Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion

Eriko Sakamoto, Yusuke Seino, Ayako Fukami, Naohiro Mizutani, Shin Tsunekawa, Kota Ishikawa, Hidetada Ogata, Eita Uenishi, Hideki Kamiya, Yoji Hamada, Hiroyuki Sato, Norio Harada, Yukiyasu Toyoda, Ichitomo Miwa, Jiro Nakamura, Nobuya Inagaki, Yutaka Oiso, Nobuaki Ozaki

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)

Abstract

Aims/Introduction: Excessive intake of sucrose can cause severe health issues, such as diabetes mellitus. In animal studies, consumption of a high-sucrose diet (SUC) has been shown to cause obesity, insulin resistance and glucose intolerance. However, several in vivo experiments have been carried out using diets with much higher sucrose contents (50-70% of the total calories) than are typically ingested by humans. In the present study, we examined the effects of a moderate SUC on glucose metabolism and the underlying mechanism. Materials and Methods: C57BL/6J mice received a SUC (38.5% sucrose), a high-starch diet (ST) or a control diet for 5weeks. We assessed glucose tolerance, incretin secretion and liver glucose metabolism. Results: An oral glucose tolerance test (OGTT) showed that plasma glucose levels in the early phase were significantly higher in SUC-fed mice than in ST-fed or control mice, with no change in plasma insulin levels at any stage. SUC-fed mice showed a significant improvement in insulin sensitivity. Glucagon-like peptide-1 (GLP-1) secretion 15min after oral glucose administration was significantly lower in SUC-fed mice than in ST-fed or control mice. Hepatic glucokinase (GCK) activity was significantly reduced in SUC-fed mice. During the OGTT, the accumulation of glycogen in the liver was suppressed in SUC-fed mice in a time-dependent manner. Conclusions: These results indicate that mice that consume a moderate SUC show glucose intolerance with a reduction in hepatic GCK activity and impairment in GLP-1 secretion.

Original languageEnglish
Pages (from-to)432-440
Number of pages9
JournalJournal of Diabetes Investigation
Volume3
Issue number5
DOIs
Publication statusPublished - 10-2012
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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