Tate ◽  
Shengxin Liu ◽  
Ruyue Zhang ◽  
Zeynep Yilmaz ◽  
Janne T. Larsen ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Type 1 Diabetes ◽  
Anorexia Nervosa ◽  
Eating Disorder ◽  
Eating Behaviors ◽  
Diabetes Diagnosis ◽  
Disordered Eating Behaviors ◽  
Increased Risk ◽  
Clinical Diagnoses

OBJECTIVE <p>To ascertain the association and co-aggregation of eating disorders and childhood-onset type 1 diabetes in families. </p> <p>RESEARCH DESIGN AND METHODS</p> <p>Using population samples from national registers in Sweden (n= 2 517 277) and Demark (n= 1 825 920) we investigated the within-individual association between type 1 diabetes and EDs, and their familial co-aggregation among full siblings, half-siblings, full cousins, and half-cousins. Based on clinical diagnoses we classified eating disorders (EDs) into: any eating disorder (AED), anorexia nervosa and atypical anorexia nervosa (AN), and other eating disorder (OED). Associations were determined with hazard ratios (HR) with confidence intervals (CI) from Cox regressions. </p> <p>RESULTS</p> <pre>Swedish and Danish individuals with a type 1 diabetes diagnosis had a greater risk of receiving an ED diagnosis (HR [95% CI] Sweden: AED 2.02 [1.80 – 2.27], AN 1.63 [1.36 – 1.96], OED 2.34 [2.07 – 2.63]; Denmark: AED 2.19 [1.84 – 2.61], AN 1.78 [1.36 – 2.33], OED 2.65 [2.20 – 3.21]). We also meta-analyzed the results: AED 2.07 [1.88 – 2.28], AN 1.68 [1.44 – 1.95], OED 2.44 [2.17 – 2.72]. There was an increased risk of receiving an ED diagnosis in full siblings in the Swedish cohort (AED 1.25 [1.07 – 1.46], AN 1.28 [1.04 – 1.57], OED 1.28 [1.07 – 1.52]), these results were non-significant in the Danish cohort.</pre> <p>CONCLUSION</p> <p>Patients with 1 diabetes are at a higher risk of subsequent EDs; however, there is conflicting support for the relationship between having a sibling with type 1 diabetes and ED diagnosis. Diabetes healthcare teams should be vigilant for disordered eating behaviors in children and adolescents with type 1 diabetes. </p>

scholarly journals Dietary Fiber's Effect on High Sensitivity C-reactive Protein Serum in Sedentary Workers

2021 ◽  
Vol 5 (1) ◽  
pp. 40
Author(s):  
Livia Kurniati Saputra ◽  
Dian Novita Chandra ◽  
Ninik Mudjihartini
Keyword(s):  
Body Weight ◽  
High Sensitivity ◽  
The Body ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Dietary Fiber Intake ◽  
Anti Inflammatory ◽  
Low Grade Inflammation ◽  
Inflammatory Effect

Low grade inflammation has been recognized of being involved in the pathogenesis of chronic disease pandemic. Individual lifestyle plays a major role in the development of low grade inflammation. Sedentary workers are at risk of low grade inflammation due to the nature of their work. Dietary habit also contributes to inflammatory status in the body. Dietary fiber intake indirectly affects the immune system. It has been hypothesized that fiber has anti-inflammatory effects, both body weight-related and body weight-unrelated This review will focus more on body weight-unrelated anti-inflammatory effect of fiber, especially through fiber’s fermentation metabolites, the short chain fatty acid (SCFA). Its anti-inflammatory effect can be seen by monitoring a biomarker of inflammation in the body, the high sensitivity C-reactive protein (hsCRP). This review’s objective is to cover the mechanisms and role of dietary fiber intake on serum hsCRP level as a marker of low grade inflammation on sedentary workers. 

scholarly journals Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects

2011 ◽  
Vol 165 (4) ◽  
pp. 639-645 ◽  
Author(s):  
Francisco J Ortega ◽  
José M Moreno-Navarrete ◽  
Mónica Sabater ◽  
Wifredo Ricart ◽  
Gema Frühbeck ◽  
...  
Keyword(s):  
Weight Loss ◽  
Glucose Tolerance ◽  
Acute Phase ◽  
Low Grade ◽  
Complement Factor ◽  
Acute Phase Reactants ◽  
Cross Sectional ◽  
Altered Glucose ◽  
Obese Subjects ◽  
Low Grade Inflammation

