Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, was recently identified in the rat stomach. Previous studies have shown that ghrelin potently increases growth hormone release and food intake. We examined the effects of the gastric peptide ghrelin on anxiety-like behavior in association with the hypothalamic-pituitary-adrenal axis in mice. Both intra-third cerebroventricular and intraperitoneal administration of ghrelin potently and significantly induced anxiogenic activities in the elevated plus maze test. Ghrelin gene expression in the stomach was increased by tail pinch stress as well as by starvation stress. Administration of a corticotropin-releasing hormone (CRH) receptor antagonist significantly inhibited ghrelin-induced anxiogenic effects. Peripherally administered ghrelin significantly increased CRH mRNA, but not urocortin mRNA expression in the hypothalamus. Furthermore, intraperitoneal injection of ghrelin produced a significant dose- dependent increase in serum corticosterone levels. These findings suggest that ghrelin may have a role in mediating neuroendocrine and behavioral responses to stressors and that the stomach could play an important role, not only in the regulation of appetite, but also in the regulation of anxiety.
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PMID:A role of ghrelin in neuroendocrine and behavioral responses to stress in mice. 1152 15

Ghrelin, a 28-amino-acid acylated peptide, produced mainly by the stomach, displays strong growth hormone-(GH)-releasing activity mediated by the hypothalamus-pituitary growth hormone potential secretagogue (GHS) receptor which had been shown to be specific for a family of synthetic, orally active GHS. GHS are reliable provocative tests for the diagnosis of GH deficiency but, as orally active growth-promoting agents, they are not comparable with human recombinant GH in terms of efficacy. The usefulness of GHS in anabolic, anti-ageing drug intervention in the somatopause is still unclear. GHS also act on central and peripheral receptors and show other actions, including an orexigenic effect, an influence on gastroentero-pancreatic functions, and cardiovascular and anti-proliferative effects. Ghrelin mediates the neuroendocrine and metabolic response to starvation. Taking into account its orexigenic effect, GHS analogues acting as agonists or antagonists on appetite could represent a new drug intervention for eating disorders.
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PMID:Ghrelin and synthetic GH secretagogues. 1246 31

The hypothalamus regulates energy intake by integrating the degree of starvation or satiation with the status of the environment through a variety of neuronal and blood-derived signals. Ghrelin, a peptide produced in the stomach and hypothalamus, stimulates feeding and GH secretion. Centrally administered ghrelin exerts an orexigenic activity through the neuropeptide Y (NPY) and agouti-related protein systems. The interaction between ghrelin and other hypothalamic orexigenic peptides, however, has not been clarified. Here, we investigated the anatomical interactions and functional relationship between ghrelin and two orexigenic peptides, orexin and melanin-concentrating hormone (MCH), present in the lateral hypothalamus. Ghrelin-immunoreactive axonal terminals made direct synaptic contacts with orexin-producing neurons. Intracerebroventricular administration of ghrelin induced Fos expression, a marker of neuronal activation, in orexin-producing neurons but not in MCH-producing neurons. Ghrelin remained competent to induce Fos expression in orexin-producing neurons following pretreatment with anti-NPY IgG. Pretreatment with anti-orexin-A IgG and anti-orexin-B IgG, but not anti-MCH IgG, attenuated ghrelin-induced feeding. Administration of NPY receptor antagonist further attenuated ghrelin-induced feeding in rats treated with anti-orexin-IgGs. Ghrelin-induced feeding was also suppressed in orexin knockout mice. This study identifies a novel hypothalamic pathway that links ghrelin and orexin in the regulation of feeding behavior and energy homeostasis.
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PMID:Ghrelin-induced food intake is mediated via the orexin pathway. 1263 35

Ghrelin is a novel gastrointestinal peptide that stimulates growth hormone secretion, food intake, and body weight gain. Increased ghrelin secretion has been reported in such negative energy states as starvation and low body weight. We investigated the dynamics of ghrelin in rats with streptozotocin-induced diabetes, because they present reduced body weight and hyperphagia. The plasma ghrelin levels and gastric preproghrelin mRNA expression levels of the diabetic rats increased significantly and their gastric ghrelin levels decreased significantly. Negative energy balance may enhance preproghrelin mRNA expression and ghrelin secretion into the bloodstream.
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PMID:Enhanced plasma ghrelin levels in rats with streptozotocin-induced diabetes. 1270 20

Ghrelin, a new gastric-derived hormone, probably plays a major role in managing energy balance and the neuroendocrine response to starvation. Information about the age-related variation in ghrelin secretion is scanty. We measured circulating ghrelin levels in 93 full term newborns adequate for gestational age, in 39 normal children and in 19 lean healthy adults. Our findings demonstrate that ghrelin levels are independent of age and gender from birth to adulthood. Interestingly, ghrelin secretion at birth is not associated to body weight and hormonal parameters such as GH, insulin and leptin levels. On the other hand, ghrelin levels seem dependent on the type of delivery, being lower in newborns after caesarean section with respect to those after normal delivery.
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PMID:Circulating ghrelin levels in newborns are not associated to gender, body weight and hormonal parameters but depend on the type of delivery. 1284 32

