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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human obesity is a manifestation of a positive energy balance. A variety of different factors influence this balance. The varieties of human obesity may be classified as follows: 1. Childhood onset with or without an increased number of adipocytes; 2. The syndromes of neuroendocrine dysfunction including hypothalamic obesity, Cushing's disease, and hyperinsulinism; 3. Dietary obesity; 4. Obesity due to physical inactivity; and 5. Genetic forms of obesity. Among the genetic form of obesity are the Laurence-Moon-Bardet-Biedl syndrome. Alstrom's syndrome, and possibly the Prader-Willi syndrome. Studies in experimental animals have increased our understanding of two of these forms of human obesity. These are: 1. Hypothalamic obesity associated with decreased sympathetic activity, hyperphagia and an increased secretion of insulin. Subdiaphragmatic vagotomy can reverse this syndrome; 2. Genetic forms of obesity inherited as recessive or dominant traits.
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PMID:Human obesity and some of its experimental counterparts. 11 2

In the horse, a syndrome of hirsutism, hyperglycemia, glucosuria, polydipsia, polyuria, polyphagia, and progressive debilitation has been recognized. Most often the syndrome has been associated with adenomas of the pars intermedia of the pituitary and bilateral adrenal hyperplasia or nodular hyperplasia involving primarily the zona fasciculata. Previously, the syndrome has been ascribed to compression of the hypothalamus by an expanding but functionally inactive pituitary neoplasm. In the present case, with RIA determination of plasma ACTH concentrations, the syndrome was ascribed to pituitary ACTH-dependent hyperadrenocorticism and likened to human Cushing's disease.
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PMID:A case of pituitary adrenocorticotropin-dependent Cushing's syndrome in the horse. 22 13

To explore whether possible differences in central nervous system neuromodulators contribute to the differential presentation of affective symptomatology in Cushing's disease and major depression, we examined the levels of immunoreactive CRH and ACTH in the cerebrospinal fluid (CSF) of 11 patients with Cushing's disease, a patient with ectopic ACTH secretion, 34 patients with major depression, and 60 healthy subjects. We elected to measure these peptides not only because both are classically involved in pituitary-adrenal regulation, but also because their primarily arousal-producing and anorexigenic behavioral effects in experimental animals suggest that they may play a role in the symptom complex of depressive syndromes. We also explored whether the CSF levels of these peptides were more helpful in determining the often difficult differential diagnosis between major depression and Cushing's disease than the plasma ACTH response to ovine CRH, a currently used but somewhat insensitive laboratory means of distinguishing these disorders. CSF levels of immunoreactive CRH and ACTH were significantly lower in Cushing's disease patients [21.9 +/- 2.7 and 15.4 +/- 1.8 pg/mL, (mean +/- SEM), respectively] compared to patients with major depression [38.4 +/- 2.3 pg/mL (P less than 0.01) and 24.5 +/- 1.6 pg/mL (P less than 0.01), respectively] and controls [38.4 +/- 1.6 pg/mL (P less than 0.001) and 26.3 +/- 1.1 pg/mL (P less than 0.001), respectively]. The coexistence of high plasma ACTH and low CSF ACTH in Cushing's disease yielded a CSF/plasma ACTH ratio consistently less than that in depressed patients, with only 2 of 31 subjects comprising both groups showing values that overlapped. In contrast, 9 of the combined patients showed ACTH responses to ovine CRH that overlapped. These data suggest that differences in centrally directed CRH secretion may account for the differential presentation of the dysphoric syndromes seen in major depression and Cushing's disease. Hence, the classic form of major depression (melancholia), is often associated with evidence of pathological hyperarousal, such as intense anxiety, sleeplessness, and anorexia, while that of Cushing's disease is associated with evidence of pathological hyperarousal, including hyperphagia, fatigue, and inertia. Moreover, measurement of the CSF/plasma ACTH ratio may serve as a clinically useful adjunct to the ovine CRH stimulation test and other laboratory measures in determining the differential diagnosis between major depression and Cushing's disease.
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PMID:Cerebrospinal fluid immunoreactive corticotropin-releasing hormone and adrenocorticotropin secretion in Cushing's disease and major depression: potential clinical implications. 199 96

CRH has been shown to produce increased locomotion, arousal, and anorexia in experimental animals. A deficiency of CRH in patients with seasonal affective disorder could contribute to the characteristic lethargy, hypersomnia, and hyperphagia characteristic of this illness. To test this hypothesis, we studied basal plasma ACTH and cortisol levels and their responses to ovine CRH in controls and depressed patients with seasonal affective disorder before and after light treatment. Untreated seasonal affective disorder patients showed normal basal plasma cortisol and ACTH levels, but their responses to CRH tended to be delayed and were significantly reduced. When patients were studied after 9 days of light treatment, a significant increase in plasma ACTH and cortisol responses to CRH was observed. Our findings in untreated patients with seasonal affective disorder are similar to those in patients with Cushing's disease 2 weeks after transsphenoidal hypophysectomy, who uniformly show sustained suppression of their CRH neuron because of long-standing hypercortisolism. This findings suggest that the CRH neuron of patients with seasonal affective disorder is hypofunctional. We postulate that the clinical symptomatology in patients with seasonal affective disorder could reflect deficient activity of this important arousal-producing system.
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PMID:Abnormal pituitary-adrenal responses to corticotropin-releasing hormone in patients with seasonal affective disorder: clinical and pathophysiological implications. 185 Nov 85

