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Acylated ghrelin secretion is acutely suppressed by oral glucose load or insulin-induced hypoglycemia independently of basal growth hormone secretion in humans

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  • معلومة اضافية
    • Contributors:
      김상완; 김경원; 신찬수; 박도준; 박경수; 조보연; 이홍규; 김성연
    • بيانات النشر:
      Karger
    • الموضوع:
      2006
    • Collection:
      Seoul National University: S-Space
    • نبذة مختصرة :
      BACKGROUND: Ghrelin has been reported to be the natural ligand of growth hormone (GH) secretagogue receptor, and it is known that exogenous ghrelin administration strongly stimulates GH release in humans. However, the effects of endogenous ghrelin on GH secretion and changes in ghrelin levels during dynamic changes in GH levels are not well understood. METHODS: Therefore, we measured circulating acylated ghrelin concentrations during oral glucose tolerance tests (OGTTs) in patients with active acromegaly (AA, n = 9) and in age/sex/BMI-matched group A controls (n = 12), and during insulin tolerance testing (ITT) in patients with GH deficiency (GHD, n = 10) and in group B controls (n = 10). Plasma acylated ghrelin, serum GH, insulin and glucose levels were measured during each test. RESULTS: Fasting plasma ghrelin levels correlated negatively with serum insulin levels in both group A and B controls (r = -0.665; p < 0.05) but not in patients with AA or GHD. During OGTTs, circulating ghrelin levels decreased significantly with a nadir at 30 min in both patients with AA (p < 0.05) and group A controls (p < 0.01). Also, ITTs were followed by a significant decrease in circulating ghrelin levels with a nadir at 30 min in patients with GHD (p < 0.05) and in group B controls (p < 0.05). CONCLUSION: The results of the study show that at baseline acylated ghrelin levels do not differ with respect to the GH status (GH excess or GH deficiency) and, furthermore, the suppression of acylated ghrelin levels during OGTT or ITT is independent of the GH response to the tests.
    • Relation:
      Horm Res. 2007;67(5):211-9. Epub 2006 Nov 16.; 0301-0163 (Print); http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17114888; http://hdl.handle.net/10371/42985
    • الرقم المعرف:
      10.1159/000097098
    • الرقم المعرف:
      edsbas.3A2ECA03