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


METHODS
C57BL/6J mice received a SUC (38.5% sucrose), a high-starch diet (ST) or a control diet for 5 weeks. 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 15 min 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. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2012.00208.x, 2012).
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Eriko
E
Sakamoto
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine ; Department of Metabolic Medicine, Nagoya University School of Medicine.
Yusuke
Y
Seino
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Ayako
A
Fukami
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Naohiro
N
Mizutani
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Shin
S
Tsunekawa
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Kota
K
Ishikawa
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Hidetada
H
Ogata
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Eita
E
Uenishi
Diabetes Center, Aichi Medical University, Nagakute.
Hideki
H
Kamiya
Department of Metabolic Medicine, Nagoya University School of Medicine.
Yoji
Y
Hamada
Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University.
Hiroyuki
H
Sato
Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Norio
N
Harada
Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University.
Yukiyasu
Y
Toyoda
Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University.
Ichitomo
I
Miwa
Diabetes Center, Aichi Medical University, Nagakute.
Jiro
J
Nakamura
Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Nobuya
N
Inagaki
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
Yutaka
Y
Oiso
Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine ; Research Center of Health, Physical Fitness and Sports, Nagoya University, Nagoya.
Nobuaki
N
Ozaki
Glucagon‐like peptide‐1; Glucokinase; High‐sucrose diet