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Stevioside does not cause increased basal insulin secretion or beta-cell desensitization as does the sulphonylurea, glibenclamide: studies in vitro

Chen, Jianguo ; Jeppesen, Per Bendix ; Abudula, Reziwanggu ; Dyrskog, Stig E U ; Colombo, Michele ; Hermansen, Kjeld

Life sciences, 06 March 2006, Vol.78(15), pp.1748-53 [Peer Reviewed Journal]

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  • Title:
    Stevioside does not cause increased basal insulin secretion or beta-cell desensitization as does the sulphonylurea, glibenclamide: studies in vitro
  • Author: Chen, Jianguo ; Jeppesen, Per Bendix ; Abudula, Reziwanggu ; Dyrskog, Stig E U ; Colombo, Michele ; Hermansen, Kjeld
  • Description: We have shown that stevioside (SVS) enhances insulin secretion and thus may have a potential role as antihyperglycemic agent in the treatment of type 2 diabetes mellitus. However, whether SVS stimulates basal insulin secretion (BIS) and/or cause desensitization of beta cells like sulphonylureas (SU), e.g. glibenclamide (GB), is not known. To explore and compare the effects of SVS pretreatment with those of GB and glucagon-like peptide-1 (GLP-1), we exposed isolated mouse islets to low or high glucose for 1 h after short-term (2 h) or long-term (24 h) pretreatment with SVS, GB or GLP-1, respectively. BIS at 3.3 or 5.5 mM glucose were not changed after short-term pretreatment with SVS (10(-7) M), while it increased about three folds after pretreatment with GB (10(-7) M). Glucose stimulated insulin secretion (GSIS) (16.7 mM) increased dose-dependently after long-term pretreatment with SVS at concentrations from 10(-7) to 10(-5) M. Pretreatment for 24 h with GB (10(-7) M) increased the subsequent...
  • Is Part Of: Life sciences, 06 March 2006, Vol.78(15), pp.1748-53
  • Identifier: ISSN: 0024-3205 ; PMID: 16260001 Version:1
  • Subjects: Diterpenes, Kaurane -- Pharmacology ; Glucosides -- Pharmacology ; Glyburide -- Pharmacology ; Hypoglycemic Agents -- Pharmacology ; Insulin -- Metabolism ; Islets of Langerhans -- Drug Effects
  • Language: English
  • Source: MEDLINE/PubMed (U.S. National Library of Medicine)

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