Insulin Secretory Defect and Insulin Resistance in Isolated Impaired Fasting Glucose and Isolated Impaired Glucose Tolerance

• Main Authors: Sae Aoyama-Sasabe, Mitsuo Fukushima, Xin Xin, Ataru Taniguchi, Yoshikatsu Nakai, Rie Mitsui, Yoshitaka Takahashi, Hideaki Tsuji, Daisuke Yabe, Koichiro Yasuda, Takeshi Kurose, Nobuya Inagaki, Yutaka Seino
• Format: Article
• Language: English
• Published: Hindawi Limited 2016-01-01
• Series: Journal of Diabetes Research
• Online Access: http://dx.doi.org/10.1155/2016/1298601

Objective. To investigate the characteristics of isolated impaired glucose tolerance (IGT) and isolated impaired fasting glucose (IFG), we analyzed the factors responsible for elevation of 2-hour postchallenge plasma glucose (2 h PG) and fasting plasma glucose (FPG) levels. Methods. We investigated the relationship between 2 h PG and FPG levels who underwent 75 g OGTT in 5620 Japanese subjects at initial examination for medical check-up. We compared clinical characteristics between isolated IGT and isolated IFG and analyzed the relationships of 2 h PG and FPG with clinical characteristics, the indices of insulin secretory capacity, and insulin sensitivity. Results. In a comparison between isolated IGT and isolated IFG, insulinogenic index was lower in isolated IGT than that of isolated IFG (0.43 ± 0.34 versus 0.50 ± 0.47, resp.; p<0.01). ISI composite was lower in isolated IFG than that of isolated IGT (6.87 ± 3.38 versus 7.98 ± 4.03, resp.; p<0.0001). In isolated IGT group, insulinogenic index showed a significant correlation with 2 h PG (r=-0.245, p<0.0001) and had the strongest correlation with 2 h PG (β=-0.290). In isolated IFG group, ISI composite showed a significant correlation with FPG (r=-0.162, p<0.0001) and had the strongest correlation with FPG (β=-0.214). Conclusions. We have elucidated that decreased early-phase insulin secretion is the most important factor responsible for elevation of 2 h PG levels in isolated IGT subjects, and decreased insulin sensitivity is the most important factor responsible for elevation of FPG levels in isolated IFG subjects.