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Food Intake

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M W Schwartz – One of the best experts on this subject based on the ideXlab platform.

  • central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, D Porte, Randy J. Seeley, Stephen C. Woods, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from inherited or acquired defects in their function.

  • Central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, S. C. Woods, D Porte, Randy J. Seeley, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its Importance to human health, Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. Se better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from Inherited or acquired defects in their function.

  • Neuroendocrine regulation of Food Intake
    Acta Paediatrica, 1999
    Co-Authors: Randy J. Seeley, M W Schwartz
    Abstract:

    Seeley RJ, Schwartz MW. Neuroendocrine regulation of Food Intake. Acta Paediatr 1999; Suppl 428: 58–61. Stockholm. ISSN 0803–5326 Maintenance of appropriate stores of metabolic fuels depends on carefully matching caloric Intake to caloric expenditure. Achieving such‘energy balance’is a product of complex interactions of peripheral hormones with effector systems in the central nervous system (CNS) that regulate Food Intake and energy expenditure. Leptin is a hormone that is made in the adipocytes, circulates in the blood and interacts with receptors in the CNS. These receptors can be found in two different types of systems. One effector system is termed‘anabolic’and is activated by low levels of leptin during negative energy balance. This system (exemplified by the hypothalamic neuropeptide Y system) increases Food Intake and decreases energy expenditure to facilitate the regaining of lost energy stores. The other effector system is termed‘catabolic’and is activated by high levels of leptin during positive energy balance. This system (exemplified by the hypothalamic melanocortin and corticotrophin-releasing hormone systems) decreases Food Intake and increases energy expenditure to facilitate the loss of excess energy stores. Further understanding of these systems is necessary to develop adequate treatments for disorders of energy balance, such as obesity and wasting. □Corticotrophin-releasing hormone, energy balance, Food Intake, leptin, melanocortin, neuropeptide Y

M.k. Unkefer – One of the best experts on this subject based on the ideXlab platform.

  • Development of Food Intake controls: Neuroendocrine and environmental regulation of Food Intake during early life
    Hormones and Behavior, 2014
    Co-Authors: Erica J. Crespi, M.k. Unkefer
    Abstract:

    Abstract This article is part of a Special Issue “Energy Balance”. The development of neuroendocrine regulation of Food Intake during early life has been shaped by natural selection to allow for optimal growth and development rates needed for survival. In vertebrates, neonates or early larval forms typically exhibit “feeding drive,” characterized by a developmental delay in 1) responsiveness of the hypothalamus to satiety signals (e.g., leptin, melanocortins) and 2) sensitivity to environmental cues that suppress Food Intake. Homeostatic regulation of Food Intake develops once offspring transition to later life history stages when growth is slower, neuroendocrine systems are more mature, and appetite becomes more sensitive to environmental or social cues. Across vertebrate groups, there is a tremendous amount of developmental plasticity in both Food Intake regulation and stress responsiveness depending on the environmental conditions experienced during early life history stages or by pregnant/brooding mothers. This plasticity is mediated through the organizing effects of hormones acting on the Food Intake centers of the hypothalamus during development, which alter epigenetic expression of genes associated with ingestive behaviors. Research is still needed to reveal the mechanisms through which environmental conditions during development generate and maintain these epigenetic modifications within the lifespan or across generations. Furthermore, more research is needed to determine whether observed patterns of plasticity are adaptive or pathological. It is clear, however, that developmental programming of Food Intake has important effects on fitness, and therefore, has ecological and evolutionary implications.

  • Development of Food Intake controls: Neuroendocrine and environmental regulation of Food Intake during early life
    Hormones and Behavior, 2014
    Co-Authors: Erica J. Crespi, M.k. Unkefer
    Abstract:

    This article is part of a Special Issue “Energy Balance”.The development of neuroendocrine regulation of Food Intake during early life has been shaped by natural selection to allow for optimal growth and development rates needed for survival. In vertebrates, neonates or early larval forms typically exhibit “feeding drive,” characterized by a developmental delay in 1) responsiveness of the hypothalamus to satiety signals (e.g., leptin, melanocortins) and 2) sensitivity to environmental cues that suppress Food Intake. Homeostatic regulation of Food Intake develops once offspring transition to later life history stages when growth is slower, neuroendocrine systems are more mature, and appetite becomes more sensitive to environmental or social cues. Across vertebrate groups, there is a tremendous amount of developmental plasticity in both Food Intake regulation and stress responsiveness depending on the environmental conditions experienced during early life history stages or by pregnant/brooding mothers. This plasticity is mediated through the organizing effects of hormones acting on the Food Intake centers of the hypothalamus during development, which alter epigenetic expression of genes associated with ingestive behaviors. Research is still needed to reveal the mechanisms through which environmental conditions during development generate and maintain these epigenetic modifications within the lifespan or across generations. Furthermore, more research is needed to determine whether observed patterns of plasticity are adaptive or pathological. It is clear, however, that developmental programming of Food Intake has important effects on fitness, and therefore, has ecological and evolutionary implications. © 2014 Elsevier Inc.

Randy J. Seeley – One of the best experts on this subject based on the ideXlab platform.

  • central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, D Porte, Randy J. Seeley, Stephen C. Woods, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from inherited or acquired defects in their function.

  • Central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, S. C. Woods, D Porte, Randy J. Seeley, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its Importance to human health, Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. Se better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from Inherited or acquired defects in their function.

