Nolan, Laurence J.,

Scheurink, Anton J.W.,

English

University of Groningen Digital Archive

Appetite, 1996, 26, 304
Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTON
J. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCE
J. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.
The mobilization, storage and utilization of the diVerent energy substrates is regulated by
sensitive and very speciﬁc hormonal and neural mechanisms. Increased parasympathetic
activity leads to storage of glucose and free fatty acids (FFA) while activation of the
sympathetic branch of the autonomic nervous system (ANS) results in the mobilization of
FFA and glucose from storage tissues. The latter is accomplished by both neuronal no-
repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.
The relation between autonomic activity and substrate availability might be bidirectional:
an increased availability of energy substrates could activate the parasympathetic branch of
the ANS, while a decreased availability of glucose and/or FFA may lead to increased
sympatheticoutﬂow.Onesetofexperimentsinvestigatedthemetabolicandhormonalresponses
that occur during food intake or intravenous or intragastric administration of glucose (Strubbe,
1992). Food intake was accompanied by the early insulin response (EIR), an increase in
plasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressed
byprior administrationof atropineorsubdiaphragmatic vagotomy.Administration ofatropine
also attenuated and delayed the insulin response to intravenous or intragastric glucose load
indicating that the parasympathetic nervous system is also involved in the dynamics of insulin
secretion during hyperglycemia.
A second set of experiments was conducted to examine the metabolic and hormonal
responses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;
Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy-
d-glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered and
catecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-
lation of adrenal E secretion combined with a small NE outﬂow. Lipoprivation stimulated
only the neuronal branch of the sympathetic nervous system without any eVect on adrenal E
release. The ﬁnding that decreased glucose availability leads to adrenomedullary secretion of
E is compatible with the fact that circulating E is an important mediator of hepatic glucose
production in rats. Likewise, the selective increase in neuronal outﬂow of NE after MA
administration can be considered a metabolically appropriate response to blockade of FFA
oxidation since neuronal NE serves as the physiological mediator of lipolysis in white adipose
tissue. These data indicate that distinct metabolic signals are capable of exerting a selective
and functional control of sympathoadrenal outﬂow.
The hypothalamus is the likely source of control (Scheurink & SteVens, 1990). A possible
mechanism is serotonin (5-HT) as it is able to aVect E outﬂow without aVecting NE release.
When administered to sleeping rats, fenﬂuramine is associated with a rise in E and has no
eVect on NE. There is also a corresponding increase in circulating glucose while FFA levels
remain unchanged. These eVects can be blocked by 5-HT-1a receptor blockade. In preliminary
studies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamus
measured by microdialysis and increased circulating levels of E. MA administration did not
aVect either medial hypothalamic 5-HT levels or plasma E.
Taken together, the data demonstrate that metabolic needs are regulated via changes in
the functioning of the diVerent branches of the autonomic nervous system. In turn, metabolic
states can also profoundly aVect the functioning of the autonomic regulatory mechanisms.
The hypothalamus may function as a center in the brain coordinating autonomic outﬂow and
energy balance.
Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-
privation in rats. Physiology and Behavior, 53, 995–1000.
Scheurink, A. J. W. & SteVens, A. B. (1990) Central and peripheral control of sympathoadrenal
activity and energy metabolism in rats. Physiology and Behavior, 48, 909–20.
Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditioned
insulin secretion in the rat. American Journal of Physiology, 263, R615–18.
Van Dijk, G., Scheurink, A. J. W., Ritter, S., & SteVens A. B. (1995) Glucose homeostasis and
sympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759–64.
Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on Appetitive
Behavior, 2 November 1995 (Harry R. KissileV, Chairman). Supported in part by HoVmann-La Roche;
McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.
Luke’s/Roosevelt Hospital.
0195–6663/96/030304+01 $18.00/0 Ó 1996 Academic Press Limited

