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Obesity is a progressive, chronic disease, which can be caused by long-term miscommunication between organs. It remains challenging to understand how chronic dysfunction in a particular tissue remotely impairs other organs to eventually imbalance organismal energy homeostasis. Here we introduce RNAi Pulse Induction (RiPI) mediated by short hairpin RNA (shRiPI) or double-stranded RNA (dsRiPI) to generate chronic, organ-specific gene knockdown in the adult Drosophila fat tissue. We show that organ-restricted RiPI targeting Stromal interaction molecule (Stim), an essential factor of store-operated calcium entry (SOCE), results in progressive fat accumulation in fly adipose tissue. Chronic SOCE-dependent adipose tissue dysfunction manifests in considerable changes of the fat cell transcriptome profile, and in resistance to the glucagon-like Adipokinetic hormone (Akh) signaling. Remotely, the adipose tissue dysfunction promotes hyperphagia likely via increased secretion of Akh from the neuroendocrine system. Collectively, our study presents a novel in vivo paradigm in the fly, which is widely applicable to model and functionally analyze inter-organ communication processes in chronic diseases.

Bariatric surgery is the most effective treatment to reduce weight permanently which is essential to avoid, to improve or even to cure life-threatening comorbidities. Little is known about changes of the psychological etiology and risk factors.The present study concentrated on psychological variables which are considered to cause or promote obesity. The changes of symptoms were measured by the AD-EVA test inventory. A total of 60 patients (24 male/36 female, age 18-71 years) were tested prior to gastric bypass or gastric banding (body mass index BMI M=44.95, SD=6.91) and postoperatively (BMI M=33.92, SD=7.23).Following surgery the variables addiction (t=11.15, p0.01) and binge eating disorder (t=2.13, p0.05) showed significant changes across all patients and therefore confirmed a positive effect but restrained eating and bulimia remained unmodified after surgery. There were significant differences between the two bariatric methods (p0.01).A precise interdisciplinary evaluation is a prerequisite for deciding between gastric banding and the bypass technique as well as to define the need for preoperative and postoperative psychotherapy.

A 4-year-old, slightly overweight (BMI 18 kg/m2, BMI SDS 1.29 approximately 90.1 (th) percentile) and otherwise healthy girl presented with accelerated linear growth (99.6 (th) percentile) and hyperphagia due to loss of satiety feeling. These findings are consistent with melanocortin-4 receptor ( MC4R) mutations. GENETIC ANALYSIS AND DIAGNOSIS: We found the partially inactivating mutation Arg (165)Trp by direct sequencing of the MC4R coding region. Interestingly, the patient's mother is also heterozygous for this mutation, but lean (BMI 19 kg/m2).Carriers of MC4R mutations develop hyperphagia due to lack of satiety feeling as a result of central dysregulation. The reduction of energy intake and the encouragement of physical activity can be successful to control the body weight.Early diagnosis can promote lifestyle intervention to prevent the development of obesity even in the presence of a genetic predisposition.

Bulimia nervosa is characterized by episodes of compulsive eating of large amounts of food that are followed by measures undertaken to avoid weight gain, and an exaggerated concern about one's figure and weight. Bulimic symptomatology comprises a complex of various interacting components such as poor self-esteem, a negative attitude towards one's own body, eating behavior and current conflicts. Treatment must take account of all of these factors, and involves both internistic and psychotherapeutic elements. The severity of the condition, possible comorbidities, and psychosocial criteria are crucial for deciding whether treatment should be on an ambulatory or an inpatient basis.

Obesity has become the most prevalent nutritional disorder in post-industrialised societies and it is associated with the development of severe and costly complications such as type 2 diabetes mellitus and coronary heart disease or cancer. A large proportion of the risk of obesity is determined by the genetic susceptibility of an individual, but environmental factors conducive for the disorder play an important role in its phenotypic expression. Several candidate genes emerged from studies in animal models of obesity, but human pathophysiology is likely to be more complex. Thus, most cases of human obesity probably result from subtle interactions of susceptibility genes with environmental factors favouring deposition of excess calories as fat. The recent surge of obesity may relate to past evolutionary pressure which favoured selection of mechanisms defending body-weight against caloric restriction rather than against caloric excess. Rapidly developing new techniques in quantitative genetics and growing information from functional genomics will help to understand the interaction of environmental factors with signalling networks that regulate energy metabolism. The role of previously unknown pathways in the aetiology of obesity will be uncovered. The typing of numerous genetic variants will become possible and allow individual risk assessment for obesity and/or its associated disorders. Thus, rational and individually tailored therapies may be developed to combat obesity and its associated disorders.

The progression of alimentary fatty liver to liver cirrhosis is a very rare observation. During the year after surgical extirpation of a suprasellar craniopharyngioma in a seven years old boy developed severe obesity and again six years later at autopsy a complete liver cirrhosis with fatty liver was established. Injury of the ventromedial hypothalamic nuclei and resulting hyperphagia is the reason for the obesity following suprasellar tumours. The pathogenesis of liver cirrhosis following alimentary fatty liver is not completely evident up to now, such a progression is possible--as shown in this case--also in children and within a short period.

According to a German play of words, man, in part, is, what he eats. Balanced nutrition is essential for health and well being; faulty nutrition may cause disease. World-wide, under-nutrition appears to be the most important nutritional problem and may exist in selected groups such as young women and geriatric patients, in Germany as well. Here, however, the most important diet related health problems result from overconsumption of energy or nutrients such as fat, cholesterol, salt and alcohol.

A report is given on a 18 year old girl with a Kleine-Levin-syndrome, which was studied 4 years after beginning in the menarche. At first there were only attacks of nausea and vertigo. One year later the attacks were combined with hypersomnia for several hours. Remarkable was a minimal overirritability of the right vestibular system and a slight hypersensitivity to touch and pain on the whole right side. Worth mentioning is also a disturbed water balance (retention). A disturbance of the hypothalamic regulation is supposed and methylphenidate-hydrochloride (Rilatin) is commanded for treatment.

For the last decade the bulimia syndrome, known since Antiquity, has been observed to be on the increase, predominantly among females, the onset of the disease occurring after puberty. Symptoms, connections with anorexia nervosa, aetiologic and pathogenetic aspects, and therapeutic approaches are being discussed.

In patients suffering from anorexia nervosa (n = 20) a significant correlation was found between pathological DST results and weight loss. In this respect, patients with bulimic symptomatology do not differ from the main anorectic group. In addition, the correlation was unaltered by the length of the disease. These results are interpreted as indicative of secondary regulatory disturbances of the hypothalamic-hypophyseal-adrenal axis, whereas they are inconsistent with a close connection between anorexia nervosa and endogenous depression. As demonstrated by other authors, weight change exerts an influence on DST results in endogenous depression as well.