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Chen J, Jeppesen PB, Nordentoft I, et al. Stevioside Counteracts Beta-Cell Lipotoxicity without Affecting Acetyl CoA Carboxylase. Rev Diabet Stud. 2007;3(4):178-88doi: 10.1900/RDS.2006.3.178.
Chen, J., Jeppesen, P. B., Nordentoft, I., & Hermansen, K. (2006). Stevioside Counteracts Beta-Cell Lipotoxicity without Affecting Acetyl CoA Carboxylase. The review of diabetic studies : RDS, 3(4), 178-88. https://doi.org/10.1900/RDS.2006.3.178
Chen, Jianguo, et al. "Stevioside Counteracts Beta-Cell Lipotoxicity without Affecting Acetyl CoA Carboxylase." The review of diabetic studies : RDS vol. 3,4 (2006): 178-88. doi: https://doi.org/10.1900/RDS.2006.3.178
Chen J, Jeppesen PB, Nordentoft I, Hermansen K. Stevioside Counteracts Beta-Cell Lipotoxicity without Affecting Acetyl CoA Carboxylase. Rev Diabet Stud. 2006;3(4):178-88. doi: 10.1900/RDS.2006.3.178. Epub 2007 Feb 10. PMID: 17487342; PMCID: PMC1828288.
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Rev Diabet Stud. 2006;3(4):178-88. doi: 10.1900/RDS.2006.3.178. Epub 2007 Feb 10.

Stevioside Counteracts Beta-Cell Lipotoxicity without Affecting Acetyl CoA Carboxylase.

The review of diabetic studies : RDS

Jianguo Chen, Per Bendix Jeppesen, Iver Nordentoft, Kjeld Hermansen

Affiliations

  1. Department of Endocrinology and Metabolism C, Aarhus Sygehus THG, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark.

PMID: 17487342 PMCID: PMC1828288 DOI: 10.1900/RDS.2006.3.178

Abstract

Chronic exposure to high levels of free fatty acids impairs beta-cell function (lipotoxicity). Then basal insulin secretion (BIS) is increased and glucose-stimulated insulin secretion (GSIS) is inhibited. Acetyl CoA carboxylase (ACC) acts as the sensor for insulin secretion in pancreatic beta-cells in response to glucose and other nutrients. Stevioside (SVS), a diterpene glycoside, has recently been shown to prevent glucotoxic effect by regulating ACC activity. The aim of this study was to investigate whether SVS can alleviate impaired beta-cell function by regulating ACC activity. We exposed isolated rat islets and the clonal beta-cell line, INS-1E, to palmitate concentrations of 1.0 or 0.6 mM, respectively, for a period of 24 h to 120 h. The results showed that lipotoxicity occurred in rat islets after 72 h exposure to 1.0 mM palmitate. The lipotoxicity was counteracted by 10(-6) M SVS (n = 8, p < 0.001). Similar results were obtained in INS-1E cells. Neither SVS nor palmitate had any effect on the gene expression of ACC, insulin 2, and glucose transporter 2 in INS-1E cells. In contrast, palmitate significantly increased the gene expression of carnitine palmitoyl transporter 1 (n = 6, p = 0.003). However, the addition of SVS to palmitate did not counteract this effect (n = 6, p = 1.0). During lipotoxicity, SVS did not alter levels of ACC protein, phosphorylated-ACC, ACC activity or glucose uptake. Our results showed that SVS counteracts the impaired insulin secretion during lipotoxicity in rat islets as well as in INS-1E cells without affecting ACC activity.

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