Brain activations show association with subsequent endocrine responses to oral glucose challenge in a satiation-level dependent manner.

Cortisol Food intake Imaging Magnetic resonance imaging

Journal

Comprehensive psychoneuroendocrinology
ISSN: 2666-4976
Titre abrégé: Compr Psychoneuroendocrinol
Pays: England
ID NLM: 101774169

Informations de publication

Date de publication:
May 2021
Historique:
received: 30 12 2020
revised: 01 03 2021
accepted: 22 03 2021
entrez: 27 6 2022
pubmed: 29 3 2021
medline: 29 3 2021
Statut: epublish

Résumé

The communication between brain and peripheral homeostatic systems is a central element of ingestive control. We set out to explore which parts of the brain have strong functional connections to peripheral signalling molecules in a physiological context. It was hypothesised that associations can be found between endocrine response to glucose ingestion and preceding brain activity in dependence of the nutritional status of the body. Young, healthy male participants underwent both a 38 ​h fasting and a control condition with standardized meals. On the second day of the experiment, participants underwent fMRI scanning followed by ingestion of glucose solution in both conditions. Subsequent endocrine responses relevant to energy metabolism were assessed. Associations between preceding brain activation and endocrine responses were examined. In both fasting and non-fasting conditions, brain activity was associated with subsequent endocrine responses after glucose administration, but relevant brain areas differed substantially between the conditions. In the fasting condition relations between the caudate nucleus and the orbitofrontal regions with insulin and C-peptide were prevailing, whereas in the non-fasting condition associations between various brain regions and adiponectin and cortisol were the predominant significant outcome. Connections between endocrine response following a glucose challenge and prior brain activity suggests that the brain is playing an active role in the networks regulating food intake and associated endocrine signals. Further studies are needed to demonstrate causation.

Identifiants

pubmed: 35757367
doi: 10.1016/j.cpnec.2021.100055
pii: S2666-4976(21)00029-1
pmc: PMC9216379
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100055

Informations de copyright

© 2021 The Authors.

Déclaration de conflit d'intérêts

Declarations of interest: none.

Références

Obesity (Silver Spring). 2014 Jun;22(6):1439-46
pubmed: 24174404
Data Brief. 2019 Oct 17;27:104676
pubmed: 31720329
Cell Metab. 2011 Nov 2;14(5):700-6
pubmed: 22000927
Neuroimage. 2006 Jul 1;31(3):968-80
pubmed: 16530430
Front Nutr. 2014 Jul 09;1:7
pubmed: 25988110
Eur Eat Disord Rev. 2013 Mar;21(2):89-98
pubmed: 23348964
Neuroinformatics. 2009 Spring;7(1):73-82
pubmed: 19140033
J Mol Med (Berl). 2002 Nov;80(11):696-702
pubmed: 12436346
Front Neurosci. 2011 May 30;5:74
pubmed: 21660101
Neuroendocrinology. 2009;89(1):38-47
pubmed: 18698133
Nature. 2007 Nov 1;450(7166):106-9
pubmed: 17934448
Int J Mol Sci. 2019 Mar 08;20(5):
pubmed: 30857216
Trends Cogn Sci. 2011 Jan;15(1):37-46
pubmed: 21109477
Physiol Behav. 2012 Jun 6;106(3):317-24
pubmed: 22450260
Cell Metab. 2008 May;7(5):400-9
pubmed: 18460331
Yale J Biol Med. 1951 Nov;24(2):123-40
pubmed: 14901884
PLoS One. 2013 Apr 10;8(4):e60393
pubmed: 23593210
Behav Neurosci. 2001 Apr;115(2):493-500
pubmed: 11345973
Psychoneuroendocrinology. 2019 Nov;109:104310
pubmed: 31404897
Diabetes. 2014 Dec;63(12):4186-96
pubmed: 25071023
J Neuroendocrinol. 2015 Jun;27(6):419-23
pubmed: 25594822
Cell. 2015 Mar 26;161(1):119-132
pubmed: 25815990
Nat Rev Neurosci. 2012 Mar 14;13(4):279-86
pubmed: 22414944
Neuroimage. 2003 Aug;19(4):1381-94
pubmed: 12948696
Nat Commun. 2017 Jul 18;8:16052
pubmed: 28719580
Front Hum Neurosci. 2019 May 14;13:162
pubmed: 31178708
Nat Med. 2004 May;10(5):524-9
pubmed: 15077108
Neuroimage. 2020 Aug 15;217:116931
pubmed: 32417450
Obes Facts. 2011;4(2):151-7
pubmed: 21577022
Am J Physiol Endocrinol Metab. 2007 Sep;293(3):E754-8
pubmed: 17566114
Science. 2007 Sep 7;317(5843):1355
pubmed: 17690262
PLoS One. 2019 Jan 25;14(1):e0211514
pubmed: 30682147
Neuroimage. 2006 Sep;32(3):1273-80
pubmed: 16815041
Nutr Neurosci. 2020 Feb;23(2):110-117
pubmed: 29806553
Brain Imaging Behav. 2018 Aug;12(4):1150-1159
pubmed: 29071464
Diabetes Obes Metab. 2011 Mar;13(3):229-34
pubmed: 21205113
CNS Neurosci Ther. 2018 Sep;24(9):763-774
pubmed: 29691988
Exp Diabetes Res. 2012;2012:764017
pubmed: 22719753
Physiol Rev. 1974 Jul;54(3):596-619
pubmed: 4601624
Eur J Neurosci. 2009 Oct;30(8):1625-35
pubmed: 19811532
Exp Brain Res. 2006 Aug;173(2):318-21
pubmed: 16710683
Diabetologia. 2012 Jun;55(6):1773-82
pubmed: 22434537
Neuron. 2011 Feb 24;69(4):664-79
pubmed: 21338878
Metabolism. 2019 Oct;99:11-18
pubmed: 31271805
Br J Pharmacol. 2012 Jan;165(2):313-27
pubmed: 21718299

Auteurs

Janis M Nolde (JM)

Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
School of Medicine, University of Western Australia, Perth, Australia.

Sophia G Connor (SG)

Royal Perth Hospital, Perth, Australia.

Arkan Al-Zubaidi (A)

Applied Neurocognitive Psychology Lab, University of Oldenburg, Oldenburg, Germany.

Martina A Obst (MA)

Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.

Jana Laupenmühlen (J)

Department of Psychiatry, University of Lübeck, Ratzeburger Allee 160, 23562, Lübeck, Germany.

Marcus Heldmann (M)

Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
Institute of Psychology II, University of Lübeck, Ratzeburger Allee 160, 23562, Lübeck, Germany.

Kamila Jauch-Chara (K)

Department of Psychiatry and Psychotherapy, Christian-Albrechts-University, Niemannsweg 147, 24105, Kiel, Germany.

Thomas F Münte (TF)

Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23562 Lübeck, Germany.
Institute of Psychology II, University of Lübeck, Ratzeburger Allee 160, 23562, Lübeck, Germany.

Classifications MeSH