Altered expression of glycoproteins and glycosphingolipids in a mouse model whose glycemic status is controlled by a low carbohydrate ketogenic diet

2014 Fiscal Year Final Research Report

• Project/Area Number: 24700859
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Eating habits, studies on eating habits
• Research Institution: National Institute of Advanced Industrial Science and Technology
• Principal Investigator: OKUDA Tetsuya 独立行政法人産業技術総合研究所, 生物プロセス研究部門, 主任研究員 (20443179)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 糖鎖抗原 / 糖尿病 / 食事療法 / ケトン食 / バイオマーカー / O-GlcNAc / スフィンゴ糖脂質 / ob/obマウス

Outline of Final Research Achievements

Abnormal modification of proteins by O-linked N-acetylglucosamine (O-GlcNAc) is known to be associated with the pathology induced by hyperglycemia. However, the dynamic mechanism of O-GlcNAc modification under hyperglycemic conditions in vivo has not been fully characterized.
Here we showed that Akt protein kinase was modified by O-GlcNAc in the liver of mice under hyperglycemic condition, and the modification levels were decreased by improvement of hyperglycemia. Furthermore, aberrant phosphorylation of Akt was found in the liver of mice under hyperglycemic condition.
In addition, we found that feeding of a very low carbohydrate diet (ketogenic diet) influenced the expression levels of sialoglycans in mouse liver. To develop a quantification method for these sialoglycans, we generated monoclonal antibodies react with these sialoglycans.

Free Research Field

糖鎖生物学、糖鎖抗原、糖鎖発現制御