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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of obesity is multifactorial and still unclear. Genetic factors play a significant role and include several gene candidates: polymorphisms of genes for ss(2)-adrenoreceptor, resistin, estrogen receptor-a and peroxisome proliferator-activated receptor-gamma. Moreover, peptides regulating hunger and satiety, e.g. leptin, galanin, cholecystokinin and neuropeptide Y, and altered nutritional patterns have been implicated. Also, factors associated with aging, e.g. decreased levels of growth hormone and dehydroepiandrosterone, and the activity of the sympathetic nervous system (resting metabolism and thermogenesis) cannot be disregarded. Participation of the sex steroids and inflammatory factors has also been postulated in the etiology of obesity. Three phenotypes of obesity are postulated; however, the visceral (abdominal) phenotype is typical of postmenopausal women and is characterized by several metabolic disorders with high risks of diabetes mellitus type 2 and cardiovascular disease. On the basis of personal experience and data from evidence-based medicine, diagnostic-therapeutic algorithms of climacteric obesity are presented.
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PMID:Climacteric obesity: from genesis to clinic. 1652 29

Diagnosis and treatment of hypoglycemia is an actual problem because glucose is the principal source of energy for central nervous system except permanent starvation when the ketone bodies are used by the central nervous system for energy. Glucose homeostasis depends on primary glucoregulatory organs--pancreas, liver, adrenal glands, and hypophysis. Insulin, glucagon, cathecholamines, cortisol, and growth hormone take part in this interaction. Hypoglycemia can develop if there are disorders of glucoregulatory organs resulting in imbalance of normal glucose homeostasis. Hypoglycemia presents with autonomic symptoms--hunger, palpitations, tremor, sweating--and with neuroglycopenic symptoms--confusion, drowsiness, odd behavior, speech difficulties, incoordination. None of these symptoms is specific just to hypoglycemia. Frequently hypoglycemia has to be differentiated with neurologic, psychiatric, and cardiovascular disorders. In this article the causes, symptoms, diagnosis, and treatment of hypoglycemia are reviewed.
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PMID:[Causes, diagnosis, and treatment of hypoglycemia]. 1709 Sep 87

Insulin-secreting pancreatic tumors and insulin-like growth hormone-secreting non-islet cell tumors can cause hypoglycemia. However, insulin-releasing paraganglioma or pheochromocytoma has almost never been reported. A 67-year-old female patient was admitted to our hospital because of headache, palpitation, perspiration, faintness, frequent sense of hunger and absent-mindedness. These intermittent symptoms had begun approximately a year before admission. On physical examination, she had high blood pressure of 150/90 mm Hg. Hormonal studies demonstrated increased urinary norepinephrine levels, and hyperinsulinemic hypoglycemia was confirmed while the patient was symptomatic. Abdominal MRI revealed a retroperitoneal mass measuring 4.5 cm in the pancreatic region. She was treated with an alpha-blocking agent to control blood pressure preceding the removal of the mass. Histopathological diagnosis was paraganglioma, and immunohistochemically insulin staining in the neoplastic cells was demonstrated. Her blood pressure normalized and hypoglycemia relieved after the operation. The patient did not have recurrence of hypoglycemia after a year of follow-up. Paraganglioma is a rare tumor of the neural crest, and co-secretion of insulin and catecholamines has been reported only by a single case report in the literature. The present patient is another case with this co-secretion.
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PMID:Hypoglycemia due to ectopic release of insulin from a paraganglioma. 1728 22

