Luis Miguel García-Segura
- Published in print:
- 2009
- Published Online:
- May 2009
- ISBN:
- 9780195326611
- eISBN:
- 9780199864881
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195326611.003.0005
- Subject:
- Neuroscience, Behavioral Neuroscience, Neuroendocrine and Autonomic
This chapter examines the role of peptide hormones in the regulation of neural mutability and the involved cellular and molecular mechanisms. It first considers the effects of vasopressin and ...
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This chapter examines the role of peptide hormones in the regulation of neural mutability and the involved cellular and molecular mechanisms. It first considers the effects of vasopressin and oxytocin—hormones released in the neurohypophysis. It then analyzes the plastic actions of corticotropin-releasing hormone, prolactin, gonadotropin-releasing hormone, insulin, growth hormone, insulin-like growth factor-I (GF-I), erythropoietin and angiotensin. Finally, the chapter considers the effects of feeding hormones leptin, ghrelin, and glucagon-like peptide-1 on neural plasticity. These hormones exert important plastic actions on the organization of neuronal circuits involved in the control of food intake and energy balance, but also promote plastic remodeling of cognitive brain areas.Less
This chapter examines the role of peptide hormones in the regulation of neural mutability and the involved cellular and molecular mechanisms. It first considers the effects of vasopressin and oxytocin—hormones released in the neurohypophysis. It then analyzes the plastic actions of corticotropin-releasing hormone, prolactin, gonadotropin-releasing hormone, insulin, growth hormone, insulin-like growth factor-I (GF-I), erythropoietin and angiotensin. Finally, the chapter considers the effects of feeding hormones leptin, ghrelin, and glucagon-like peptide-1 on neural plasticity. These hormones exert important plastic actions on the organization of neuronal circuits involved in the control of food intake and energy balance, but also promote plastic remodeling of cognitive brain areas.
Edmund T. Rolls
- Published in print:
- 2005
- Published Online:
- September 2009
- ISBN:
- 9780198570035
- eISBN:
- 9780191693793
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780198570035.003.0005
- Subject:
- Neuroscience, Behavioral Neuroscience
This chapter covers peripheral signals for hunger and satiety. Internal regulators of appetite and body weight are described, such as hormones including leptin. Brain mechanisms are explained and the ...
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This chapter covers peripheral signals for hunger and satiety. Internal regulators of appetite and body weight are described, such as hormones including leptin. Brain mechanisms are explained and the question asked: What make food taste pleasant? Sensory-specific satiety is described. The effect of variety on food intake; the hypothalamus, orbitofrontal cortex, and amygdale; the normal and abnormal control of appetite, including obesity and anorexia, are also covered.Less
This chapter covers peripheral signals for hunger and satiety. Internal regulators of appetite and body weight are described, such as hormones including leptin. Brain mechanisms are explained and the question asked: What make food taste pleasant? Sensory-specific satiety is described. The effect of variety on food intake; the hypothalamus, orbitofrontal cortex, and amygdale; the normal and abnormal control of appetite, including obesity and anorexia, are also covered.
Barry E. Levin and Alison M. Strack
- Published in print:
- 2011
- Published Online:
- May 2011
- ISBN:
- 9780195306637
- eISBN:
- 9780199894130
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195306637.003.0017
- Subject:
- Neuroscience, Neuroendocrine and Autonomic
Energy homeostasis, the balance of energy intake, assimilation, expenditure, and storage, is regulated by a distributed network of specialized metabolic sensing neurons that receive viscerosensory ...
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Energy homeostasis, the balance of energy intake, assimilation, expenditure, and storage, is regulated by a distributed network of specialized metabolic sensing neurons that receive viscerosensory afferent input and hormonal and metabolic signals from the periphery. These neurons then activate autonomic pathways controlling physiological functions, metabolism, and hormone secretion. Leptin and insulin levels, which reflect the size of adipose stores, act centrally to inhibit food intake and increase sympathetically-mediated thermogenesis as adipose stores increase when energy intake exceeds expenditure. As stores are depleted during fasting, leptin and insulin promote hunger and food seeking. The effects of leptin and insulin on metabolic sensing neurons are modulated by autonomic afferent, gut hormone and metabolic substrate feedback. This finely controlled regulation of energy and glucose homeostasis is perturbed by the superimposition of obesity and diabetes, particularly in genetically predisposed individuals.Less
Energy homeostasis, the balance of energy intake, assimilation, expenditure, and storage, is regulated by a distributed network of specialized metabolic sensing neurons that receive viscerosensory afferent input and hormonal and metabolic signals from the periphery. These neurons then activate autonomic pathways controlling physiological functions, metabolism, and hormone secretion. Leptin and insulin levels, which reflect the size of adipose stores, act centrally to inhibit food intake and increase sympathetically-mediated thermogenesis as adipose stores increase when energy intake exceeds expenditure. As stores are depleted during fasting, leptin and insulin promote hunger and food seeking. The effects of leptin and insulin on metabolic sensing neurons are modulated by autonomic afferent, gut hormone and metabolic substrate feedback. This finely controlled regulation of energy and glucose homeostasis is perturbed by the superimposition of obesity and diabetes, particularly in genetically predisposed individuals.