  • Neuroendocrine regulation of Food Intake
    Acta Paediatrica, 1999
    Co-Authors: Randy J. Seeley, M W Schwartz
    Abstract:

    Seeley RJ, Schwartz MW. Neuroendocrine regulation of Food Intake. Acta Paediatr 1999; Suppl 428: 58–61. Stockholm. ISSN 0803–5326 Maintenance of appropriate stores of metabolic fuels depends on carefully matching caloric Intake to caloric expenditure. Achieving such‘energy balance’is a product of complex interactions of peripheral hormones with effector systems in the central nervous system (CNS) that regulate Food Intake and energy expenditure. Leptin is a hormone that is made in the adipocytes, circulates in the blood and interacts with receptors in the CNS. These receptors can be found in two different types of systems. One effector system is termed‘anabolic’and is activated by low levels of leptin during negative energy balance. This system (exemplified by the hypothalamic neuropeptide Y system) increases Food Intake and decreases energy expenditure to facilitate the regaining of lost energy stores. The other effector system is termed‘catabolic’and is activated by high levels of leptin during positive energy balance. This system (exemplified by the hypothalamic melanocortin and corticotrophin-releasing hormone systems) decreases Food Intake and increases energy expenditure to facilitate the loss of excess energy stores. Further understanding of these systems is necessary to develop adequate treatments for disorders of energy balance, such as obesity and wasting. □Corticotrophin-releasing hormone, energy balance, Food Intake, leptin, melanocortin, neuropeptide Y

Stephen R. Bloom – One of the best experts on this subject based on the ideXlab platform.

  • Increased Food Intake with oxyntomodulin analogues
    Peptides, 2015
    Co-Authors: Samantha L. Price, James Minnion, Stephen R. Bloom
    Abstract:

    Oxyntomodulin analogues offer a novel treatment for obesity. However during analogue screening in a rat model increased Food Intake was consistently observed. To further investigate this finding, a series of representative analogues (OXM14 and OXM15) and their Glu-3 equivalents (OXM14E3 and OXM15E3) were administered to rats for 7 days and Food Intake and bodyweight measurements taken. To investigate the role of glucagon receptor activation glutamate (Glu/E) was substituted at amino acid position 3. GLP-1 and glucagon receptor efficacy of the oxyntomodulin analogues and their Glu-3 counterparts were measured at the rat receptors in vitro. Doses of 25 n mol/kg of OXM14 and OXM15 increased Food Intake by up to 20%. Bodyweight was not significantly increased. Food Intake was not increased with the Glu-3 peptides, indicating that a glucagon receptor mechanism may be responsible for the increase in Food Intake.

  • Neuroendocrine control of Food Intake
    Current Opinion in Gastroenterology, 2005
    Co-Authors: Adrian J. Park, Stephen R. Bloom
    Abstract:

    Purpose of review Obesity is a major public health problem and substantially increases the risk of type 2 diabetes, hypertension, stroke, cardiovascular, respiratory problems, gall bladder disease, osteoarthritis and sleep apnoea, as well as certain cancers. The prevalence of obesity is rapidly increasing worldwide. However, for individuals weight is regulated within a narrow range. This regulation depends on energy Intake (in the form of Food) and energy expenditure. Recently, there has been a remarkable increase in our understanding of the homeostatic mechanisms that control Food Intake and energy homeostasis. Recent findings There is increased understanding of the central regulation of appetite. In particular, this includes new knowledge about the hypothalamus and brainstem and their relation to Food Intake regulation. Peripheral hormones (notably adipostat factors and gut hormones) have now been found to be important in Food Intake regulation. Summary Complex central circuitry controls Food Intake. Circulating hormones, in particular the gut hormones have unexpectedly been found to be very important in appetite control. The gut hormones are thus new and exciting targets for future obesity therapies.

  • pancreatic polypeptide reduces appetite and Food Intake in humans
    The Journal of Clinical Endocrinology and Metabolism, 2003
    Co-Authors: Rachel L Batterham, C Le W Roux, Mark Cohen, Adrian Park, Sandra M Ellis, Michael Patterson, Gary Frost, M A Ghatei, Stephen R. Bloom
    Abstract:

    Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to ingestion of Food. Plasma PP has been shown to be reduced in conditions associated with increased Food Intake and elevated in anorexia nervosa. In addition peripheral administration of PP has been shown to decrease Food Intake in rodents. These findings suggest that PP may act as a circulating factor that regulates Food Intake. Therefore we investigated the effect of intravenous infusion of PP (10 pmol/kg/min) on appetite and Food Intake in a randomised double-blind placebo-controlled crossover study in ten healthy volunteers. Infusion of PP reduced appetite and decreased the energy Intake at a buffet lunch two hours post-infusion by 21.8 ± 5.7% (P < 0.01). More importantly the inhibition of Food Intake was sustained, such that energy Intake, as assessed by Food diaries, was significantly reduced both the evening of the study and the following morning. Overall PP infusion reduced cumulative 24-hour energy Intake by 25.3…

D. G. Baskin – One of the best experts on this subject based on the ideXlab platform.

  • central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, D Porte, Randy J. Seeley, Stephen C. Woods, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from inherited or acquired defects in their function.

  • Central nervous system control of Food Intake
    Nature, 2000
    Co-Authors: M W Schwartz, S. C. Woods, D Porte, Randy J. Seeley, D. G. Baskin
    Abstract:

    New information regarding neuronal circuits that control Food Intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy Intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its Importance to human health, Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity the growing number of such signalling molecules indicates that Food Intake is controlled by a highly complex process. Se better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of Food Intake and the means by which obesity can arise from Inherited or acquired defects in their function.