Food Intake, Fuel Homeostasis, and the Autonomic Nervous System

Scheurink, AJW

Nolan, LJ

University of Groningen Research Database

  
 University of Groningen
Food intake, fuel homeostasis, and the autonomic nervous system.
Scheurink, Antonius; Nolan, LJ
Published in:
Appetite
DOI:
10.1006/appe.1996.0026
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from
it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date:
1996
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
Scheurink, A. J. W., & Nolan, L. J. (1996). Food intake, fuel homeostasis, and the autonomic nervous
system. Appetite, 26(3), 304-304. DOI: 10.1006/appe.1996.0026
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the
author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately
and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the
number of authors shown on this cover page is limited to 10 maximum.
Download date: 10-02-2018
Appetite, 1996, 26, 304
Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTON
J. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCE
J. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.
The mobilization, storage and utilization of the different energy substrates is regulated by
sensitive and very speci®c hormonal and neural mechanisms. Increased parasympathetic
activity leads to storage of glucose and free fatty acids (FFA) while activation of the
sympathetic branch of the autonomic nervous system (ANS) results in the mobilization of
FFA and glucose from storage tissues. The latter is accomplished by both neuronal no-
repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.
The relation between autonomic activity and substrate availability might be bidirectional:
an increased availability of energy substrates could activate the parasympathetic branch of
the ANS, while a decreased availability of glucose and/or FFA may lead to increased
sympathetic out¯ow. One set of experiments investigated the metabolic and hormonal responses
that occur during food intake or intravenous or intragastric administration of glucose (Strubbe,
1992). Food intake was accompanied by the early insulin response (EIR), an increase in
plasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressed
by prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropine
also attenuated and delayed the insulin response to intravenous or intragastric glucose load
indicating that the parasympathetic nervous system is also involved in the dynamics of insulin
secretion during hyperglycemia.
A second set of experiments was conducted to examine the metabolic and hormonal
responses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;
Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy-
-glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered and
catecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-
lation of adrenal E secretion combined with a small NE out¯ow. Lipoprivation stimulated
only the neuronal branch of the sympathetic nervous system without any effect on adrenal E
release. The ®nding that decreased glucose availability leads to adrenomedullary secretion of
E is compatible with the fact that circulating E is an important mediator of hepatic glucose
production in rats. Likewise, the selective increase in neuronal out¯ow of NE after MA
administration can be considered a metabolically appropriate response to blockade of FFA
oxidation since neuronal NE serves as the physiological mediator of lipolysis in white adipose
tissue. These data indicate that distinct metabolic signals are capable of exerting a selective
and functional control of sympathoadrenal out¯ow.
The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possible
mechanism is serotonin (5-HT) as it is able to affect E out¯ow without affecting NE release.
When administered to sleeping rats, fen¯uramine is associated with a rise in E and has no
effect on NE. There is also a corresponding increase in circulating glucose while FFA levels
remain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminary
studies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamus
measured by microdialysis and increased circulating levels of E. MA administration did not
affect either medial hypothalamic 5-HT levels or plasma E.
Taken together, the data demonstrate that metabolic needs are regulated via changes in
the functioning of the different branches of the autonomic nervous system. In turn, metabolic
states can also profoundly affect the functioning of the autonomic regulatory mechanisms.
The hypothalamus may function as a center in the brain coordinating autonomic out¯ow and
energy balance.
Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-
privation in rats. Physiology and Behavior, 53, 995±1000.
Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenal
activity and energy metabolism in rats. Physiology and Behavior, 48, 909±20.
Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditioned
insulin secretion in the rat. American Journal of Physiology, 263, R615±18.
Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis and
sympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759±64.
Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on Appetitive
Behavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;
McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.
Luke's/Roosevelt Hospital.
0195±6663/96/030304+01 $18.00/0  1996 Academic Press Limited


Food intake, fuel homeostasis, and the autonomic nervous system.

