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. 2018 May 23;13(5):e0197663.
doi: 10.1371/journal.pone.0197663. eCollection 2018.

CPR-IR is an insulin resistance index that is minimally affected by hepatic insulin clearance-A preliminary research

Tsuyoshi Okura  1 , Risa Nakamura  1 , Yohei Fujioka  1 , Sonoko Kawamoto-Kitao  1 , Yuichi Ito  1 , Kazuhisa Matsumoto  1 , Kyoko Shoji  1 , Keisuke Sumi  1 , Kazuhiko Matsuzawa  1 , Shoichiro Izawa  1 , Etsuko Ueta  2 , Masahiko Kato  1 , Takeshi Imamura  3 , Shin-Ichi Taniguchi  4 , Kazuhiro Yamamoto  1
Affiliations

CPR-IR is an insulin resistance index that is minimally affected by hepatic insulin clearance-A preliminary research

Tsuyoshi Okura et al. PLoS One. .

Abstract

Background: Increased hepatic insulin clearance (HIC) is important in the pathophysiology of type 2 diabetes mellitus (T2DM). The aim of this study is to analyze an effective insulin resistance (IR) index that is minimally affected by HIC.

Methods: Our study involved 20 participants with T2DM and 21 healthy participants without diabetes (Non-DM). Participants underwent a meal tolerance test from which plasma glucose, insulin and serum C-peptide immunoreactivity (CPR) were measured, and HOMA-IR and HIC were calculated. Participants then underwent a hyperinsulinemic-euglycemic clamp from which the glucose disposal rate (GDR) was measured.

Results: The index CPR-IR = 20/(fasting CPR × fasting plasma glucose) was correlated more strongly with GDR, than was HOMA-IR, and CPR-IR could be used to estimate GDR. In T2DM participants with HIC below the median, HOMA-IR and CPR-IR were equally well correlated with GDR. In T2DM with high HIC, CPR-IR correlated with GDR while HOMA-IR did not. In Non-DM, CPR-IR and HOMA-IR were equally well correlated with GDR regardless of HIC. The mean HIC value in T2DM was significantly higher than that of Non-DM.

Conclusions: CPR-IR could be a simple and effective index of insulin resistance for patients with type 2 diabetes that is minimally affected by HIC.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1
The correlation between the glucose disposal rate (GDR) and C-peptide immunoreactivity insulin resistance (CPR-IR; A, B) or homeostasis model assessment of insulin resistance (HOMA-IR; C, D), where black circles depict results from study participants with type 2 diabetes mellitus and white circles depict results from study participants without diabetes.
See this image and copyright information in PMC

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References

    1. DeFronzo RA. Lilly lecture 1987. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM. Diabetes 1988; 37: 667–687. - PubMed
    1. DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol 1979; 237: 214–223. - PubMed
    1. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28: 412–419. - PubMed
    1. Kang ES, Yun YS, Park SW, Kim HJ, Ahn CW, Song YD, et al. Limitation of the validity of the homeostasis model assessment as an index of insulin resistance in Korea. Metabolism 2005; 54: 206–211. doi: 10.1016/j.metabol.2004.08.014 - DOI - PubMed
    1. Kadowaki T, Miyake Y, Kajinuma H. Risk factors for worsening to diabetes in subjects with impaired glucose tolerance. Diabetologia 1984; 26: 44–49. - PubMed

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Grants and funding

This work was supported by a JSPS KAKENHI Grant-in-Aid for Scientific Research (C) grant number 16K08935 (2016-2019), JSPS KAKENHI Grant-in-Aid for Young Scientists (B) grant number 26870373 (2014–2015), the Japan Diabetes Foundation (2013), grants for young researchers from the Japan Association for Diabetes Education and Care (2013, 2014), Tottori University Faculty of Medicine Research Grant (2013) and Tottori University Hospital Research Grant (2013). This work also supported by the MSD research grant (2013, 2015).