William R. Clark and Michael Grunstein
- Published in print:
- 2004
- Published Online:
- April 2010
- ISBN:
- 9780195178005
- eISBN:
- 9780199893331
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780195178005.003.0010
- Subject:
- Biology, Evolutionary Biology / Genetics
Obesity is an increasing medical problem in Western societies. There is little question that body weight, like many other physical features, is under genetic control. Each person has a genetically ...
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Obesity is an increasing medical problem in Western societies. There is little question that body weight, like many other physical features, is under genetic control. Each person has a genetically determined “set point” weight that is maintained within a narrow range with normal caloric intake. What are the factors that determine the set point? Are genes involved in the behaviors that lead to overeating and undereating that moves the body above or below the set point? Leptin is a normal protein that has a powerful effect on the perception of satiety. Others are being studied for similar effects. Neuropeptide Y also affects appetite. Disorders such as anorexia and bulemia have a strong genetic component, likely through genes and receptors for serotonin, which is also involved in impulsive behaviors and depression.Less
Obesity is an increasing medical problem in Western societies. There is little question that body weight, like many other physical features, is under genetic control. Each person has a genetically determined “set point” weight that is maintained within a narrow range with normal caloric intake. What are the factors that determine the set point? Are genes involved in the behaviors that lead to overeating and undereating that moves the body above or below the set point? Leptin is a normal protein that has a powerful effect on the perception of satiety. Others are being studied for similar effects. Neuropeptide Y also affects appetite. Disorders such as anorexia and bulemia have a strong genetic component, likely through genes and receptors for serotonin, which is also involved in impulsive behaviors and depression.
Richard G. Bribiescas and Peter T. Ellison
- Published in print:
- 2007
- Published Online:
- April 2010
- ISBN:
- 9780199207466
- eISBN:
- 9780191728167
- Item type:
- chapter
- Publisher:
- Oxford University Press
- DOI:
- 10.1093/acprof:oso/9780199207466.003.0007
- Subject:
- Biology, Evolutionary Biology / Genetics
Trade-offs between reproduction and maintenance can compromise health. Male hormones such as testosterone regulate energy allocation between reproductive effort and survival; this is made evident ...
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Trade-offs between reproduction and maintenance can compromise health. Male hormones such as testosterone regulate energy allocation between reproductive effort and survival; this is made evident when immunological challenges cause changes in reproductive hormones. Female hormones adjust energy allocation between investment in ovarian function, somatic investment, and present offspring (lactation), implementing trade-offs between present and future reproduction. Metabolic hormones respond to environmental cues to sequester or liberate energetic resources such as glucose and fat. Mismatch between environmental conditions and the expression of metabolic hormones are likely to underlie variation in obesity and diabetes. Lifetime variation in endogenous reproductive hormones suggests a trade-off between early benefits for reproduction and later costs against survivorship expressed in population differences in the incidence of reproductive tumors, such as breast and prostate cancer.Less
Trade-offs between reproduction and maintenance can compromise health. Male hormones such as testosterone regulate energy allocation between reproductive effort and survival; this is made evident when immunological challenges cause changes in reproductive hormones. Female hormones adjust energy allocation between investment in ovarian function, somatic investment, and present offspring (lactation), implementing trade-offs between present and future reproduction. Metabolic hormones respond to environmental cues to sequester or liberate energetic resources such as glucose and fat. Mismatch between environmental conditions and the expression of metabolic hormones are likely to underlie variation in obesity and diabetes. Lifetime variation in endogenous reproductive hormones suggests a trade-off between early benefits for reproduction and later costs against survivorship expressed in population differences in the incidence of reproductive tumors, such as breast and prostate cancer.
Linda A. Parker
- Published in print:
- 2017
- Published Online:
- September 2017
- ISBN:
- 9780262035798
- eISBN:
- 9780262338448
- Item type:
- chapter
- Publisher:
- The MIT Press
- DOI:
- 10.7551/mitpress/9780262035798.003.0007
- Subject:
- Neuroscience, Research and Theory
The endcoannabinoid system is an important regulator of appetite, food preference and body weight. It not only regulates metabolic feeding related hormones (leptin, ghrelin) in the brain and gut, but ...
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The endcoannabinoid system is an important regulator of appetite, food preference and body weight. It not only regulates metabolic feeding related hormones (leptin, ghrelin) in the brain and gut, but also regulates the brain reward circuitry involved in palatability based feeding. One of the primary roles of the endocannabinoid system is in the homeostatic regulation of feeding behaviour. New treatments for obesity are being developed that attempt to harvest the anti-obesity effects of the CB1 antagonist, rimonabant, but that are devoid of the psychiatric side effects that became clearly known only after it was widely prescribed.Less
The endcoannabinoid system is an important regulator of appetite, food preference and body weight. It not only regulates metabolic feeding related hormones (leptin, ghrelin) in the brain and gut, but also regulates the brain reward circuitry involved in palatability based feeding. One of the primary roles of the endocannabinoid system is in the homeostatic regulation of feeding behaviour. New treatments for obesity are being developed that attempt to harvest the anti-obesity effects of the CB1 antagonist, rimonabant, but that are devoid of the psychiatric side effects that became clearly known only after it was widely prescribed.
