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

The influence of protein in exchange for carbohydrates on the energy maintenance requirement was studied with nearly fully-grown rats at ambient temperatures between 33 and 21 degrees C. The levels of the crude protein content were 10, 25, 40 and 70%. At an ambient temperature of 33 and 30 degrees C energy maintenance requirement increased with the growing protein content in the feed. At a temperature of 30 degrees C the following values of energy maintenance requirement were measured in the sequence of the protein levels mentioned: 330 +/- 11, 347 +/- 18, 360 +/- 15 and 399 +/- 15 kJ metabolizable energy/kg live weight 0.75 X d. The occurring changes largely coincide with the expected values calculated from the efficiency of the ATP synthesis in the oxidative catabolization of protein and carbohydrates. At ambient temperatures of less than 30 degrees C, thermogenous effects after the exchange of protein versus carbohydrates could only be observed partly or not. 30 degrees C in feeding on the maintenance level and 33 degrees C in the state of hunger are estimated as the lower critical temperatures. Below the critical temperatures down to 24 degrees C heat production increased less per 1 degree C temperature decrease both in hungry and fed rats than in the temperature range between 24 and 21 degrees C. By the decrease of the ambient temperature from 24 to 21 degrees C the heat production of the hungry or fed rats increased by 39 or 33 kJ/degrees C X kg live weight 0.75 X d.
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PMID:[Nutrient dependence of energy preservation requirements in rats. 2. Effect of the protein level of feed and the environmental temperature on the energy preservation requirement and heat production in fully-grown rats]. 381 76

The fructose analogue 2,5-anhydro-D-mannitol (2,5-AM), that inhibits glucose release and ATP formation in liver cells, seems to stimulate feeding by acting on the liver, because hepatic portal injection was more effective than jugular vein injection and because hepatic branch vagotomy attenuated 2,5-AM's hyperphagic effect. Russek's "potentiostatic" hypothesis postulates a role for the hepatic membrane potential in the control of food intake with depolarization of hepatocytes signaling hunger and hyperpolarization representing a satiety signal. Therefore, the aim of the present study was to find out, whether 2,5-AM affects the hepatic membrane potential under in vivo conditions. The membrane potential was measured with microelectrodes in anesthetized rats after intraperitoneal (i.p.) or intraportal (i.p.v.) administration of 2,5-AM or control solution. 2,5-AM significantly hyperpolarized the hepatocyte membrane 50 min after i.p. injection (100 mg/kg: 3.6 mV; 300 mg/kg: 9.9 mV). In a second experiment, 2,5-AM (300 mg/kg) elicited a significant hyperpolarization of hepatocytes as soon as 5-9 min after i.p.v. infusion. These effects occurred at doses that have been shown to increase the afferent discharge rate in the common hepatic vagus branch, and to stimulate food intake. 2,5-AM's hyperphagic effect therefore is associated with an increase in the hepatic membrane potential. These findings contradict the predictions of the "potentiostatic" hypothesis and are consistent with the notion, that the feeding response to 2,5-AM might be due to ATP depletion in the terminals of vagal afferents.
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PMID:Hyperpolarization of the rat hepatocyte membrane by 2,5-anhydro-D-mannitol in vivo. 958 70

Studies using metabolic inhibitors suggest that a reduction in hepatic ATP generates a stimulus that triggers feeding behavior. To investigate the relationship between changes in liver ATP and food intake under physiological conditions, we assessed changes in feeding behavior and liver adenine nucleotides during refeeding after 24 h of food deprivation. Deprived rats consumed 14 g of food in the first 3 h of refeeding; the rate of consumption declined markedly thereafter for the next 9 h, but remained higher than that seen in nonfasted rats. Fasting produced substantial reductions in ATP, ATP/ADP, and phosphorylation potential relative to fed levels. Refeeding restored liver ATP by 6 h, whereas ATP/ADP and phosphorylation potential did not fully recover until 12 h of refeeding. Restricting food intake during refeeding limited recovery of liver energy status. These results show that liver energy production recovers slowly during refeeding with a time course that parallels the compensatory change in eating behavior. These findings raise the possibility that changes in hepatic energy status play a role in satiation as well as in hunger.
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PMID:Compensatory hyperphagia after fasting tracks recovery of liver energy status. 1062 79

