Abstract

BackgroundProxies are mathematical calculations based on fasting glucose and/or insulin concentrations developed to allow prediction of insulin sensitivity (IS) and β-cell response. These proxies have not been evaluated in horses with insulin dysregulation. The first objective of this study was to evaluate how fasting insulin (FI) and proxies for IS (1/Insulin, reciprocal of the square root of insulin (RISQI) and the quantitative insulin sensitivity check index (QUICKI)) and β-cell response (the modified insulin-to-glucose ratio (MIRG) and the homeostatic model assessment of β-cell function (HOMA-β)) were correlated to measures of IS (M index) using the euglycemic hyperinsulinemic clamp (EHC) in horses with insulin resistance (IR) and normal IS. A second objective was to evaluate the repeatability of FI and proxies in horses based on sampling on consecutive days. The last objective was to investigate the most appropriate cut-off value for the proxies and FI.ResultsThirty-four horses were categorized as IR and 26 as IS based on the M index. The proxies and FI had coefficients of variation (CVs) ≤ 25.3 % and very good reliability (intraclass correlation coefficients ≥ 0.89). All proxies and FI were good predictors of the M index (r = 0.76–0.85; P < 0.001). The proxies for IS had a positive linear relationship with the M index whereas proxies for β-cell response and FI had an inverse relationship with the M index. Cut-off values to distinguish horses with IR from horses with normal IS based on the M index were established for all proxies and FI using receiver operating characteristic curves, with sensitivity between 79 % and 91 % and specificity between 85 % and 96 %. The cut-off values to predict IR were < 0.32 (RISQI), < 0.33 (QUICKI) and > 9.5 µIU/mL for FI.ConclusionsAll proxies and FI provided repeatable estimates of horses’ IS. However, there is no advantage of using proxies instead of FI to estimate IR in the horse. Due to the heteroscedasticity of the data, proxies and FI in general are more suitable for epidemiological studies and larger clinical studies than as a diagnostic tool for measurement of IR in individual horses.

Highlights

  • Proxies are mathematical calculations based on fasting glucose and/or insulin concentrations developed to allow prediction of insulin sensitivity (IS) and β-cell response

  • Correlation between proxies and insulin sensitivity measures from the euglycemic hyperinsulinemic clamp (EHC) Scatter plots showing the correlation between fasting indices for β-cell response (FI, Modified insulin-to-glucose ratio (MIRG) and homeostatic model assessment of β-cell function (HOMA-β)) and the M index demonstrate an inverse relationship (Fig. 2, a - c)

  • The fasting indices for β-cell response were highly correlated with the M index derived from the EHC; r = 0.85, 0.76 and 0.84 for fasting insulin (FI), MIRG and HOMA-β respectively (P < 0.001)

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Summary

Introduction

Proxies are mathematical calculations based on fasting glucose and/or insulin concentrations developed to allow prediction of insulin sensitivity (IS) and β-cell response These proxies have not been evaluated in horses with insulin dysregulation. The first objective of this study was to evaluate how fasting insulin (FI) and proxies for IS (1/Insulin, reciprocal of the square root of insulin (RISQI) and the quantitative insulin sensitivity check index (QUICKI)) and β-cell response (the modified insulin-to-glucose ratio (MIRG) and the homeostatic model assessment of β-cell function (HOMA-β)) were correlated to measures of IS (M index) using the euglycemic hyperinsulinemic clamp (EHC) in horses with insulin resistance (IR) and normal IS. Proxies are mathematical calculations based on fasting glucose concentration (FG) and/or fasting insulin (FI) concentrations developed to allow prediction of insulin sensitivity (IS) and β-cell response [4] In both humans and horses, proxies correlate well with quantitative measurements of IS [5,6,7]. The proxies for IS are linearly correlated with quantitative measurements for IS, whereas proxies for β-cell response are inversely related [5, 6]

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