Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-9
pubmed:abstractText
Long-term exposure to fatty acids impairs beta-cell function in type 2 diabetes, but little is known about the chronic effects of fatty acids on alpha-cells. We therefore studied the prolonged impact of palmitate on alpha-cell function and on the expression of genes related to fuel metabolism. We also investigated whether the antihyperglycemic agent stevioside was able to counteract these effects of palmitate. Clonal alpha-TC1-6 cells were cultured with palmitate in the presence or absence of stevioside. After 72 h, we evaluated glucagon secretion, glucagon content, triglyceride (TG) content, and changes in gene expression. Glucagon secretion was dose-dependently increased after 72-h culture, with palmitate at concentrations >or=0.25 mM (P< 0.05). Palmitate (0.5 mM) enhanced TG content of alpha-cells by 73% (P< 0.01). Interestingly, stevioside (10(-8) and 10(-6) M) reduced palmitate-stimulated glucagon release by 22 and 45%, respectively (P< 0.01). There was no significant change in glucagon content after 72-h culture with palmitate and/or stevioside. Palmitate increased carnitine palmitoyltransferase I (CPT I) mRNA level, whereas stevioside enhanced CPT I, peroxisome proliferator-activated receptor-gamma, and stearoyl-CoA desaturase gene expressions in the presence of palmitate (P<0.05). In conclusion, long-term exposure to elevated fatty acids leads to a hypersecretion of glucagon and an accumulation of TG content in clonal alpha-TC1-6 cells. Stevioside was able to counteract the alpha-cell hypersecretion caused by palmitate and enhanced the expression of genes involved in fatty acid metabolism. This indicates that stevioside may be a promising antidiabetic agent in treatment of type 2 diabetes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E416-22
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16204336-Acetyl-CoA Carboxylase, pubmed-meshheading:16204336-Animals, pubmed-meshheading:16204336-Carnitine O-Palmitoyltransferase, pubmed-meshheading:16204336-Cell Line, Tumor, pubmed-meshheading:16204336-Diterpenes, Kaurane, pubmed-meshheading:16204336-Drug Interactions, pubmed-meshheading:16204336-Gene Expression, pubmed-meshheading:16204336-Glucagon, pubmed-meshheading:16204336-Glucagon-Secreting Cells, pubmed-meshheading:16204336-Glucosides, pubmed-meshheading:16204336-Hypoglycemic Agents, pubmed-meshheading:16204336-Mice, pubmed-meshheading:16204336-Mice, Transgenic, pubmed-meshheading:16204336-PPAR gamma, pubmed-meshheading:16204336-Palmitates, pubmed-meshheading:16204336-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16204336-Secretory Rate, pubmed-meshheading:16204336-Stearoyl-CoA Desaturase, pubmed-meshheading:16204336-Sterol Regulatory Element Binding Protein 1
pubmed:year
2006
pubmed:articleTitle
Stevioside counteracts the alpha-cell hypersecretion caused by long-term palmitate exposure.
pubmed:affiliation
Department of Endocrinology and Metabolism, Aarhus University Hospital, Odense, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't