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Spranger, J.* ; Ristow, M.* ; Otto, B.* ; Heldwein, W.* ; Tschöp, M.H. ; Pfeiffer, A.F.* ; Möhlig, M.*

Post-prandial decrease of human plasma ghrelin in the absence of insulin.

J. Endocrinol. Invest. 26, RC19-22 (2003)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Ghrelin is the most powerful orexigenic hormone in mammalian physiology. Ghrelin plasma concentrations increase prior to meal onset, but decrease post-prandially. We and others reported previously that insulin reduces circulating ghrelin levels and might therefore be a driving force for post-prandial suppression of ghrelin. To test the influence of insulin on post-prandial ghrelin regulation, a patient with Type I diabetes with complete insulin deficiency received a low glycemic index meal and subsequently an additional high glycemic index meal in the absence of insulin substitution. Subsequently, a sc injection of 0.08 IU Lispro insulin per kg body weight was given. Results were compared to those of a healthy control subject matched for sex, age and body mass index, which was undergoing the same test series (without Lispro bolus) in the presence of endogenous post-prandial insulin secretion. A substantial decrease of plasma ghrelin levels was observed in the insulin-deficient patient following low glycemic index carbohydrate load (27% plasma ghrelin decrease). The subsequent exposure to a high glycemic index meal resulted in a slight additional reduction of ghrelin levels (32% from baseline), while Lispro bolus did not induce further changes in circulating ghrelin (27% of baseline at termination). This post-prandial response was comparable to that of the healthy control subject (33% reduction after the first meal, 40% after the second meal). These data tentatively suggest that post-prandial secretion of ghrelin is not exclusively regulated by plasma insulin or plasma glucose but may depend on other metabolic factors yet to be identified.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Sprache
Veröffentlichungsjahr 2003
HGF-Berichtsjahr 2003
ISSN (print) / ISBN 0391-4097
e-ISSN 1720-8386
Quellenangaben Band: 26, Heft: 8, Seiten: RC19-22 Artikelnummer: , Supplement: ,
Verlag Springer
Begutachtungsstatus Peer reviewed
PubMed ID 14669821
Erfassungsdatum 2020-02-20