BackgroundAcute phase mediators promote metabolic changes by modifying circulating hormones. However, there is virtually no data about the link between glucagon and inflammatory parameters in obesity-related chronic low-grade inflammation.Study designWe performed both cross-sectional and longitudinal (diet-induced weight loss) studies.MethodsCirculating glucagon concentrations (ELISA), parameters of glucose and lipid metabolism, interleukin 6 (IL6), and complement factor B (CFB) were analyzed in 316 subjects (250 men and 66 women). The effects of weight loss were investigated in an independent cohort of 20 subjects.ResultsCirculating glucagon significantly correlated with glucose (r=0.407,P<0.0001), HbAlc (r=0.426,P<0.0001), fasting triglycerides (r=0.356,P=0.001), and parameters of innate immune response system such as IL6 (r=0.342,P=0.050) and CFB (r=0.404,P=0.002) in obese subjects with altered glucose tolerance, but not in individuals with normal glucose tolerance (NGT). In obese and NGT subjects, glucagon was associated with fasting triglycerides (r=0.475,P=0.003) and CFB (r=0.624,P=0.001). In obese subjects, glucagon (P=0.019) and CFB (P=0.002) independently contributed to 26% of fasting triglyceride variance (P<0.0001) after controlling for the effects of age and fasting serum glucose concentration in multiple lineal regression models. Moreover, concomitant with fat mass, fasting triglycerides, and CFB, weight loss led to significantly decreased circulating glucagon (−23.1%,P=0.004).ConclusionsAccording to the current results, acute phase reactants such as IL6 and CFB are associated with fasting glucagon in metabolically compromised subjects. This suggests that glucagon may be behind the association between inflammatory and metabolic parameters in obesity-associated chronic low-grade inflammation.

Eating Disorders

2017 ◽  
pp. 179-186
Author(s):  
Myrna M. Weissman ◽  
John C. Markowitz ◽  
Gerald L. Klerman
Keyword(s):  
Eating Disorders ◽  
Anorexia Nervosa ◽  
Eating Disorder ◽  
Bulimia Nervosa ◽  
Binge Eating ◽  
Binge Eating Disorder ◽  
Eating Behaviors ◽  
Negative Mood ◽  
Few Data ◽  
Maladaptive Eating

This chapter provides an overview of the use of IPT for patients with eating disorders. The most common eating disorders are anorexia nervosa, bulimia nervosa, and binge eating disorder. The chapter discusses the adaptations of IPT that have been used for the treatment of eating disorders and evaluates their performance in research studies. The assumption for testing IPT with eating disorders is that they occur in response to distress at poor social and interpersonal functioning and consequent negative mood, to which the patient responds with maladaptive eating behaviors. For anorexia nervosa, few data provide evidence for the benefit of IPT. For bulimia and binge eating disorder, however, IPT is considered a viable option for treatment and is recommended in numerous guidelines. A case example of a woman with bulimia nervosa is provided.

scholarly journals Adiponectin as Link Factor between Adipose Tissue and Cancer

2019 ◽  
Vol 20 (4) ◽  
pp. 839 ◽  
Author(s):  
Erika Di Zazzo ◽  
Rita Polito ◽  
Silvia Bartollino ◽  
Ersilia Nigro ◽  
Carola Porcile ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Active Role ◽  
Low Grade ◽  
Poor Clinical Outcome ◽  
Different Types ◽  
Obesity And Cancer ◽  
Low Grade Inflammation ◽  
Circulating Levels ◽  
Proliferation And Invasion

Adipose tissue is a key regulator of energy balance playing an active role in lipid storage as well as in synthesizing several hormones directly involved in the pathogenesis of obesity. Obesity represents a peculiar risk factor for a growing list of cancers and is frequently associated to poor clinical outcome. The mechanism linking obesity and cancer is not completely understood, but, amongst the major players, there are both chronic low-grade inflammation and deregulation of adipokines secretion. In obesity, the adipose tissue is pervaded by an abnormal number of immune cells that create an inflammatory environment supporting tumor cell proliferation and invasion. Adiponectin (APN), the most abundant adipokine, shows anti-inflammatory, anti-proliferative and pro-apoptotic properties. Circulating levels of APN are drastically decreased in obesity, suggesting that APN may represent the link factor between obesity and cancer risk. The present review describes the recent advances on the involvement of APN and its receptors in the etiology of different types of cancer.