Neuronal modules, or 'cell-assemblies', comprising millions of mutually interconnected cells have been postulated to form the basis of many functions of the brain, such as mood, sleep, hunger, vigilance, and more. Depending on the extent of the module, neurocommunication in cell-assemblies might exceed metabolic resources. A medium-size (10000 neurons) module would require at least 10 J per l of brain, based on a calculated cost of an isolated action potential (AP) of 10(11)-10(12) molecules of ATP per cm(2) of cell membrane, with an absolute minimum of 10(6) ATP at a node of Ranvier. The figure matches the cost of depolarizing the unmyelinated axon of the large monopolar cell in the blowfly retina. A circuit model of the cell membrane, based on abrupt changes of Na(+) and K(+) conductances, is used to emulate the AP and to assess the resulting ionic unbalance. The cost of an AP is equated to the metabolic energy necessary to fuel ATP-based pumps that restore intracellular K(+). The high metabolic demand of a cell-assembly suggests that less expensive means of neurocommunication may be involved, such as non-synaptic diffusion neurotransmission (NDN), which would comply with a proposed law of conservation of space and energy in the brain.
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PMID:The cost of an action potential. 1108 6

The objective of this experiment was to evaluate effects of salt type on hypophagic effects of intraruminal infusion of propionate in lactating dairy cows. Our working hypothesis is that oxidative metabolism of propionate causes satiety by increasing hepatic ATP concentration and decreasing the discharge rate of the hepatic vagus. We hypothesized that hypophagic effects of propionate are reduced by ammonium and potassium. We speculated that ammonium infusion lowers hepatic ATP concentration because ATP is used for urea synthesis and potassium increases the discharge rate of the hepatic vagus. Eight ruminally cannulated Holstein cows in midlactation were used in a duplicated 4 x 4 Latin square design experiment. Treatments were intraruminal infusion of propionic acid, ammonium propionate, sodium propionate, and potassium propionate. Treatment solutions were 0.93 M for propionate and 0.67 M for salts among the treatments except for propionic acid. Treatment solutions were infused over 14 h starting 2 h before feeding at 17.9 ml/min, which is equivalent to 16.7 and 11.9 mmol/min for propionate and salts, respectively. Infusion of ammonium propionate decreased dry matter intake compared with sodium propionate and potassium propionate (P < 0.04; 11.0 vs. 14.0 and 13.9 kg/12 h) by decreasing meal frequency without affecting meal size, indicating that ammonium delayed the sense of hunger. No difference in DMI and feeding behavior was observed between infusion of sodium and potassium propionate. Contrary to the hypothesis, ammonium infusion did not reduce hypophagic effects of propionate, possibly because the urea cycle indirectly stimulated oxidative metabolism in the liver by generating oxidizable carbon from amino acid catabolism.
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PMID:Effects of intraruminal infusion of sodium, potassium, and ammonium on hypophagia from propionate in lactating dairy cows. 1274 64

To test the hypothesis that decreased hepatocyte ATP is transduced into a hepatic neuronal signal via a change in sodium pump activity, we examined the effect of 2,5-anhydro-D-mannitol (2,5-AM), which stimulates feeding behavior in rats, on intracellular sodium levels using 23Na nuclear magnetic resonance (NMR) spectroscopy. Isolated hepatocytes suspended in agarose beads were superfused with either 2.5 mM 2,5-AM or fructose in the presence of the paramagnetic shift reagent, thulium(III)(1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylenephosphonate)). Superfusion with 2,5-AM decreased hepatocyte ATP and increased intracellular sodium levels compared with superfusion with either fructose or shift reagent alone starting within 15 min of exposure, reaching a maximum level of 120% of baseline by 30 min and declining gradually thereafter over the next 90 min. Superfusion with fructose, which also decreased hepatocyte ATP but by less than half the amount seen with 2,5-AM, had no significant effect on cellular sodium levels. The results support the hypothesis that changes in sodium pump activity could participate in transducing a hunger stimulus associated with hepatocyte energy status into a signal for hunger.
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PMID:2,5-Anhydro-D-mannitol increases hepatocyte sodium: transduction of a hepatic hunger stimulus? 1297 93

Etomoxir, an inhibitor of fatty acid oxidation, increases food intake and reported hunger in humans. Work with animal models suggests that other inhibitors of fatty acid oxidation stimulate feeding behavior by acting on the liver. In the following study, we assessed whether etomoxir would increase food intake in rats and to what degree the effects of etomoxir on feeding were associated with changes in hepatic energy status. The effects of etomoxir on hepatic energy status were assessed by measuring liver ATP, ADP, phosphorylation potential, and glycogen content. Blood glucose, free fatty acids, and ketone bodies were also measured to determine the availability of circulating fuels following etomoxir treatment. Etomoxir and methyl palmoxirate (MP; another inhibitor of fatty acid oxidation) increased food intake. Etomoxir, like MP, also reduced hepatic ATP/ADP ratio and phosphorylation potential. In combination with 2,5-anhydro-D-mannitol (an analogue of fructose that produces an increase in feeding by action on the liver), etomoxir synergistically increased food intake and reduced hepatic ATP/ADP ratio. In summary, etomoxir increased food intake and decreased hepatic energy status in the rat. This suggests that etomoxir stimulates feeding by action on the liver.
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PMID:Etomoxir, a fatty acid oxidation inhibitor, increases food intake and reduces hepatic energy status in rats. 1505 95

