Brain-derived neurotrophic factor (BDNF) in the hypothalamic ventromedial nucleus increases energy expenditure
Abstract Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated th...
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| Published in | Brain research Vol. 1336; pp. 66 - 77 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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Amsterdam
Elsevier B.V
08.06.2010
Elsevier |
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| Online Access | Get full text |
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| Abstract | Abstract Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 μg) was injected into the VMH of male Sprague–Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24 h in an indirect calorimeter. Animals were sacrificed 4 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9 h immediately after BDNF injection. BDNF increased SPA and EE during SPA (aEE) within 9 h after injection although BDNF had no effect on 0–24 h SPA and aEE. BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. |
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| AbstractList | Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 μg) was injected into the VMH of male Sprague Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24 h in an indirect calorimeter. Animals were sacrificed 4 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9 h immediately after BDNF injection. BDNF increased SPA and aEE within 9 h after injection although BDNF had no effect on 0–24h SPA and EE during SPA (aEE). BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 microg) was injected into the VMH of male Sprague-Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24h in an indirect calorimeter. Animals were sacrificed 4h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9h immediately after BDNF injection. BDNF increased SPA and EE during SPA (aEE) within 9h after injection although BDNF had no effect on 0-24h SPA and aEE. BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5I14g) was injected into the VMH of male Sprague-Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24h in an indirect calorimeter. Animals were sacrificed 4h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9h immediately after BDNF injection. BDNF increased SPA and EE during SPA (aEE) within 9h after injection although BDNF had no effect on 0-24h SPA and aEE. BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. Abstract Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 μg) was injected into the VMH of male Sprague–Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24 h in an indirect calorimeter. Animals were sacrificed 4 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9 h immediately after BDNF injection. BDNF increased SPA and EE during SPA (aEE) within 9 h after injection although BDNF had no effect on 0–24 h SPA and aEE. BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy expenditure. The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism. Our previous work indicated that BDNF in the VMH reduced food intake. The purposes of the study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 μg) was injected into the VMH of male Sprague–Dawley rats and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24 h in an indirect calorimeter. Animals were sacrificed 4 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food and water intake, and body weight gain. Heat production and RMR were significantly elevated for 9 h immediately after BDNF injection. BDNF increased SPA and EE during SPA (aEE) within 9 h after injection although BDNF had no effect on 0–24 h SPA and aEE. BDNF did not induce a significant increase in BAT UCP1 expression. In conclusion, VMH BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence energy balance. |
| Author | Levine, Allen S Wang, ChuanFeng Billington, Charles J Bomberg, Eric Kotz, Catherine M |
| AuthorAffiliation | 1 Veterans Affairs Medical Center, One Veterans Drive, Research Route 151, Minneapolis, MN 55417, USA 4 Graduate Program in Neuroscience, University of Minnesota, 1334 Eckles Avenue, Saint Paul, MN 55108, USA 2 Minnesota Obesity Center, One Veterans Drive, Research Route 151, Minneapolis, MN 55417, USA 3 Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, Saint Paul, MN 55108, USA |
| AuthorAffiliation_xml | – name: 3 Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, Saint Paul, MN 55108, USA – name: 1 Veterans Affairs Medical Center, One Veterans Drive, Research Route 151, Minneapolis, MN 55417, USA – name: 2 Minnesota Obesity Center, One Veterans Drive, Research Route 151, Minneapolis, MN 55417, USA – name: 4 Graduate Program in Neuroscience, University of Minnesota, 1334 Eckles Avenue, Saint Paul, MN 55108, USA |
| Author_xml | – sequence: 1 fullname: Wang, ChuanFeng – sequence: 2 fullname: Bomberg, Eric – sequence: 3 fullname: Billington, Charles J – sequence: 4 fullname: Levine, Allen S – sequence: 5 fullname: Kotz, Catherine M |
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| Keywords | EE aEE EE during SPA Food intake regulation BDNF SPA UCP1 mean resting metabolic rate energy expenditure VMH hypothalamic ventromedial nucleus uncoupling protein 1 rEE EE during resting Thermogenesis brown adipose tissue BAT RMR spontaneous physical activity mRMR Energy homeostasis resting metabolic rate brain-derived neurotrophic factor Resting metabolic rate Spontaneous physical activity Rat Rodentia Central nervous system Homeostasis Hypothalamus Feeding Encephalon Vertebrata Rest Mammalia Food intake Energetic cost Animal Ventromedial nucleus Brain derived neurotrophic factor |
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| Snippet | Abstract Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on... Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified for its effect on energy... |
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| SubjectTerms | Adipose Tissue, Brown - metabolism Animals Basal Metabolism Biological and medical sciences Brain-Derived Neurotrophic Factor - metabolism Carbon Dioxide - metabolism Eating - physiology Energy homeostasis Energy Metabolism - physiology Feeding. Feeding behavior Food intake regulation Fundamental and applied biological sciences. Psychology Gene Expression Ion Channels - biosynthesis Ion Channels - genetics Male Mitochondrial Proteins - biosynthesis Mitochondrial Proteins - genetics Motor Activity - physiology Neurology Oxygen Consumption - physiology Rats Rats, Sprague-Dawley Resting metabolic rate Reverse Transcriptase Polymerase Chain Reaction Spontaneous physical activity Thermogenesis Thermogenesis - physiology Uncoupling Protein 1 Ventromedial Hypothalamic Nucleus - metabolism Vertebrates: anatomy and physiology, studies on body, several organs or systems Weight Gain |
| Title | Brain-derived neurotrophic factor (BDNF) in the hypothalamic ventromedial nucleus increases energy expenditure |
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