scholarly journals Aerobic training reduces immune cell recruitment and cytokine levels in adipose tissue in obese mice

2019 ◽  
Vol 44 (5) ◽  
pp. 512-520 ◽  
Author(s):  
Débora Romualdo Lacerda ◽  
Michele Macedo Moraes ◽  
Albená Nunes-Silva ◽  
Kátia Anunciação Costa ◽  
Débora Fernandes Rodrigues ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Aerobic Training ◽  
Immune Cell ◽  
Control Diet ◽  
Moderate Intensity ◽  
Low Grade ◽  
Carbohydrate Diet ◽  
Cytokine Levels ◽  
Low Grade Inflammation

Obesity is associated with an energy imbalance that results from excessive energy intake, low diet quality, and a sedentary lifestyle. The increased consumption of a high-refined carbohydrate (HC) diet is strongly related to higher adiposity and low-grade inflammation. Aerobic training is a well-known nonpharmacological intervention to treat obesity and metabolic disturbances. However, the mechanisms through which aerobic training ameliorates the low-grade inflammation induced by an HC diet should be further investigated. Our hypothesis herein was that aerobic training would decrease the recruitment of leukocytes in adipose tissue, thereby reducing the levels of cytokines and improving metabolism in mice fed an HC diet. Male Balb/c mice were assigned to the following groups: control diet/nontrained (C-NT), control diet/trained (C-T), high-refined carbohydrate diet/nontrained (HC-NT), and high-refined carbohydrate diet/trained (HC-T). Mice were submitted to moderate-intensity training sessions that consisted of running 60 min per day for 8 weeks. An intravital microscopy technique was performed in vivo in anesthetized mice to visualize the microvasculature of the adipose tissue. The HC diet induced obesity and increased the influx of immune cells into the adipose tissue. In contrast, HC-T mice presented a lower adiposity and adipocyte area. Furthermore, relative to HC-NT mice, HC-T mice showed increased resting energy expenditure, decreased recruitment of immune cells in the adipose tissue, reduced cytokine levels, and ameliorated hyperglycemia and fatty liver deposition. Collectively, our data enhance understanding about the anti-inflammatory effect of aerobic training and shed light on the adipose tissue-mediated mechanisms by which training promotes a healthier metabolic profile.

scholarly journals Whole grain-rich diet reduces body weight and systemic low-grade inflammation without inducing major changes of the gut microbiome: a randomised cross-over trial

Gut ◽  
2017 ◽  
Vol 68 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Henrik Munch Roager ◽  
Josef K Vogt ◽  
Mette Kristensen ◽  
Lea Benedicte S Hansen ◽  
Sabine Ibrügger ◽  
...  
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Gut Microbiome ◽  
Inflammatory Markers ◽  
Dietary Intervention ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Whole Grain ◽  
Intestinal Transit Time ◽  
Low Grade Inflammation

ObjectiveTo investigate whether a whole grain diet alters the gut microbiome and insulin sensitivity, as well as biomarkers of metabolic health and gut functionality.Design60 Danish adults at risk of developing metabolic syndrome were included in a randomised cross-over trial with two 8-week dietary intervention periods comprising whole grain diet and refined grain diet, separated by a washout period of ≥6 weeks. The response to the interventions on the gut microbiome composition and insulin sensitivity as well on measures of glucose and lipid metabolism, gut functionality, inflammatory markers, anthropometry and urine metabolomics were assessed.Results50 participants completed both periods with a whole grain intake of 179±50 g/day and 13±10 g/day in the whole grain and refined grain period, respectively. Compliance was confirmed by a difference in plasma alkylresorcinols (p<0.0001). Compared with refined grain, whole grain did not significantly alter glucose homeostasis and did not induce major changes in the faecal microbiome. Also, breath hydrogen levels, plasma short-chain fatty acids, intestinal integrity and intestinal transit time were not affected. The whole grain diet did, however, compared with the refined grain diet, decrease body weight (p<0.0001), serum inflammatory markers, interleukin (IL)-6 (p=0.009) and C-reactive protein (p=0.003). The reduction in body weight was consistent with a reduction in energy intake, and IL-6 reduction was associated with the amount of whole grain consumed, in particular with intake of rye.ConclusionCompared with refined grain diet, whole grain diet did not alter insulin sensitivity and gut microbiome but reduced body weight and systemic low-grade inflammation.Trial registration numberNCT01731366; Results.

Sign in / Sign up

Export Citation Format

Share Document