Integration of peripheral and central anabolic and catabolic inputs within the hypothalamic arcuate nucleus (ARC) is believed to be central to the maintenance of energy balance. In order to perform this complex task, neurons in the ARC express receptors for all major humoral and central transmitters involved in the maintenance of energy homeostasis. The integration of these inputs occurs at the cellular and circuit level and the resulting electrical output forms the origins for the activation of feeding and energy balance-related networks. Here, we discuss the role that active intrinsic membrane conductances, K(ATP) channels and intracellular second messenger systems play in the integration of metabolic stimuli at the cellular level in the ARC. We conclude that the research into the integration of hunger and satiety signals in the ARC has made substantial progress in the last decade, but we are far from unraveling the complex neuronal networks involved in the maintenance of energy homeostasis. The diverse range of inputs, neuronal integrative properties, targets, output signals and how these signals relate to the physiological output provides us with a colossal challenge for years to come. However, to battle the current obesity epidemic, target-specific drugs need to be developed for which the knowledge of neuronal pathways involved in the maintenance of energy homeostasis will be crucial.
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PMID:Integration of metabolic stimuli in the hypothalamic arcuate nucleus. 1687 73

The hypothalamus is the central regulatory unit that balances a number of body functions including metabolic rate, hunger, and satiety signals. Hypothalamic neurons monitor and respond to alterations of circulating nutrients and hormones that reflect the peripheral energy status. These extracellular signals are integrated within the cell at the ATP:AMP ratio and at the level of ROS, triggering gene expression associated with glucose and lipid metabolism. In order to identify new molecular factors potentially associated with the control of energy homeostasis, metabolic adaptation, and regulation of feed intake, hypothalami from ad libitum fed and energy restricted cows were characterized using 2-DE and MALDI-TOF-MS. Among 189 different protein spots identified, nine proteins were found to be differentially expressed between groups. Beside the 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase, stress-induced phosphoprotein-1, heat shock protein 70 kDa-protein-5, dihydropyrimidinase-related protein-2, [Cu-Zn]-superoxide dismutase, ubiquitin carboxy-terminal hydrolase-L1, and inorganic pyrophosphatase were found to be up-regulated, whereas glyceraldehyde 3-phosphate dehydrogenase and aconitase-2 were down-regulated in the restricted group. In conclusion, differentially expressed proteins are related to energy and nucleotide metabolism and cellular stress under conditions of dietary energy deficiency. These proteins may be new candidate molecules that are potentially involved in signaling for maintaining energy homeostasis.
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PMID:Proteomics analysis of hypothalamic response to energy restriction in dairy cows. 1790 70

Orexin A and Orexin B (also known as hypocretins) are neuropeptides that bind two related G-coupled protein receptors (OXR1 and OXR2) and thus induce wakefulness, food consumption, and locomotion. Conversely, deletion of the orexin gene in mice produces a condition similar to canine and human narcolepsy. Despite the central importance of the orexin system in regulating wakefulness and feeding behavior, little is known about the downstream signaling mechanisms that achieve these effects. In this study, genomics techniques are used to probe this question and reveal that orexin activates the hypoxia-inducible factor 1 (HIF-1), a heterodimeric transcription factor whose pathogenic role in stimulating angiogenesis in hypoxic tumors has been the focus of intense investigation. Orexin-stimulated HIF-1 activity is due to both increased HIF-1alpha gene transcription and a down-regulation of von Hippel-Lindau (VHL), the E3 ubiquitin ligase that mediates the turnover of HIF-1 via the ubiquitin-proteasome pathway. Orexin-mediated activation of HIF-1 results in increased glucose uptake and higher glycolytic activity, as expected from studies of hypoxic cells. However, orexin receptor-expressing cells somehow override the HIF-1-mediated preference for funneling pyruvate into anaerobic glycolysis and instead favor ATP production through the tricarboxylic acid cycle and oxidative phosphorylation. These findings implicate HIF-1 as an important transcription factor in the hormone-mediated regulation of hunger and wakefulness.
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PMID:The neurohormone orexin stimulates hypoxia-inducible factor-1 activity. 1800 90


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