Scheurink, A J W

Nolan, L J

ARTS repository - University of Groningen

   University of GroningenFood intake, fuel homeostasis, and the autonomic nervous systemScheurink, A J W; Nolan, L JPublished in:AppetiteDOI:10.1006/appe.1996.0026IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1996Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Scheurink, A. J. W., & Nolan, L. J. (1996). Food intake, fuel homeostasis, and the autonomic nervoussystem. Appetite, 26(3), 304-304. https://doi.org/10.1006/appe.1996.0026CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 30-10-2023Appetite, 1996, 26, 304Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTONJ. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCEJ. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.The mobilization, storage and utilization of the different energy substrates is regulated bysensitive and very specific hormonal and neural mechanisms. Increased parasympatheticactivity leads to storage of glucose and free fatty acids (FFA) while activation of thesympathetic branch of the autonomic nervous system (ANS) results in the mobilization ofFFA and glucose from storage tissues. The latter is accomplished by both neuronal no-repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.The relation between autonomic activity and substrate availability might be bidirectional:an increased availability of energy substrates could activate the parasympathetic branch ofthe ANS, while a decreased availability of glucose and/or FFA may lead to increasedsympathetic outflow. One set of experiments investigated the metabolic and hormonal responsesthat occur during food intake or intravenous or intragastric administration of glucose (Strubbe,1992). Food intake was accompanied by the early insulin response (EIR), an increase inplasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressedby prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropinealso attenuated and delayed the insulin response to intravenous or intragastric glucose loadindicating that the parasympathetic nervous system is also involved in the dynamics of insulinsecretion during hyperglycemia.A second set of experiments was conducted to examine the metabolic and hormonalresponses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy--glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered andcatecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-lation of adrenal E secretion combined with a small NE outflow. Lipoprivation stimulatedonly the neuronal branch of the sympathetic nervous system without any effect on adrenal Erelease. The finding that decreased glucose availability leads to adrenomedullary secretion ofE is compatible with the fact that circulating E is an important mediator of hepatic glucoseproduction in rats. Likewise, the selective increase in neuronal outflow of NE after MAadministration can be considered a metabolically appropriate response to blockade of FFAoxidation since neuronal NE serves as the physiological mediator of lipolysis in white adiposetissue. These data indicate that distinct metabolic signals are capable of exerting a selectiveand functional control of sympathoadrenal outflow.The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possiblemechanism is serotonin (5-HT) as it is able to affect E outflow without affecting NE release.When administered to sleeping rats, fenfluramine is associated with a rise in E and has noeffect on NE. There is also a corresponding increase in circulating glucose while FFA levelsremain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminarystudies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamusmeasured by microdialysis and increased circulating levels of E. MA administration did notaffect either medial hypothalamic 5-HT levels or plasma E.Taken together, the data demonstrate that metabolic needs are regulated via changes inthe functioning of the different branches of the autonomic nervous system. In turn, metabolicstates can also profoundly affect the functioning of the autonomic regulatory mechanisms.The hypothalamus may function as a center in the brain coordinating autonomic outflow andenergy balance.Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-privation in rats. Physiology and Behavior, 53, 995–1000.Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenalactivity and energy metabolism in rats. Physiology and Behavior, 48, 909–20.Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditionedinsulin secretion in the rat. American Journal of Physiology, 263, R615–18.Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis andsympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759–64.Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on AppetitiveBehavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.Luke’s/Roosevelt Hospital.0195–6663/96/030304+01 $18.00/0  1996 Academic Press Limited

Food intake, fuel homeostasis, and the autonomic nervous system

University of Groningen

   University of GroningenFood intake, fuel homeostasis, and the autonomic nervous system.Scheurink, AJW; Nolan, LJPublished in:AppetiteDOI:10.1006/appe.1996.0026IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1996Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Scheurink, AJW., & Nolan, LJ. (1996). Food intake, fuel homeostasis, and the autonomic nervous system.Appetite, 26(3), 304-304. https://doi.org/10.1006/appe.1996.0026CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 12-11-2019Appetite, 1996, 26, 304Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTONJ. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCEJ. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.The mobilization, storage and utilization of the different energy substrates is regulated bysensitive and very speci®c hormonal and neural mechanisms. Increased parasympatheticactivity leads to storage of glucose and free fatty acids (FFA) while activation of thesympathetic branch of the autonomic nervous system (ANS) results in the mobilization ofFFA and glucose from storage tissues. The latter is accomplished by both neuronal no-repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.The relation between autonomic activity and substrate availability might be bidirectional:an increased availability of energy substrates could activate the parasympathetic branch ofthe ANS, while a decreased availability of glucose and/or FFA may lead to increasedsympathetic out¯ow. One set of experiments investigated the metabolic and hormonal responsesthat occur during food intake or intravenous or intragastric administration of glucose (Strubbe,1992). Food intake was accompanied by the early insulin response (EIR), an increase inplasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressedby prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropinealso attenuated and delayed the insulin response to intravenous or intragastric glucose loadindicating that the parasympathetic nervous system is also involved in the dynamics of insulinsecretion during hyperglycemia.A second set of experiments was conducted to examine the metabolic and hormonalresponses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy--glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered andcatecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-lation of adrenal E secretion combined with a small NE out¯ow. Lipoprivation stimulatedonly the neuronal branch of the sympathetic nervous system without any effect on adrenal Erelease. The ®nding that decreased glucose availability leads to adrenomedullary secretion ofE is compatible with the fact that circulating E is an important mediator of hepatic glucoseproduction in rats. Likewise, the selective increase in neuronal out¯ow of NE after MAadministration can be considered a metabolically appropriate response to blockade of FFAoxidation since neuronal NE serves as the physiological mediator of lipolysis in white adiposetissue. These data indicate that distinct metabolic signals are capable of exerting a selectiveand functional control of sympathoadrenal out¯ow.The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possiblemechanism is serotonin (5-HT) as it is able to affect E out¯ow without affecting NE release.When administered to sleeping rats, fen¯uramine is associated with a rise in E and has noeffect on NE. There is also a corresponding increase in circulating glucose while FFA levelsremain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminarystudies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamusmeasured by microdialysis and increased circulating levels of E. MA administration did notaffect either medial hypothalamic 5-HT levels or plasma E.Taken together, the data demonstrate that metabolic needs are regulated via changes inthe functioning of the different branches of the autonomic nervous system. In turn, metabolicstates can also profoundly affect the functioning of the autonomic regulatory mechanisms.The hypothalamus may function as a center in the brain coordinating autonomic out¯ow andenergy balance.Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-privation in rats. Physiology and Behavior, 53, 995±1000.Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenalactivity and energy metabolism in rats. Physiology and Behavior, 48, 909±20.Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditionedinsulin secretion in the rat. American Journal of Physiology, 263, R615±18.Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis andsympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759±64.Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on AppetitiveBehavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.Luke's/Roosevelt Hospital.0195±6663/96/030304+01 $18.00/0  1996 Academic Press Limited

