Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit
ObjectiveButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate.DesignA...
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| Published in | Gut Vol. 67; no. 7; pp. 1269 - 1279 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BMJ Publishing Group LTD
01.07.2018
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| Subjects | |
| Online Access | Get full text |
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| Abstract | ObjectiveButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate.DesignAcute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice.ResultsAcute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT.ConclusionButyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT. |
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| AbstractList | OBJECTIVEButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate.DESIGNAcute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice.RESULTSAcute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT.CONCLUSIONButyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT. Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate. Acute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice. Acute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT. Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT. Objective Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate. Design Acute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice. Results Acute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT. Conclusion Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT. Objective Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate. Design Acute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice. Results Acute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT. Conclusion Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT. |
| Author | Katiraei, Saeed Berbée, Jimmy F P van den Heuvel, José K Meijer, Onno C Kooijman, Sander Gao, Yuanqing Chung, Chih Kit Zhou, Enchen Heijink, Marieke Willems van Dijk, Ko Wang, Yanan Li, Zhuang Yi, Chun-Xia Giera, Martin Rensen, Patrick C N Groen, Albert K |
| Author_xml | – sequence: 1 givenname: Zhuang surname: Li fullname: Li, Zhuang email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 2 givenname: Chun-Xia surname: Yi fullname: Yi, Chun-Xia email: y.Wang@lumc.nl organization: Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands – sequence: 3 givenname: Saeed surname: Katiraei fullname: Katiraei, Saeed email: y.Wang@lumc.nl organization: Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands – sequence: 4 givenname: Sander surname: Kooijman fullname: Kooijman, Sander email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 5 givenname: Enchen surname: Zhou fullname: Zhou, Enchen email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 6 givenname: Chih Kit surname: Chung fullname: Chung, Chih Kit email: y.Wang@lumc.nl organization: Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 7 givenname: Yuanqing surname: Gao fullname: Gao, Yuanqing email: y.Wang@lumc.nl organization: Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands – sequence: 8 givenname: José K surname: van den Heuvel fullname: van den Heuvel, José K email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 9 givenname: Onno C surname: Meijer fullname: Meijer, Onno C email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 10 givenname: Jimmy F P surname: Berbée fullname: Berbée, Jimmy F P email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 11 givenname: Marieke surname: Heijink fullname: Heijink, Marieke email: y.Wang@lumc.nl organization: Center for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, The Netherlands – sequence: 12 givenname: Martin surname: Giera fullname: Giera, Martin email: y.Wang@lumc.nl organization: Center for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, The Netherlands – sequence: 13 givenname: Ko surname: Willems van Dijk fullname: Willems van Dijk, Ko email: y.Wang@lumc.nl organization: Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands – sequence: 14 givenname: Albert K surname: Groen fullname: Groen, Albert K email: y.Wang@lumc.nl organization: Department of Pediatrics, University of Groningen, Groningen, The Netherlands – sequence: 15 givenname: Patrick C N surname: Rensen fullname: Rensen, Patrick C N email: y.Wang@lumc.nl organization: Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands – sequence: 16 givenname: Yanan surname: Wang fullname: Wang, Yanan email: y.Wang@lumc.nl organization: Department of Pediatrics, University of Groningen, Groningen, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29101261$$D View this record in MEDLINE/PubMed |
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| Snippet | ObjectiveButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate... Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on... Objective Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate... Objective Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate... OBJECTIVEButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate... |
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| SubjectTerms | Acute effects Adipose tissue Adipose tissue (brown) Appetite Body fat Brain stem Clinical medicine Diabetes Diet Dietary supplements Energy Energy expenditure Energy intake Energy metabolism Epigenetics Fatty acids Fatty liver Food Food intake Gastrointestinal surgery High fat diet Hypothalamus Insulin resistance Intravenous administration Metabolic syndrome Nervous system Neuropeptide Y Obesity Oxidation Rodents Satiety Solitary tract nucleus Steatosis Studies Vagotomy Vagus nerve Weight control |
| Title | Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit |
| URI | http://dx.doi.org/10.1136/gutjnl-2017-314050 https://www.ncbi.nlm.nih.gov/pubmed/29101261 https://www.proquest.com/docview/2067714024 https://search.proquest.com/docview/1960930738 |
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