Oxytocin improves β-Cell responsivity and glucose tolerance in healthy men

Johanna Klement*, Volker Ott, Kristina Rapp, Swantje Brede, Francesca Piccinini, Claudio Cobelli, Hendrik Lehnert, Manfred Hallschmid

*Corresponding author for this work
59 Citations (Scopus)

Abstract

In addition to its pivotal role in psychosocial behavior, the hypothalamic neuropeptide oxytocin contributes to metabolic control by suppressing eating behavior. Its involvement in glucose homeostasis is less clear, although pilot experiments suggest that oxytocin improves glucose homeostasis. We assessed the effect of intranasal oxytocin (24 IU) administered to 29 healthy, fasted male subjects on glucose homeostasis measured by means of an oral glucose tolerance test. Parameters of glucose metabolism were analyzed according to the oral minimal model. Oxytocin attenuated the peak excursion of plasma glucose and augmented the early increases in insulin and C-peptide concentrations in response to the glucose challenge, while slightly blunting insulin and C-peptide peaks. Oral minimal model analyses revealed that oxytocin compared with placebo induced a pronounced increase in b-cell responsivity (PHItotal) that was largely due to an enhanced dynamic response (PHId), and a more than twofold improvement in glucose tolerance (disposition index). Adrenocorticotropic hormone (ACTH), cortisol, glucagon, and nonesterified fatty acid (NEFA) concentrations were not or were only marginally affected. These results indicate that oxytocin plays a significant role in the acute regulation of glucose metabolism in healthy humans and render the oxytocin system a potential target of antidiabetic treatment.

Original languageEnglish
JournalDiabetes
Volume66
Issue number2
Pages (from-to)264-271
Number of pages8
ISSN0012-1797
DOIs
Publication statusPublished - 01.02.2017

Funding

FundersFunder number
Helmholtz Alliance Imaging and Curing Environmental Metabolic Diseases
Deutsche ForschungsgemeinschaftSFB/Transregio 134
Bundesministerium für Bildung und Forschung01GI0925

    Research Areas and Centers

    • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

    DFG Research Classification Scheme

    • 2.22-17 Endocrinology, Diabetology, Metabolism

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    • CRC/Transregio TRR 134: Ingestive Behaviour: Homeostasis and Reward

      Lehnert, H. (Speaker, Coordinator), Brüning, J. C. (Principal Investigator (PI)), Scholz, H. (Principal Investigator (PI)), Kloppenburg, P. (Principal Investigator (PI)), Hausen, A. C. (Principal Investigator (PI)), Jöhren, O. (Principal Investigator (PI)), Schulz, C. (Principal Investigator (PI)), Schwaninger, M. (Principal Investigator (PI)), Wunderlich, F. T. (Principal Investigator (PI)), Schmid, S. (Principal Investigator (PI)), Oster, H. (Principal Investigator (PI)), Klement, J. (Principal Investigator (PI)), Ott, V. (Principal Investigator (PI)), Stephan, K. E. (Principal Investigator (PI)), Tittgemeyer, M. (Principal Investigator (PI)), Oltmanns, K. (Principal Investigator (PI)), Münte, T. (Principal Investigator (PI)), Tronnier, V. M. (Principal Investigator (PI)), Schweiger, U. (Principal Investigator (PI)), Brassen, S. (Principal Investigator (PI)), Büchel, C. (Principal Investigator (PI)), Peters, J. (Principal Investigator (PI)), Schilbach, L. (Principal Investigator (PI)), Anders, S. (Principal Investigator (PI)), Martinetz, T. (Principal Investigator (PI)), Park, S. Q. (Principal Investigator (PI)), Brabant, E. G. (Principal Investigator (PI)), Kasten, M. (Principal Investigator (PI)), Klein, C. (Principal Investigator (PI)) & Krämer, U. (Principal Investigator (PI))

      01.01.1431.12.18

      Project: DFG Joint ResearchDFG Collaborative Research Centers (CRC)

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