Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropeptide Y (NPY), acting through various medial hypothalamic nuclei, is found to have potent effects on a variety of endocrine, physiological and behavioral systems that modulate energy balance. This peptide affects the release of various hormones, such as corticosterone, insulin, aldosterone and vasopressin, which modulate energy metabolism, as well as food intake. It also has direct impact on energy metabolism through an effect on substrate utilization and lipogenesis. Finally, NPY has a remarkably potent stimulatory effect on feeding behavior, which is characterized by a selective increase in carbohydrate ingestion that is strongest at the beginning of the active feeding cycle and is dependent upon circulating levels of corticosterone. This evidence has led to the proposal that NPY exerts anabolic effects to restore energy balance at specific times of energy depletion. Increased NPY activity may occur at the beginning of the active cycle or after a period of food deprivation. Further evidence, that chronic NPY stimulation produces profound hyperphagia and obesity and that endogenous NPY concentration is increased in genetically obese animals, strongly suggests that hypothalamic NPY may contribute to the development of eating disorders and obesity.
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PMID:Brain neuropeptide Y: an integrator of endocrine, metabolic and behavioral processes. 195 27

We studied a patient with lung cancer, who exhibited severe systemic derangements of metabolism causing cachexia preceding the appearance of a large bulky tumor. The data described herein left no doubt that lung cancer growing in the patient acted as a powerful hypoglycemic factor, setting in motion widespread metabolic disorders. Inappropriate secretion of insulin may be involved in the manifestation of hypoglycemia. However, no ectopic secretion of insulin, glucagon, ACTH and aldosterone appeared to be associated with the carcinoma in the patient. From the present and previous observations, it is stressed that progressive energy loss from the patient occurs by virtue of a combination of severe anorexia and the establishment of a systemic energy-losing cycle dependent on an interplay of glycolysis in the cancer cells and stimulated gluconeogenesis in the host tissues, which in turn results in derangements of protein, lipid and electrolyte metabolism. Attempts to ameliorate the patient's distress and counterbalance the effect of the tumor by parenteral hyperalimentation were not satisfactory and resulted in only a temporary improvement. This study also demonstrated that marked granulocytosis was the result of production of an excess granulopoietic colony stimulating activity by the cancer cells.
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PMID:Hypoglycemia, hypopotassemia and hyperleukocytosis associated with squamous cell carcinoma of the lung. 697 22

Ventromedial hypothalamic (VMH) lesion-induced obesity is accompanied by hyperinsulinemia and hyperphagia, which are dependent upon corticosterone (Cort) for their expression. Whether Cort exerts these actions through its stimulation of type I or II Cort receptor populations is unknown. Therefore, food intake and weight gain were measured in obese adrenalectomized VMH-lesioned rats given continuous infusion of various doses of either a type I-receptor agonist (aldosterone), a type II-receptor agonist (RU-28362), or several combination doses. Similarly, the receptor population responsible for lesion-induced hyperinsulinemia was identified. Type II receptor stimulation restored the hyperphagia, weight gain, and hyperinsulinemia of adrenalectomized VMH-lesioned animals, while type I receptor stimulation blocked their weight loss.
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PMID:Relative contribution of type I and II corticosterone receptors in VMH lesion-induced obesity and hyperinsulinemia. 820 42

Eating disorders are a group of disease states including anorexia nervosa, bulimia nervosa and binge eating on one end as well as episodic or chronic overeating resulting in obesity at the other end of the spectrum. These disorders are characterized by decreased and/or increased energy intake and are frequently associated with hormonal and metabolic disorders. The discovery of leptin, an adipocyte-secreted hormone acting in the brain to regulate energy homeostasis, and its subsequent study in human physiology have significantly advanced our understanding of normal human physiology and have provided new opportunities for understanding and possibly treating disease states, such as anorexia and bulimia nervosa. It has been recently discovered that leptin levels above a certain threshold are required to activate the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid axes in men, whereas the hypothalamic-pituitary-adrenal, renin-aldosterone, and growth hormone-IGF-1 axes may be largely independent of circulating leptin levels in humans. In this review, we summarize the latest findings related to the role of leptin in the regulation of several neuroendocrine axes, such as the hypothalamic-pituitary-gonadal and the hypothalamic-pituitary-thyroid axes in humans and discuss its potential pathophysiologic role in eating disorders.
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PMID:The role of leptin in regulating neuroendocrine function in humans. 1533 44