University of GroningenFood intake, fuel homeostasis, and the autonomic nervous systemScheurink, A J W; Nolan, L JPublished in:AppetiteDOI:10.1006/appe.1996.0026IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1996Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Scheurink, A. J. W., & Nolan, L. J. (1996). Food intake, fuel homeostasis, and the autonomic nervoussystem. Appetite, 26(3), 304-304. https://doi.org/10.1006/appe.1996.0026CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 23-12-2025Appetite, 1996, 26, 304Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTONJ. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCEJ. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.The mobilization, storage and utilization of the different energy substrates is regulated bysensitive and very specific hormonal and neural mechanisms. Increased parasympatheticactivity leads to storage of glucose and free fatty acids (FFA) while activation of thesympathetic branch of the autonomic nervous system (ANS) results in the mobilization ofFFA and glucose from storage tissues. The latter is accomplished by both neuronal no-repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.The relation between autonomic activity and substrate availability might be bidirectional:an increased availability of energy substrates could activate the parasympathetic branch ofthe ANS, while a decreased availability of glucose and/or FFA may lead to increasedsympathetic outflow. One set of experiments investigated the metabolic and hormonal responsesthat occur during food intake or intravenous or intragastric administration of glucose (Strubbe,1992). Food intake was accompanied by the early insulin response (EIR), an increase inplasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressedby prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropinealso attenuated and delayed the insulin response to intravenous or intragastric glucose loadindicating that the parasympathetic nervous system is also involved in the dynamics of insulinsecretion during hyperglycemia.A second set of experiments was conducted to examine the metabolic and hormonalresponses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy--glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered andcatecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-lation of adrenal E secretion combined with a small NE outflow. Lipoprivation stimulatedonly the neuronal branch of the sympathetic nervous system without any effect on adrenal Erelease. The finding that decreased glucose availability leads to adrenomedullary secretion ofE is compatible with the fact that circulating E is an important mediator of hepatic glucoseproduction in rats. Likewise, the selective increase in neuronal outflow of NE after MAadministration can be considered a metabolically appropriate response to blockade of FFAoxidation since neuronal NE serves as the physiological mediator of lipolysis in white adiposetissue. These data indicate that distinct metabolic signals are capable of exerting a selectiveand functional control of sympathoadrenal outflow.The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possiblemechanism is serotonin (5-HT) as it is able to affect E outflow without affecting NE release.When administered to sleeping rats, fenfluramine is associated with a rise in E and has noeffect on NE. There is also a corresponding increase in circulating glucose while FFA levelsremain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminarystudies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamusmeasured by microdialysis and increased circulating levels of E. MA administration did notaffect either medial hypothalamic 5-HT levels or plasma E.Taken together, the data demonstrate that metabolic needs are regulated via changes inthe functioning of the different branches of the autonomic nervous system. In turn, metabolicstates can also profoundly affect the functioning of the autonomic regulatory mechanisms.The hypothalamus may function as a center in the brain coordinating autonomic outflow andenergy balance.Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-privation in rats. Physiology and Behavior, 53, 995–1000.Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenalactivity and energy metabolism in rats. Physiology and Behavior, 48, 909–20.Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditionedinsulin secretion in the rat. American Journal of Physiology, 263, R615–18.Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis andsympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759–64.Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on AppetitiveBehavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.Luke’s/Roosevelt Hospital.0195–6663/96/030304+01 $18.00/0  1996 Academic Press Limited