Genetically obese and hypertensive rats (Obese/SHR) were subjected to sham or bilateral adrenalectomy at 4-5 weeks of age with the onset of hyperphagia. The sham-operated Obese/SHR ate voraciously and by 180 days of age males weighed 700 g and females 590 g. The adrenalectomized Obese/SHR ate much less and weighed 325 and 225 g. The systolic blood pressure of the intact Obese/SHR ranged from 160 to 170 mmHg, whereas the blood pressure of the adrenalectomized animals ranged from 108 to 110 mmHg. The thymi of the intact Obese/SHR were massive compared to those of the adrenalectomized rats. Adrenalectomy effectively reduced the hyperinsulinaemia, adiposity, hyperlipidaemia, hyperglycaemia, and elevated BUN levels of the obese rats. Several obese rats had old or new myocardial infarcts, fatty livers, giant-sized islets of Langerhans, nodular and hyperaemic adrenal glands, narrow zona glomerulosa devoid of lipid, vacuolated inner cortical zones, foci of intimal fibrinohyalin deposits in mesenteric arteries, early glomerulosclerosis, and large, rounded bladder calculi. The adrenalectomized Obese/SHR displayed none of these stigmata. It is suggested that the genetically programmed obesity and hypertension in these SHR are mediated by abnormal activity of the hypothalamic-pituitary-adrenal-gonadal axis, may be likened to Cushing's disease in the human, and is associated with accelerated ageing.
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PMID:Ameliorative effects of adrenalectomy on the hyperphagia, hyperlipidaemia, hyperglycaemia and hypertension of obese, spontaneously hypertensive rats (Obese/SHR). 701 60

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression. Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression. In a series of studies, commencing in patients with Cushing's disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide. In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.
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PMID:Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. 859 44

Human (visceral) obesity is associated with alterations hypothalamus-pituitary-adrenal (HPA) axis functioning. It is however not completely clear whether the HPA axis is causally or co-incidentally related to (visceral) obesity. This review summarizes supporting data of an involvement of the HPA axis in the development of (visceral) obesity. First, several DNA polymorphisms related to HPA axis functioning are correlated to the development of obesity. Second, chronic elevation of circulatory glucocorticoid concentrations, as in Cushing's disease, results in increased abdominal adiposity. Third, (visceral) obesity is associated with a diminished capacity of cortisol to suppress its own secretion. HPA axis functioning might affect energy balance through affecting energy intake. Both CRH and cortisol influence physiological, central mechanisms involved in the regulation of food intake. Still, general activation of the HPA axis has shown to have inconsistent effects on food intake in humans. This inconsistency may partially be explained by gender differences, individual differences in the functioning of the HPA axis, as well as differences in attitude towards eating. In particular, women with high scores on dietary restraint are prone to stress-induced hyperphagia. Dietary restraint scores, in turn, are positively correlated to basal and dexamethasone-suppressed cortisol levels, indicating a complex dual relationship between stress, HPA axis functioning, attitude towards eating and the risk for stress-induced hyperphagia. In the Western society, with chronically high ambient levels of stress and the availability of high caloric foods, this relationship may imply a risk for the development of (visceral) obesity and the metabolic syndrome.
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PMID:The hypothalamic-pituitary-adrenal-axis in the regulation of energy balance. 1827 77

Depressive syndromes are a group of heterogeneous disorders. Atypical depression (AD) with reversed vegetative signs, such as hyperphagia or hypersomnia, is traditionally neglected, demonstrated by the fact that in the most widely used depression scales, such as the Hamilton Depression Scale (HAMD), melancholic symptoms have a specific weight, while, by contrast, reversed vegetative signs are not included. However, epidemiologically and phenomenologically related disorders to AD do exist, such as somatoform disorders, neurasthenia (chronic fatigue syndrome) and fibromyalgia (FM). In this spectrum, here called the AD spectrum, instead a decrease in hypothalamus-pituitary-adrenocortical (HPA) axis activity seems to exist. This has similarities to Cushing's disease, where a suppression of central HPA system activity is accompanied by features of AD and somatization in a considerable number of patients. Opposite vegetative features might therefore be related to the opposite dysregulation of the HPA system. The psychopharmacological intervention in the AD spectrum should therefore differ from that used in typical major depression. MAO inhibitors, low-dose tricyclic antidepressants and 5-HT3 antagonists demonstrated therapeutic efficacy, but the existing studies focused on different aspects. Hypericum extracts might be an alternative pharmacological intervention, which demonstrated therapeutic efficacy in the symptom range of the spectrum.
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PMID:Atypical depression spectrum disorder - neurobiology and treatment. 2698 70