A 52-year-old lean woman was admitted to hospital for a medical examination in July 2010. A 75 g oral glucose test (75 g OGTT) revealed postprandial hyperglycemia (above 200 mg/dl at 120 min) and she was diagnosed with diabetes mellitus. She was negative for diabetes-related autoantibodies. The 75 g OGTT also revealed a very low insulinogenic index (I. I.) of 0. 024 μU/ml/mg/dl; however, her plasma C-peptide immunoreactivity (CPR) response to glucagon was preserved (0. 94 and 5. 56 at 0 and 6 min, respectively). At the same time, she also suffered from Fe-deficiency anemia due to endometriosis, for which treatment with leuprorelin was initiated after hospitalization in August 2010. Meanwhile, her postprandial plasma glucose level continued to increase. Subsequently, on November 30, 2010, alogliptin therapy at a dose of 6. 25 mg was initiated, which was increased to 25 mg on December 28, 2010. Leuprorelin therapy was discontinued on January 14, 2011; however, her plasma glucose level remained high despite the alogliptin therapy. Administration of 0. 3 mg liraglutide was initiated on March 15, 2011, and the dose was increased to 0. 6 mg on June 7, 2011. The plasma glucose level, glycosylated hemoglobin (HbA1c) level, and 1. 5 anhydroglucitol level gradually improved, as did her I. I. Moreover, fasting plasma glucagon levels were suppressed by liraglutide. Her fasting serum CPR to plasma glucose ratio and homeostasis model assessment (HOMA-R) were low both before and after liraglutide administration. These results suggest that the fasting CPR to glucose ratio may underestimate residual islet function in lean patients with high insulin sensitivity. Thus, a glucagon test may be useful to estimate residual islet function when administering liraglutide treatment in lean diabetes patients.
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