Pharmacological studies show that ghrelin stimulates growth hormone release, appetite, and fat deposition, but ghrelin's physiological role in energy homeostasis has not been established. Ghrelin was also proposed to regulate leptin and insulin release and to be important for the normal function of stomach, heart, kidney, lung, testis, and placenta. To help determine a definable physiological role for ghrelin, we generated ghrelin-null mice. In contrast to predictions made from the pharmacology of ghrelin, ghrelin-null mice are not anorexic dwarfs; their size, growth rate, food intake, body composition, reproduction, gross behavior, and tissue pathology are indistinguishable from wild-type littermates. Fasting produces identical decreases in serum leptin and insulin in null and wild-type mice. Ghrelin-null mice display normal responses to starvation and diet-induced obesity. As in wild-type mice, the administration of exogenous ghrelin stimulates appetite in null mice. Our data show that ghrelin is not critically required for viability, fertility, growth, appetite, bone density, and fat deposition and not likely to be a direct regulator of leptin and insulin. Therefore, antagonists of ghrelin are unlikely to have broad utility as antiobesity agents.
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PMID:Deletion of ghrelin impairs neither growth nor appetite. 1458 59

Ghrelin, a 28 amino-acid acylated peptide predominantly produced by the stomach, displays strong GH-releasing activity mediated by the hypothalamus-pituitary GH secretagogues (GHS) receptors which had been shown specific for a family of synthetic, orally active GHS. GHS also act on central and peripheral receptors and show other actions including an orexigenic effect, influence on gastro-entero-pancreatic functions, cardiovascular and anti-proliferative effects. Ghrelin manages the neuroendocrine and metabolic response to starvation. Taking into account its orexigenic effect, GHS analogues acting as agonists or antagonists on appetite could represent new drug intervention in eating disorders.
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PMID:Central and peripheral activities of ghrelin, a ligand of the growth hormone secretagogue receptor. 1461 18

Ghrelin, a 28-amino acid acylated peptide predominantly produced by the stomach, displays strong GH-releasing activity mediated by the hypothalamic-pituitary GH secretagogues (GHS) receptors (GHS-R) which had been shown specific for a family of synthetic, orally active molecules known as GHS. However, ghrelin and GHS, acting on central and peripheral receptors, also exert other actions. These include influence on pituitary functions, orexigenic action, influence on exocrine and endocrine gastro-entero-pancreatic functions, cardiovascular and anti-proliferative effects. In particular, the effect of ghrelin in promoting food intake and modulating energy metabolism strongly suggested that ghrelin has a key role in managing the neuroendocrine and metabolic response to starvation and that could be involved in the pathogenesis and/or in the metabolic and neuro-hormonal alterations of obesity and eating disorders. Although specific alterations in ghrelin secretion and/or action in obesity and anorexia nervosa (AN) have already been reported, the possibility that ghrelin analogues acting as agonists or antagonists has clinical perspectives for treatment of eating disorders presently remains a dream.
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PMID:Ghrelin: a link between eating disorders, obesity and reproduction. 1568 22

Ghrelin is a peptidic hormone composed of 28 aminoacid residues. It is produced by enteroendocrine cells of stomach and intestine. It is also produced in pancreas, kidney, placental tissue, thyroid gland, hypothalamus, and hypophysis. Gastrectomy leads to 65-80% decrease of plasma levels of ghrelin. In human organism, ghrelin stimulates secretion of growth hormone, prolactin, and ACTH. Ghrelin also has orexigenic activity (increases food intake), influences the sleep/wake cycle, gastric motility and secretion, cardiovascular functions, regulates endocrine function of pancreas and metabolism of glucose and shows an antiproliferative effect. Ghrelin is an important regulatory part of the homeostasis of the organism, and iterconnects neuroendocrine and metabolic response of the organism to starvation, and it is considered as a counterpart to leptin. Ghrelin was discovered by Japanese scientists in 1999 as a natural ligand of an "orphan" receptor GHS1a, which is specific for a group of synthetic peptides (growth hormone secretagogues--GHS) stimulating secretion of growth hormone. Plasma levels of ghrelin reflect short-time changes of food intake, as well as long-time changes of the nutritional state of the organism. Plasma levels of ghrelin are decreased after food intake and in obese humans, and they are increased during starvation and in patients with mental anorexia. Plasma levels of ghrelin in humans correlate negatively with body mass index, amount of body fat, size of adipocytes, and plasma levels of insulin, glucose, and leptin. Thus, ghrelin probably plays a role as a metabolic signal of hunger.
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PMID:[Ghrelin--structure, function and clinical applications]. 1570 43

The oxyntic mucosa of rat and mouse stomach harbors histamine-producing ECL cells and ghrelin-producing A-like cells. The ECL cells are known to be active when the circulating gastrin levels are elevated in response to food intake. The A-like cells are the main source of circulating ghrelin. In response to starvation, the circulating ghrelin is elevated as a hunger signal. The aim of the present work was to study the correlation between the immunoreactivities and cellular activities of the ECL cells and A-like cells. Rats were either fed or fasted for 48 h and mice for 24 h. Immunohistochemical examination with antiserum against chromogranin A-derived fragment pancreastatin revealed both the ECL cells and the A-like cells without a difference between fasted and fed animals. Histamine was limited to the ECL cells with no significant difference between fasted and fed animals. Histidine decarboxylase (HDC) immunoreactivity occurred predominately in the ECL cells of the fed, but not fasted, animals in which the HDC enzymatic activity in the oxyntic mucosa was higher than in fasted animals. Ghrelin immunoreactivity was increased in terms of intensity, but not cell density in fasted animals. Thus, the immunoreactivities of ECL cells and A-like cells might be affected by starvation.
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PMID:Immunoreactivity of gastric ECL and A-like cells in fasted and fed rats and mice. 1580 23


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