Ghrelin is produced primarily in the stomach in response to hunger, and circulates in the blood. Plasma ghrelin levels increase during fasting and decrease after ingesting glucose and lipid, but not protein. The efferent vagus nerve contributes to the fasting-induced increase in ghrelin secretion. Ghrelin secreted by the stomach stimulates the afferent vagus nerve and promotes food intake. Ghrelin also stimulates pituitary gland secretion of growth hormone (GH) via the afferent vagus nerve. GH inhibits stomach ghrelin secretion. These findings indicate that the vagal circuit between the central nervous system and stomach has a crucial role in regulating plasma ghrelin levels. Moreover, body mass index modulates plasma ghrelin levels. In a lean state and anorexia nervosa, plasma ghrelin levels are increased, whereas in obesity, except in Prader-Willi syndrome, plasma ghrelin levels are decreased and the feeding- and sleeping-induced decline in plasma ghrelin levels is disrupted. There are two forms of ghrelin: active n-octanoyl-modified ghrelin and des-acyl ghrelin. Fasting increases both ghrelin types compared with the fed state. Hyperphagia and obesity are likely to decrease plasma des-acyl ghrelin, but not n-octanoyl-modified ghrelin levels. Hypothalamic serum and glucocorticoid-inducible kinase-1 and serotonin 5-HT2C/1B receptor gene expression levels are likely to be proportional to plasma des-acyl ghrelin levels during fasting, whereas they are likely to be inversely proportional to plasma des-acyl ghrelin levels in an increased energy storage state such as obesity. Thus, a dysfunction of the ghrelin feedback systems might contribute to the pathophysiology of obesity and eating disorders.
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PMID:Ghrelin and feedback systems. 1798 56

The endogenous ligand for growth-hormone secretagogue receptor (GHS-R) was purified from the stomach and we named it "ghrelin", after a word root ("ghre") in Proto-Indo-European languages meaning "grow", since ghrelin has potent growth hormone (GH) releasing activity. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. Ghrelin is orexigenic; it is secreted from the stomach and circulates in the blood stream under fasting conditions, indicating that it transmits a hunger signal from the periphery to the central nervous system. Taking into account all these activities, ghrelin plays important roles for maintaining growth hormone release and energy homeostasis in vertebrates. The diverse functions of ghrelin raise the possibility of its clinical application for GH deficiency, eating disorder, gastrointestinal disease, cardiovascular disease, osteoporosis and aging, etc.
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PMID:Structure and function of ghrelin. 1819 77

In normal individuals hypoglycemic counterregulation is a multifactorial, redundant process that involves reduction of insulin secretion, increasing glucagon secretion, adrenergic activation, and increased growth hormone and cortisol secretion. Metabolically, these lead to increased glucose production, initially through glycogenolysis and later through gluconeogenesis, decreased muscle glucose oxidation and storage and increased release and use of alternative fuels, primarily free fatty acids. They also lead to hypoglycemic symptoms and hunger which increase food intake. These systems are designed to provide as much glucose as possible for brain glucose use. In patients with type 1 diabetes there are multiple impairments of these responses. Insulin does not decrease. Glucagon secretion is decreased or absent. Recovery from hypoglycemia is therefore dependent on the adrenergic response. Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase. Increased beta-activity increases free fatty acid release which increase glucose production and decrease glucose utilization. The increased alpha-adrenergic activity's primary role is to counteract beta-adrenergic vasodilation. It may also reduce neurogenic and neuroglycopenic symptoms. Lastly, there is evidence that both cardiac and adrenergic sensitivity are altered in type 1 diabetes. It is hoped that this information can be used in the future to help develop ways to protect patients with type 1 diabetes from hypoglycemia and its adverse effects.
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PMID:Sympathetic mechanisms of hypoglycemic counterregulation. 1822 Jun 70

The mechanisms of appetite and body-weight regulation by peripheral signals are highly complex in vertebrates and remain poorly understood. It is intuitively apparent that such regulation must involve interactions between peripheral metabolic status and the brain, but what are the signals recognized by the brain to initiate feeding? The hypothalamus has long been recognized as central in "recognition" of peripheral nutrient and metabolic signals (and, perhaps, body weight status) and in "regulation" of hunger and satiety responses and, therefore, is a logical site on which to focus research aimed at understanding interactions between and regulation of the periphery and central nervous system. Recent studies demonstrating modulation of hypothalamic neurotransmitter expression by peripheral metabolic status may yield insights into regulation of appetite and metabolism in obesity and aberrant metabolic homeostasis. This review concentrates on summarizing data regarding regulation of expression of neuropeptide Y and growth hormone-releasing hormone as model peptide systems for addressing questions relating peripheral metabolism and hypothalamic neuropeptide expression.
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PMID:Regulation of hypothalamic neuropeptide expression by peripheral metabolism. 1840 91

Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health.
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PMID:Metabolic consequences of sleep and sleep loss. 1892 15

The central nervous system undertakes the homeostatic role of sensing nutrient intake and body reserves, integrating the information, and regulating energy intake and/or energy expenditure. Few tasks regulated by the brain hold greater survival value, particularly important in farmed ruminant species, where the demands of pregnancy, lactation and/or growth are not easily met by often bulky plant-based and sometimes nutrient-sparse diets. Information regarding metabolic state can be transmitted to the appetite control centres of the brain by a diverse array of signals, such as stimulation of the vagus nerve, or metabolic 'feedback' factors derived from the pituitary gland, adipose tissue, stomach/abomasum, intestine, pancreas and/or muscle. These signals act directly on the neurons located in the arcuate nucleus of the medio-basal hypothalamus, a key integration, and hunger (orexigenic) and satiety (anorexigenic) control centre of the brain. Interest in human obesity and associated disorders has fuelled considerable research effort in this area, resulting in increased understanding of chronic and acute factors influencing feed intake. In recent years, research has demonstrated that these results have relevance to animal production, with genetic selection for production found to affect orexigenic hormones, feeding found to reduce the concentration of acute controllers of orexigenic signals, and exogenous administration of orexigenic hormones (i.e. growth hormone or ghrelin) reportedly increasing DM intake in ruminant animals as well as single-stomached species. The current state of knowledge on factors influencing the hypothalamic orexigenic and anorexigenic control centres is reviewed, particularly as it relates to domesticated ruminant animals, and potential avenues for future research are identified.
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PMID:Neuroendocrine and physiological regulation of intake with particular reference to domesticated ruminant animals. 1908 72

The discovery of ghrelin (GRLN) has broadened our understanding of the regulation of energy homeostasis in vertebrates. In addition to stimulating growth hormone release from the pituitary, GRLN has been implicated as a hunger signal stimulating food intake in mammals and goldfish. Indeed, GRLN levels rise preprandial and fall following a meal. The current study investigated pre- and postprandial changes (3 h before and after a meal) in GRLN signaling in the tilapia (Oreochromis mossambicus). Significant elevations in preprandial brain mRNA levels of the GRLN receptor (GHS-R1a) and GRLN were observed; though not significant brain neuropeptide Y (NPY) mRNA levels did increase preprandially. GHS-R1b, and NPY mRNA levels were reduced significantly 3 h after a meal; whereas GHS-R1a levels were unaltered postprandially. Brain ghrelin mRNA levels exhibited a transient significant increase 1 h postprandially. Tilapia that missed the scheduled feeding exhibited no changes in brain GHS-R1a, GRLN and NPY postprandial mRNA levels; whereas GHS-R1b mRNA levels were significantly reduced 1 and 3 h postprandially. Brain GHSR preprocessed RNA (heteronuclear mRNA) levels were significantly elevated 3 h preprandially. GHS-R hnRNA levels were significantly elevated 1h postprandial in fed and fasted tilapia. No preprandial rise in plasma GRLN was observed. Following a meal, plasma GRLN levels were significantly elevated; whereas there was no change in tilapia missing the scheduled feeding. Stomach mRNA levels of GRLN rose preprandially and remained unchanged following a meal. In animals that missed the scheduled feeding stomach GRLN levels dropped significantly 1 h following a meal. There was no change in plasma growth hormone levels in the fed fish, although there was a significant rise in the fasted fish 1h after the scheduled feeding. Postprandial levels of plasma IGF-I were elevated in both fed and fasted tilapia. These results suggest that brain derived GRLN is likely driving day-to-day appetite through GHS-R1a and NPY; while systemic GRLN may play a role in postprandial metabolism.
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PMID:Pre- and postprandial effects on ghrelin signaling in the brain and on the GH/IGF-I axis in the Mozambique tilapia (Oreochromis mossambicus). 1924 15


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