Metabolic syndrome and related disorders · 2017
Prediabetes Exhibits Decreased Disposition Index Correlated with Deterioration of Glycemic Parameters in Nonobese Japanese Subjects: A Cross-Sectional Study from Medical Examination.
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Takeda Yasutaka, Fujita Yukihiro, Yanagimachi Tsuyoshi, Honjo Jun, Abiko Atsuko, Asai Mahito, Haneda Masakazu
Аннотация
BACKGROUND: Prediabetes, defined as impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), likely develops to type 2 diabetes mellitus (DM) and independently increases cardiovascular risk. We employed disposition index (DI), a new metabolic parameter indicating the pancreatic beta cell function adjusted for insulin resistance, and investigated whether it could be altered in Japanese population with prediabetes and associated with early glucose intolerance.
METHODS: A total of 102 adults who underwent an oral glucose tolerance test at the medical screening were designated to normal glucose tolerance (NGT), IFG, IGT, and DM. We calculated insulinogenic index (IGI) and homeostasis model assessment (HOMA) of β cell function (HOMA-β) as insulin secretory function, HOMA-insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) as insulin resistance and DI, and assessed correlations between these indices and glycemic parameters.
RESULTS: We observed graded increase of glycemic parameters in the order of NGT, IFG, IGT, and DM. HOMA-IR was significantly higher only in DM compared with NGT, although HOMA-β, IGI, and QUICKI showed no significant differences among the groups. In contrast, DI was significantly lower in IFG, IGT, and DM compared with NGT. In correlation analysis, glycemic parameters related positively to HOMA-IR, but inversely to DI. Only two parameters, IGI and particularly DI, were significantly decreased in the subjects with 1-hr postload glucose >8.6 mmol/L previously proposed as a predictor of type 2 diabetes.
CONCLUSIONS: Our results suggest that reduction of DI promptly reflects the alteration of early glucose intolerance in Japanese population presenting with prediabetes.
METHODS: A total of 102 adults who underwent an oral glucose tolerance test at the medical screening were designated to normal glucose tolerance (NGT), IFG, IGT, and DM. We calculated insulinogenic index (IGI) and homeostasis model assessment (HOMA) of β cell function (HOMA-β) as insulin secretory function, HOMA-insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) as insulin resistance and DI, and assessed correlations between these indices and glycemic parameters.
RESULTS: We observed graded increase of glycemic parameters in the order of NGT, IFG, IGT, and DM. HOMA-IR was significantly higher only in DM compared with NGT, although HOMA-β, IGI, and QUICKI showed no significant differences among the groups. In contrast, DI was significantly lower in IFG, IGT, and DM compared with NGT. In correlation analysis, glycemic parameters related positively to HOMA-IR, but inversely to DI. Only two parameters, IGI and particularly DI, were significantly decreased in the subjects with 1-hr postload glucose >8.6 mmol/L previously proposed as a predictor of type 2 diabetes.
CONCLUSIONS: Our results suggest that reduction of DI promptly reflects the alteration of early glucose intolerance in Japanese population presenting with prediabetes.