A role for the endogenous opioid β-endorphin in energy homeostasis
Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and β-endorphin neuropeptides are processed from POMC and putatively coreleased at axon...
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2003
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n5_p1753_Appleyard http://hdl.handle.net/20.500.12110/paper_00137227_v144_n5_p1753_Appleyard |
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paper:paper_00137227_v144_n5_p1753_Appleyard2023-06-08T14:36:10Z A role for the endogenous opioid β-endorphin in energy homeostasis beta endorphin leptin melanocortin naloxone neuropeptide opiate opiate antagonist proopiomelanocortin beta endorphin glucose leptin naloxone narcotic antagonist neuropeptide Y animal experiment animal model animal tissue anorexia article body weight controlled study energy balance food intake hyperphagia hypothalamus male mouse nerve ending nonhuman obesity priority journal animal blood drug effect eating energy metabolism homeostasis hyperinsulinism hyperphagia metabolism mouse mutant obesity physiology reference value Animals beta-Endorphin Eating Energy Metabolism Glucose Homeostasis Hyperinsulinism Hyperphagia Leptin Male Mice Mice, Knockout Naloxone Narcotic Antagonists Neuropeptide Y Obesity Reference Values Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and β-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack β-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, β-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to β-endorphin that physiologically stimulates feeding. These genetic data indicate that β-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of β-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis. 2003 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n5_p1753_Appleyard http://hdl.handle.net/20.500.12110/paper_00137227_v144_n5_p1753_Appleyard |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
beta endorphin leptin melanocortin naloxone neuropeptide opiate opiate antagonist proopiomelanocortin beta endorphin glucose leptin naloxone narcotic antagonist neuropeptide Y animal experiment animal model animal tissue anorexia article body weight controlled study energy balance food intake hyperphagia hypothalamus male mouse nerve ending nonhuman obesity priority journal animal blood drug effect eating energy metabolism homeostasis hyperinsulinism hyperphagia metabolism mouse mutant obesity physiology reference value Animals beta-Endorphin Eating Energy Metabolism Glucose Homeostasis Hyperinsulinism Hyperphagia Leptin Male Mice Mice, Knockout Naloxone Narcotic Antagonists Neuropeptide Y Obesity Reference Values |
| spellingShingle |
beta endorphin leptin melanocortin naloxone neuropeptide opiate opiate antagonist proopiomelanocortin beta endorphin glucose leptin naloxone narcotic antagonist neuropeptide Y animal experiment animal model animal tissue anorexia article body weight controlled study energy balance food intake hyperphagia hypothalamus male mouse nerve ending nonhuman obesity priority journal animal blood drug effect eating energy metabolism homeostasis hyperinsulinism hyperphagia metabolism mouse mutant obesity physiology reference value Animals beta-Endorphin Eating Energy Metabolism Glucose Homeostasis Hyperinsulinism Hyperphagia Leptin Male Mice Mice, Knockout Naloxone Narcotic Antagonists Neuropeptide Y Obesity Reference Values A role for the endogenous opioid β-endorphin in energy homeostasis |
| topic_facet |
beta endorphin leptin melanocortin naloxone neuropeptide opiate opiate antagonist proopiomelanocortin beta endorphin glucose leptin naloxone narcotic antagonist neuropeptide Y animal experiment animal model animal tissue anorexia article body weight controlled study energy balance food intake hyperphagia hypothalamus male mouse nerve ending nonhuman obesity priority journal animal blood drug effect eating energy metabolism homeostasis hyperinsulinism hyperphagia metabolism mouse mutant obesity physiology reference value Animals beta-Endorphin Eating Energy Metabolism Glucose Homeostasis Hyperinsulinism Hyperphagia Leptin Male Mice Mice, Knockout Naloxone Narcotic Antagonists Neuropeptide Y Obesity Reference Values |
| description |
Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and β-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack β-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, β-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to β-endorphin that physiologically stimulates feeding. These genetic data indicate that β-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of β-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis. |
| title |
A role for the endogenous opioid β-endorphin in energy homeostasis |
| title_short |
A role for the endogenous opioid β-endorphin in energy homeostasis |
| title_full |
A role for the endogenous opioid β-endorphin in energy homeostasis |
| title_fullStr |
A role for the endogenous opioid β-endorphin in energy homeostasis |
| title_full_unstemmed |
A role for the endogenous opioid β-endorphin in energy homeostasis |
| title_sort |
role for the endogenous opioid β-endorphin in energy homeostasis |
| publishDate |
2003 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n5_p1753_Appleyard http://hdl.handle.net/20.500.12110/paper_00137227_v144_n5_p1753_Appleyard |
| _version_ |
1768544894147624960 |