Display options
Cite
Sakamoto E, Seino Y, Fukami A, et al. Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. J Diabetes Investig. 2012;3(5):432-40doi: 10.1111/j.2040-1124.2012.00208.x.
Sakamoto, E., Seino, Y., Fukami, A., Mizutani, N., Tsunekawa, S., Ishikawa, K., Ogata, H., Uenishi, E., Kamiya, H., Hamada, Y., Sato, H., Harada, N., Toyoda, Y., Miwa, I., Nakamura, J., Inagaki, N., Oiso, Y., & Ozaki, N. (2012). Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. Journal of diabetes investigation, 3(5), 432-40. https://doi.org/10.1111/j.2040-1124.2012.00208.x
Sakamoto, Eriko, et al. "Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion." Journal of diabetes investigation vol. 3,5 (2012): 432-40. doi: https://doi.org/10.1111/j.2040-1124.2012.00208.x
Sakamoto E, Seino Y, Fukami A, Mizutani N, Tsunekawa S, Ishikawa K, Ogata H, Uenishi E, Kamiya H, Hamada Y, Sato H, Harada N, Toyoda Y, Miwa I, Nakamura J, Inagaki N, Oiso Y, Ozaki N. Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. J Diabetes Investig. 2012 Oct 18;3(5):432-40. doi: 10.1111/j.2040-1124.2012.00208.x. PMID: 24843603; PMCID: PMC4019243.
Copy Download .nbib Format: NLM
Share it on

J Diabetes Investig. 2012 Oct 18;3(5):432-40. doi: 10.1111/j.2040-1124.2012.00208.x.

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

Journal of diabetes investigation

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

Affiliations

  1. Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine.
  2. Department of Endocrinology and Diabetes, Field of Internal Medicine, Nagoya University Graduate School of Medicine ; Department of Metabolic Medicine, Nagoya University School of Medicine.
  3. Diabetes Center, Aichi Medical University, Nagakute.
  4. Department of Metabolic Medicine, Nagoya University School of Medicine.
  5. Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University.
  6. Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
  7. 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.

PMID: 24843603 PMCID: PMC4019243 DOI: 10.1111/j.2040-1124.2012.00208.x

Abstract

UNLABELLED: 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 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).

Keywords: Glucagon‐like peptide‐1; Glucokinase; High‐sucrose diet

References

  1. Diabetes. 2010 Nov;59(11):2697-707 - PubMed
  2. Diabetes Care. 1992 Mar;15(3):318-68 - PubMed
  3. J Nutr. 2006 Mar;136(3):582-7 - PubMed
  4. Am J Clin Nutr. 2007 Oct;86(4):899-906 - PubMed
  5. Am J Clin Nutr. 1988 Mar;47(3):420-7 - PubMed
  6. Gastroenterology. 2007 May;132(6):2131-57 - PubMed
  7. Am J Physiol. 1995 Sep;269(3 Pt 2):R641-6 - PubMed
  8. Diabetes. 2007 Apr;56(4):1000-9 - PubMed
  9. Nutr Metab (Lond). 2005 Feb 21;2(1):5 - PubMed
  10. Am J Physiol. 1996 Nov;271(5 Pt 2):R1319-26 - PubMed
  11. J Biol Chem. 1999 Nov 5;274(45):31833-8 - PubMed
  12. J Clin Endocrinol Metab. 2001 Aug;86(8):3717-23 - PubMed
  13. J Biol Chem. 1999 Jan 1;274(1):305-15 - PubMed
  14. Diabetes. 2011 Apr;60(4):1246-57 - PubMed
  15. Obes Rev. 2009 Mar;10 Suppl 1:24-33 - PubMed
  16. Physiol Behav. 1993 Jan;53(1):139-43 - PubMed
  17. Diabetes. 1989 May;38(5):550-7 - PubMed
  18. Diabetes. 2003 Feb;52(2):252-9 - PubMed
  19. Medscape J Med. 2008 Jul 09;10(7):160 - PubMed
  20. J Nutr. 2003 Dec;133(12):4095-101 - PubMed
  21. J Clin Invest. 2004 Jun;113(11):1571-81 - PubMed
  22. Nature. 1992 Apr 23;356(6371):721-2 - PubMed
  23. Am J Physiol. 1997 Feb;272(2 Pt 2):R526-31 - PubMed
  24. J Biol Chem. 1994 Sep 2;269(35):21925-8 - PubMed
  25. Diabetes. 1985 Jun;34(6):580-8 - PubMed
  26. Biochem Biophys Res Commun. 2006 Sep 8;347(4):1138-44 - PubMed
  27. Diabetes. 1983 Jul;32(7):675-9 - PubMed
  28. Am J Physiol. 1994 May;266(5 Pt 2):R1637-44 - PubMed
  29. J Nutr. 2003 Jan;133(1):127-33 - PubMed
  30. Physiol Rev. 2007 Oct;87(4):1409-39 - PubMed
  31. J Endocrinol. 1993 Jul;138(1):159-66 - PubMed
  32. J Clin Endocrinol Metab. 1986 Aug;63(2):492-8 - PubMed
  33. Diabetes. 2001 Mar;50(3):609-13 - PubMed
  34. J Clin Invest. 1992 Oct;90(4):1323-7 - PubMed
  35. Diabetes. 2008 May;57(5):1340-8 - PubMed
  36. Chem Pharm Bull (Tokyo). 1986 Nov;34(11):4731-7 - PubMed
  37. Am J Clin Nutr. 2004 Apr;79(4):537-43 - PubMed
  38. Clin Sci (Lond). 1999 Apr;96(4):335-42 - PubMed
  39. Diabetes. 2006 Jul;55(7):2015-20 - PubMed
  40. J Biol Chem. 1988 Jan 15;263(2):740-4 - PubMed
  41. J Clin Invest. 2006 Jun;116(6):1494-505 - PubMed
  42. Biochem J. 2008 Aug 15;414(1):1-18 - PubMed
  43. J Physiol. 2009 Jan 15;587(1):27-32 - PubMed
  44. Mol Cell. 2000 Jul;6(1):87-97 - PubMed
  45. Endocrinology. 1999 Apr;140(4):1687-94 - PubMed
  46. Endocrinology. 1991 Jun;128(6):3169-74 - PubMed
  47. J Diabetes Investig. 2010 Apr 22;1(1-2):8-23 - PubMed

Publication Types