IL28B gene variants and glucose metabolism in Type 2 Diabetes

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• 作者：Y. Morá ; n-Auth^a ; ^{yasmin_moran@gmx.de} ; M. Penna-Martinez^a ; D. Perner^a ; S. Susser^a ; S. Wicker^b ; S. Zeuzem^a ; C. Sarrazin^a ; K. Badenhoop^a
• 关键词：T2D ; Type 2 Diabetes ; HC ; healthy controls ; IL28B ; interleukin-28B ; HCV ; hepatitis C virus ; HOMA-IR ; homeostasis model assessment of insulin resistance ; BMI ; body mass index ; HbA1c ; hemoglobin A1c
• 刊名：Human Immunology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：77
• 期：12
• 页码：1280-1283
• 全文大小：310 K
• 卷排序：77

文摘

Type 2 Diabetes (T2D) develops, when β-cell insulin response fails to compensate for insulin resistance. Recent studies reported associations between the IL28B polymorphisms (rs12979860 and rs8099917) and T2D development in Hepatitis C virus (HCV) patients. To identify possible association with T2D independent from virus infection, we investigated both IL28B polymorphisms in T2D patients and healthy controls (HC). No association was found comparing the genotype and allele frequencies of both IL28B polymorphisms between T2D patients and HC. However, higher glucose levels were found in T2D patients carrying the IL28B CT/TT rs12979860 and GT/GG rs8099917 HCV risk genotypes compared to those with the protective CC and TT genotype (p = 0.06 and p = 0.02, respectively). Moreover, T2D patients with CT/TT rs12979860 HCV risk genotypes possessed significantly higher HbA1c levels than CC carriers (p = 0.04). In conclusion, the IL28B HCV risk genotypes may influence glucose homeostasis in T2D patients without HCV.