title: Oxytocin Improves β-Cell Responsivity and Glucose Tolerance in Healthy Men.
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 β-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.
authors.affiliation: Department of Internal Medicine I, University of Lübeck, Lübeck, Germany johanna.klement@uksh.de.
authors.forename: Johanna
authors.initials: J
authors.lastname: Klement
authors.affiliation: Department of Internal Medicine I, University of Lübeck, Lübeck, Germany.
authors.forename: Volker
authors.initials: V
authors.lastname: Ott
authors.affiliation: Department of Internal Medicine I, University of Lübeck, Lübeck, Germany.
authors.forename: Kristina
authors.initials: K
authors.lastname: Rapp
authors.affiliation: Department of Internal Medicine I, University of Lübeck, Lübeck, Germany.
authors.forename: Swantje
authors.initials: S
authors.lastname: Brede
authors.affiliation: Department of Information Engineering, University of Padua, Padua, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: Piccinini
authors.affiliation: Department of Information Engineering, University of Padua, Padua, Italy.
authors.forename: Claudio
authors.initials: C
authors.lastname: Cobelli
authors.affiliation: Department of Internal Medicine I, University of Lübeck, Lübeck, Germany.
authors.forename: Hendrik
authors.initials: H
authors.lastname: Lehnert
authors.affiliation: Department of Medical Psychology and Behavioural Neurobiology, University of Tübingen, Tübingen, Germany.|German Center for Diabetes Research (DZD), Tübingen, Germany.|Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen (IDM), Tübingen, Germany.
authors.forename: Manfred
authors.initials: M
authors.lastname: Hallschmid
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000187:drug effects / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism; D002096:C-Peptide / Q000187:drug effects / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005934:Glucagon / Q000187:drug effects / Q000378:metabolism; D005951:Glucose Tolerance Test; D064368:Healthy Volunteers; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010120:Oxytocics / Q000494:pharmacology*; D010121:Oxytocin / Q000494:pharmacology*; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D010120:Oxytocics; D010121:Oxytocin; D000324:Adrenocorticotropic Hormone; D005934:Glucagon; D006854:Hydrocortisone