Horm Metab Res 1998; 30(4): 195-199
DOI: 10.1055/s-2007-978865
Originals Clinical

© Georg Thieme Verlag Stuttgart · New York

A High-Sucrose Diet Alters the Lipid Composition and Fluidity of Liver Sinusoidal Membranes

D. A. Podolin1 , E. Sutherland2 , M. Iwahashi2 , F. R. Simon2 , M. J. Pagliassotti1
  • 1Department of Pediatrics and Center for Human Nutrition, University of Colorado Health Sciences Center, Denver, CO, USA
  • 2Hepatobiliary Research Center, University of Colorado Health Sciences Center, Denver, CO, USA
Further Information

Publication History

1997

1997

Publication Date:
20 April 2007 (online)

Impaired insulin suppression of hepatic glucose production and accumulation of hepatic triglycerides occur after 1 week on a high-sucrose diet. The purpose of this study was to ascertain whether changes in structural lipids, fatty acid composition and/or fluidity occur after 1 week on a high-sucrose diet, and therefore might contribute to the sucrose-induced impairment in hepatic glucose metabolism. Male Wistar rats (n = 28) were fed a purified high starch (68% of energy) diet for a 2-week baseline period. Fourteen animals were then switched to a high sucrose (68% of energy) diet for 1 (n = 7) or 5 (n = 7) weeks. Analyses were performed on liver sinusoidal membranes (due to this membrane's involvement in nutrient transport) from overnight fasted rats. The degree of saturation of sinusoidal membrane phospholipids and liver triglyceride fatty acids was significantly greater in sucrose vs. starch at 1 and 5 weeks. This resulted in significantly lower sinusoidal membrane fluidity at 1 and 5 weeks in the sucrose group. In contrast, hepatic sinusoidal membrane cholesterol content (0.60 ± 0.05 vs. 0.42 ± 0.04 µmol/mg protein) and the cholesterol to phospholipid molar ratio (0.66 ± 0.04 vs. 0.50 ± 0.03) were significantly greater in sucrose vs. starch animals at 5 weeks only. Minimal differences were observed in individual phospholipid species between groups. These data suggest that changes in fatty acid composition and fluidity may contribute to the development of sucrose-induced hepatic insulin resistance.

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