pituitrin and Feeding-and-Eating-Disorders

Vasopressin (AVP) and oxytocin (OT) are hypothalamic neuropeptides having distinct peripherally and centrally directed cell populations. While principally responsible for the regulation of osmotic equilibrium, AVP also participates in stress-mediated adrenocorticotropic hormone (ACTH) release, and in consolidation and retrieval of aversively conditioned behaviors. OT is principally known for its role in parturition and lactation, but also has effects opposite of AVP, antagonizing stress-mediated ACTH release and impairing the consolidation and retrieval of aversively conditioned behaviors. Our group has demonstrated novel peripheral osmoregulatory defects in underweight anorexics, coupled with hypersecretion of AVP into the cerebrospinal fluid (CSF). Conversely, a relative reduction of CSF OT is seen in underweight anorexics. Speculatively, these reciprocal changes in neurohypophyseal peptides in the underweight anorexic may enhance the observed neuroendocrine and cognitive abnormalities. In addition, the alterations in CSF OT may occur as a consequence of the abnormal gastrointestinal function present during the acute stages of anorexia nervosa.

Topics: Feeding and Eating Disorders; Humans; Oxytocin; Pituitary Gland, Posterior; Vasopressins

Topics: Adolescent; Adult; Amino Acids; Anemia, Sickle Cell; Blood Cell Count; Chromatography, Gas; Clinical Trials as Topic; Cyanates; Diuresis; Feeding and Eating Disorders; Female; Hemoglobins; Humans; Hydantoins; Injections, Intravenous; Male; Middle Aged; Reticulocytes; Thyrotropin; Time Factors; Valine; Vasopressins

Disturbances of volume-regulating mechanisms have already been implicated in the pathophysiology of eating disorders like anorexia or bulimia nervosa with the peptide hormones vasopressin and atrial natriuretic peptide (ANP) being of special interest. Aim of the present study was to investigate, whether the expression of the corresponding genes was altered and if so, if these changes could be explained by epigenetic mechanisms such as DNA methylation. We analyzed blood samples of 46 women suffering from anorexia (n=22) or bulimia nervosa (n=24) as well as of 30 healthy controls. Peripheral mRNA expression and DNA methylation of the vasopressin and the ANP precursor genes were assessed using real-time PCR. We found significantly lower levels of ANP mRNA in patients with eating disorders. This downregulation was accompanied by a hypermethylation of the ANP gene promoter in the bulimic subgroup. We did not find differences regarding expression or methylation of the vasopressin gene. ANP mRNA expression was inversely associated with impaired impulse regulation. We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders.

Topics: Adolescent; Adult; Atrial Natriuretic Factor; DNA Methylation; Down-Regulation; Epigenesis, Genetic; Feeding and Eating Disorders; Female; Gene Expression Regulation; Humans; Impulsive Behavior; Middle Aged; Promoter Regions, Genetic; RNA, Messenger; Vasopressins

Topics: Adult; Aged; Autopsy; Beer; Blood Urea Nitrogen; Coma; Diarrhea; Electroencephalography; Feeding and Eating Disorders; Female; Hemiplegia; Humans; Hypokalemia; Hyponatremia; Male; Middle Aged; Nutrition Disorders; Sodium; Tremor; Vasopressins; Vomiting; Water Intoxication

Triamcinolone acetonide was administered in excessive dosage to dogs to study the renal mechanism responsible for polyuria which is a clinically undesirable side effect of long term glucocorticoid therapy.Polyuria occurred coincident with a significant increase in urinary solute output. Although continuous administration of triamcinolone acetonide at 0.1 or 0.2 mg/lb/day caused a small but significant increase in creatinine output, the primary mechanism for the polyuria was increased solute excretion. Associated with the polyuria was pronounced hyperphagia and polydipsia. The cause of the hyperphagia was not established. The increase in electrolyte excretion caused by this synthetic steroid was probably compensated for by the hyperphagia. Because all the dogs showed muscle weakness and loss of body condition, it is likely that alteration in protein and amino acid metabolism was responsible for the hyperphagia.

Topics: Animals; Blood Glucose; Creatinine; Diuresis; Dog Diseases; Dogs; Feeding and Eating Disorders; Humans; Kidney; Kidney Function Tests; Muscular Diseases; Polyuria; Potassium; Sodium; Thirst; Time Factors; Triamcinolone Acetonide; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Blood Glucose; Body Height; Body Weight; Brain Neoplasms; Child; Craniopharyngioma; Exercise Test; Feeding and Eating Disorders; Female; Glucose Tolerance Test; Gonadotropins; Growth; Growth Hormone; Humans; Hypothalamus; Insulin; Male; Obesity; Pituitary Neoplasms; Postoperative Complications; Radioimmunoassay; Thirst; Thyrotropin; Vasopressins; Vision Disorders

Topics: Biopsy; Body Temperature; Body Weight; Brain Diseases; Calcium; Child; Child, Preschool; Chlorides; Creatine; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Diet; Diuresis; Feeding and Eating Disorders; Female; Humans; Hydrochlorothiazide; Hypothalamus; Infant; Kidney; Male; Mineralocorticoid Receptor Antagonists; Obesity; Osmolar Concentration; Osmosis; Piperidines; Potassium; Sodium; Urography; Vasopressins