Type 2 diabetes is associated with obesity, insulin resistance, hyperglycemia, hyperphagia, polyuria, body weight gain, excessive secretion of glucocorticoids (GCs), thymus involution, adrenal gland hypertrophy, diabetic nephropathy, etc. We examined the effect of cerebrocrast, a new antidiabetic agent (synthesized in the Latvian Institute of Organic Synthesis), on body weight, food and water intake, urine output, and on changes of organ weight: that is, kidney, thymus, adrenal gland of normal rats. Cerebrocrast was administered at doses of 0.05 and 0.5 mg kg(-1) per os (p.o.) once a day for three consecutive days, and its effects were observed from 3 to 27 days after the last administration. Cerebrocrast, during the experimental period, decreased body weight by an average of approximately 32.3%, food intake by about 10-15% at the beginning of the experiments and by 22.6% at the end of the experiments, especially at a dose of 0.5 mg kg(-1). Water intake and urine output in comparison with controls were decreased. The daily food intake decreased about 1.0 and 2.1 g by administering single cerebrocrast doses of 0.05 and 0.5 mg kg(-1) body weight (b.w.), respectively, but by administering for three consecutive days, food intake decreased by about 2.2 and 3.4 g, respectively. The weekly body weight gain decreased by administering a single dose of cerebrocrast by 2.61 and 2.51 g, respectively, and by triple administration it decreased by 4.36 and 3.07 g, respectively. Cerebrocrast has long-lasting effects on these parameters and on thymus and adrenal gland weight. As cerebrocrast decreased glucose levels in normal and streptozotocin (STZ)-induced diabetic rats, it also promoted glucose uptake by the brain, intensified insulin action and formation de novo of insulin receptors. We can conclude that cerebrocrast may regulate food intake and body weight through glucose sensing by proopiomelanocortin (POMC) neurons, that are involved in control of glucose homeostasis, stimulation of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion, activation of MC4-Rs and inhibition of neuropeptide Y (NPY) in the ARC of the hypothalamus, affecting the kidney, and causing decreased urine output and water intake. Moreover, it could stimulate secretion of vasopressin. By administration of cerebrocrast thymus mass was increased, thereby preventing the action of GCs. As cerebrocrast inhibited L- and T-type calcium channels, it can prevent vasoconstriction of kidney arterioles and aldosterone secretion that have significant roles in the development of hypertension and diabetic nephropathy. These properties of cerebrocrast are important for treatment of Type 2 diabetes and its consequent development of hypertension and diabetic nephropathy.
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PMID:Effect of cerebrocrast on body and organ weights, food and water intake, and urine output of normal rats. 1903 18

The concept of fetal programming of disease in later life after intrauterine growth restriction (IUGR) has opened a potential new perspective on the treatment and prevention of arterial hypertension. Numerous large studies have recently confirmed the relationship between low birth weight and raised blood pressure. Hyperalimentation after birth appears to add to the risk of higher blood pressure later in life. However, there is still a controversy and clear intervention studies have not yet been possible. Therefore, the gain of knowledge about the underlying mechanisms of fetal programming is of utmost importance.Two major groups of mechanisms may be identified: renal and extrarenal mechanisms. Renal mechanisms include the reduction of nephron number, which is encountered in patients and animals with low birth weight. According to the so-called Brenner hypothesis, this may lead to increased arterial blood pressure. Another important renal system is the renin-angiotensin-aldosterone system, which appears to be more active on a number of levels in low birth weight individuals. Finally, there is the conversion of cortisol to inactive cortisone by the 11beta-hydroxysteroid dehydrogenase in distal tubule cells, which is reduced after intrauterine growth restriction. This enables a more powerful activation of mineralocorticoid receptors by cortisol. Extrarenal mechanisms include alterations in vascular structure (primary and secondary), increased activity of the sympathetic nerve system, and maybe most interestingly, an impairment of endothelial function. The latter is at least partially caused by an inactivation of nitric oxide by an excess of free oxygen radicals. In summary, mechanisms of fetal programming are only in the process of being revealed, and research has to focus on finding the key mechanism that might allow for successful intervention.
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PMID:Renal and extrarenal mechanisms of perinatal programming after intrauterine growth restriction. 1926 94

A 13-year-old female domestic shorthair cat presented with polyphagia and weight loss. Marked systolic hypertension was found on examination. Elevated total thyroxine levels confirmed hyperthyroidism, and hypokalaemia was also documented. A euthyroid state and normotension were achieved following 4 weeks of treatment with carbimazole and amlodipine. Despite potassium supplementation, the hypokalaemia worsened. Abdominal ultrasonography revealed left adrenomegaly. Plasma aldosterone concentrations were initially in the lower half of the reference interval and, when repeated 2 months later, were undetectable. Urea and creatinine remained in the lower half of the reference interval throughout treatment, and urine specific gravity suggested good urine concentrating ability. The fractional excretion of potassium confirmed a renal source of potassium loss. Blood gas analysis was unremarkable. It was theorised that an aldosterone precursor was causing signs of mineralocorticoid excess and undetectable plasma aldosterone levels. Treatment with an aldosterone receptor antagonist successfully increased the serum potassium concentration. Owing to difficulties administering medication and associated effects on life quality the cat was euthanased. Adrenal hyperplasia was apparent on post-mortem histopathology.
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PMID:Hypokalaemia in a hyperthyroid domestic shorthair cat with adrenal hyperplasia. 2462 55