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Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Acute ketosis inhibits appetite and decreases plasma concentrations of acyl ghrelin in healthy young men

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  1. Cholecystokinin and panic disorder: reflections on the history and some unsolved questions

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  2. Expression of cholecystokinin and its receptors in the intestinal tract of type 2 diabetes patients and healthy controls

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  3. Gastrin and the moderate hypergastrinemias

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

  • Esben Thyssen Vestergaard
  • Natasa Brkovic Zubanovic
  • Nikolaj Rittig
  • Niels Møller
  • Rune Ehrenreich Kuhre
  • Jens J Holst
  • Jens F Rehfeld
  • Henrik Holm Thomsen
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AIM: To investigate the acute effect of ketone ester (KE) ingestion on appetite and plasma concentrations of acyl ghrelin (AG), unacylated ghrelin (UAG) and glucagon-like peptide-1 (GLP-1) secretion, and to compare responses with those elicited by isocaloric glucose (GLU) administration.

METHODS: We examined 10 healthy young men on three separate occasions using a placebo (PBO)-controlled crossover design. A KE versus taste-matched isovolumetric and isocaloric 50% GLU and taste-matched isovolumetric PBO vehicle was orally administered. Our main outcome measures were plasma concentrations of AG, UAG, glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 along with appetite sensation scores assessed by visual analogue scale.

RESULTS: KE ingestion resulted in an average peak beta-hydroxybutyrate concentration of 5.5 mM. AG and UAG were lowered by approximately 25% following both KE and GLU intake compared with PBO. In the case of AG, the differences were -52.1 (-79.4, -24.8) for KE and -48.4 (-75.4, -21.5) pg/mL for GLU intake (P < .01). Concentrations of AG remained lower with KE but returned to baseline and were comparable with PBO levels after GLU intake. GLP-1, GIP, gastrin and cholecystokinin were not affected by KE ingestion.

CONCLUSION: Our results suggest that the suppressive effects on appetite sensation scores associated with hyperketonaemia are more probable to be mediated through reduced ghrelin concentrations than by increased activity of cholecystokinin, gastrin, GIP or GLP-1.

OriginalsprogEngelsk
TidsskriftDiabetes, Obesity and Metabolism
Vol/bind23
Udgave nummer8
Sider (fra-til)1834-1842
Antal sider9
ISSN1462-8902
DOI
StatusUdgivet - aug. 2021

ID: 66793404