NARCIS 

   University of GroningenFood intake, fuel homeostasis, and the autonomic nervous systemScheurink, A J W; Nolan, L JPublished in:AppetiteDOI:10.1006/appe.1996.0026IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1996Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Scheurink, A. J. W., & Nolan, L. J. (1996). Food intake, fuel homeostasis, and the autonomic nervoussystem. Appetite, 26(3), 304-304. https://doi.org/10.1006/appe.1996.0026CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 25-04-2023Appetite, 1996, 26, 304Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTONJ. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCEJ. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.The mobilization, storage and utilization of the different energy substrates is regulated bysensitive and very specific hormonal and neural mechanisms. Increased parasympatheticactivity leads to storage of glucose and free fatty acids (FFA) while activation of thesympathetic branch of the autonomic nervous system (ANS) results in the mobilization ofFFA and glucose from storage tissues. The latter is accomplished by both neuronal no-repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.The relation between autonomic activity and substrate availability might be bidirectional:an increased availability of energy substrates could activate the parasympathetic branch ofthe ANS, while a decreased availability of glucose and/or FFA may lead to increasedsympathetic outflow. One set of experiments investigated the metabolic and hormonal responsesthat occur during food intake or intravenous or intragastric administration of glucose (Strubbe,1992). Food intake was accompanied by the early insulin response (EIR), an increase inplasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressedby prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropinealso attenuated and delayed the insulin response to intravenous or intragastric glucose loadindicating that the parasympathetic nervous system is also involved in the dynamics of insulinsecretion during hyperglycemia.A second set of experiments was conducted to examine the metabolic and hormonalresponses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy--glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered andcatecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-lation of adrenal E secretion combined with a small NE outflow. Lipoprivation stimulatedonly the neuronal branch of the sympathetic nervous system without any effect on adrenal Erelease. The finding that decreased glucose availability leads to adrenomedullary secretion ofE is compatible with the fact that circulating E is an important mediator of hepatic glucoseproduction in rats. Likewise, the selective increase in neuronal outflow of NE after MAadministration can be considered a metabolically appropriate response to blockade of FFAoxidation since neuronal NE serves as the physiological mediator of lipolysis in white adiposetissue. These data indicate that distinct metabolic signals are capable of exerting a selectiveand functional control of sympathoadrenal outflow.The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possiblemechanism is serotonin (5-HT) as it is able to affect E outflow without affecting NE release.When administered to sleeping rats, fenfluramine is associated with a rise in E and has noeffect on NE. There is also a corresponding increase in circulating glucose while FFA levelsremain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminarystudies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamusmeasured by microdialysis and increased circulating levels of E. MA administration did notaffect either medial hypothalamic 5-HT levels or plasma E.Taken together, the data demonstrate that metabolic needs are regulated via changes inthe functioning of the different branches of the autonomic nervous system. In turn, metabolicstates can also profoundly affect the functioning of the autonomic regulatory mechanisms.The hypothalamus may function as a center in the brain coordinating autonomic outflow andenergy balance.Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-privation in rats. Physiology and Behavior, 53, 995–1000.Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenalactivity and energy metabolism in rats. Physiology and Behavior, 48, 909–20.Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditionedinsulin secretion in the rat. American Journal of Physiology, 263, R615–18.Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis andsympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759–64.Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on AppetitiveBehavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.Luke’s/Roosevelt Hospital.0195–6663/96/030304+01 $18.00/0  1996 Academic Press Limited

