3.8 Article

Association of serum kynurenine/tryptophan ratio with poor glycemic control in patients with type2 diabetes

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JOURNAL OF DIABETES AND METABOLIC DISORDERS
卷 20, 期 2, 页码 1521-1527

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SPRINGER INT PUBL AG
DOI: 10.1007/s40200-021-00895-z

关键词

Type 2 diabetes mellitus; Insulin resistance; Indoleamine 2; 3 dioxygenase; Oxidative stress

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The study found that T2DM patients had higher levels of FBS, HbA1c, HOMA-IR, and KTR compared to controls, while TAC and HOMA-B were significantly lower. KTR was significantly correlated with HbA1c levels, and T2DM patients with poor glycemic control had higher KTR levels. HOMA-B was significantly correlated with serum tryptophan and inversely correlated with HbA1c.
Purpose The role of indoleamine 2,3-dioxygenase (IDO) has been shown in insulin resistance and metabolic syndrome. The present study aimed to measure serum IDO activity in patients with type 2 diabetes (T2DM) and to determine its association with glycemic control, oxidative stress, and insulin resistance. Methods Seventy-four patients with T2DM and 74 healthy subjects were selected to participate in this study. Fasting serum biochemical parameters including fasting blood sugar (FBS), HbA1c, insulin, uric acid, albumin, tryptophan, kynurenine, and total antioxidant capacity (TAC) were measured. HOMA-IR, QUICKI, and HOMA-B were calculated using serum FBS and insulin values. IDO activity was estimated using kynurenine/tryptophan ratio (KTR). Data were analyzed using SPSS software (Version 15) and p < 0.05 was considered as a significant difference. Results The findings showed higher levels of FBS, HbA1c, HOMA-IR, and KTR in the patients compared to the controls. TAC and HOMA-B were significantly lowered in the T2DM patients compared to controls. KTR was significantly correlated with the level of HbA1c, and T2DM patients with poor glycemic control (HbA1c <= 8) had significantly higher level of KTR. HOMA-B was significantly correlated with serum tryptophan and inversely correlated with HbA1c. Conclusion Serum KTR is increased in T2DM patients with poor glycemic control. Potential clinical implications and possible pathogenic roles of IDO in T2DM development should be further elucidated.

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