University of GroningenFood intake, fuel homeostasis, and the autonomic nervous systemScheurink, A J W; Nolan, L JPublished in:AppetiteDOI:10.1006/appe.1996.0026IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1996Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Scheurink, A. J. W., & Nolan, L. J. (1996). Food intake, fuel homeostasis, and the autonomic nervoussystem. Appetite, 26(3), 304-304. https://doi.org/10.1006/appe.1996.0026CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 30-12-2025Appetite, 1996, 26, 304Food Intake, Fuel Homeostasis, and the Autonomic Nervous System. ANTONJ. W. SCHEURINK, University of Groningen, Haren, The Netherlands and LAURENCEJ. NOLAN, Obesity Research Center, Columbia University, New York, N.Y., U.S.A.The mobilization, storage and utilization of the different energy substrates is regulated bysensitive and very specific hormonal and neural mechanisms. Increased parasympatheticactivity leads to storage of glucose and free fatty acids (FFA) while activation of thesympathetic branch of the autonomic nervous system (ANS) results in the mobilization ofFFA and glucose from storage tissues. The latter is accomplished by both neuronal no-repinephrine (NE) in the periphery and hormonal epinephrine (E) from the adrenal medulla.The relation between autonomic activity and substrate availability might be bidirectional:an increased availability of energy substrates could activate the parasympathetic branch ofthe ANS, while a decreased availability of glucose and/or FFA may lead to increasedsympathetic outflow. One set of experiments investigated the metabolic and hormonal responsesthat occur during food intake or intravenous or intragastric administration of glucose (Strubbe,1992). Food intake was accompanied by the early insulin response (EIR), an increase inplasma insulin that occurs immediately after the onset of a meal. The EIR could be suppressedby prior administration of atropine or subdiaphragmatic vagotomy. Administration of atropinealso attenuated and delayed the insulin response to intravenous or intragastric glucose loadindicating that the parasympathetic nervous system is also involved in the dynamics of insulinsecretion during hyperglycemia.A second set of experiments was conducted to examine the metabolic and hormonalresponses to a reduction in the availability of energy substrates (Scheurink & Ritter, 1993;Van Dijk et al., 1995). Hypoglycemic doses of insulin or drugs that block glucose (2-deoxy--glucose, 2DG) or FFA (mercaptoacetate, MA) utilization were i.v. administered andcatecholamine responses were measured. Glucoprivation was accompanied by a robust stimu-lation of adrenal E secretion combined with a small NE outflow. Lipoprivation stimulatedonly the neuronal branch of the sympathetic nervous system without any effect on adrenal Erelease. The finding that decreased glucose availability leads to adrenomedullary secretion ofE is compatible with the fact that circulating E is an important mediator of hepatic glucoseproduction in rats. Likewise, the selective increase in neuronal outflow of NE after MAadministration can be considered a metabolically appropriate response to blockade of FFAoxidation since neuronal NE serves as the physiological mediator of lipolysis in white adiposetissue. These data indicate that distinct metabolic signals are capable of exerting a selectiveand functional control of sympathoadrenal outflow.The hypothalamus is the likely source of control (Scheurink & Steffens, 1990). A possiblemechanism is serotonin (5-HT) as it is able to affect E outflow without affecting NE release.When administered to sleeping rats, fenfluramine is associated with a rise in E and has noeffect on NE. There is also a corresponding increase in circulating glucose while FFA levelsremain unchanged. These effects can be blocked by 5-HT-1a receptor blockade. In preliminarystudies, i.v. administration of 2DG increased hypothalamic 5-HT in medial hypothalamusmeasured by microdialysis and increased circulating levels of E. MA administration did notaffect either medial hypothalamic 5-HT levels or plasma E.Taken together, the data demonstrate that metabolic needs are regulated via changes inthe functioning of the different branches of the autonomic nervous system. In turn, metabolicstates can also profoundly affect the functioning of the autonomic regulatory mechanisms.The hypothalamus may function as a center in the brain coordinating autonomic outflow andenergy balance.Scheurink, A. & Ritter, S. (1993) Sympathoadrenal responses to glucoprivation and lipo-privation in rats. Physiology and Behavior, 53, 995–1000.Scheurink, A. J. W. & Steffens, A. B. (1990) Central and peripheral control of sympathoadrenalactivity and energy metabolism in rats. Physiology and Behavior, 48, 909–20.Strubbe, J. H. (1992) Parasympathetic involvement in rapid meal-associated conditionedinsulin secretion in the rat. American Journal of Physiology, 263, R615–18.Van Dijk, G., Scheurink, A. J. W., Ritter, S., & Steffens A. B. (1995) Glucose homeostasis andsympathoadrenal activity after lipoprivation in rats. Physiology and Behavior, 57, 759–64.Report by Laurence J. Nolan of a presentation to the Columbia University Seminar on AppetitiveBehavior, 2 November 1995 (Harry R. Kissileff, Chairman). Supported in part by Hoffmann-La Roche;McNeil Specialty Co.; Miles, Inc./Bayer, AG; Pepsico and the New York Obesity Research Center, St.Luke’s/Roosevelt Hospital.0195–6663/96/030304+01 $18.00/0  1996 Academic Press Limited

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Food Intake, Fuel Homeostasis, and the Autonomic Nervous System

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