Abstract
Insulin increases muscle microvascular perfusion and enhances tissue insulin and nutrient delivery. Our aim was to determine phenotypic traits that foretell human muscle microvascular insulin responses. Hyperinsulinemic euglycemic clamps were performed in 97 adult humans who were lean and healthy, had class 1 obesity without comorbidities, or controlled type 1 diabetes without complications. Insulin-mediated whole-body glucose disposal rates (M-value) and insulin-induced changes in muscle microvascular blood volume (ΔMBV) were determined. Univariate and multivariate analyses were conducted to examine bivariate and multivariate relationships between outcomes, ΔMBV and M-value, and predictor variables, body mass index (BMI), total body weight (WT), percent body fat (BF), lean body mass, blood pressure, maximum consumption of oxygen (VO2max), plasma LDL (LDL-C) and HDL cholesterol, triglycerides (TG), and fasting insulin (INS) levels. Among all factors, only M-value (r = 0.23, p = 0.02) and VO2max (r = 0.20, p = 0.047) correlated with ΔMBV. Conversely, INS (r = − 0.48, p ≤ 0.0001), BF (r = − 0.54, p ≤ 0.001), VO2max (r = 0.5, p ≤ 0.001), BMI (r = − 0.40, p < 0.001), WT (r = − 0.33, p = 0.001), LDL-C (r = − 0.26, p = 0.009), TG (r = − 0.25, p = 0.012) correlated with M-value. While both ΔMBV (p = 0.045) and TG (p = 0.03) provided significant predictive information about M-value in the multivariate regression model, only M-value was uniquely predictive of ΔMBV (p = 0.045). Thus, both M-value and VO2max correlated with ΔMBV but only M-value provided unique predictive information about ΔMBV. This suggests that metabolic and microvascular insulin responses are important predictors of one another, but most metabolic insulin resistance predictors do not predict microvascular insulin responses.
Highlights
Insulin increases muscle microvascular perfusion and enhances tissue insulin and nutrient delivery
In order to sample from a range of insulin resistance patterns without the confounding influence of clinically significantly metabolic disarrays, we prospectively studied 97 adult human subjects who were either lean and healthy, had a diagnosis of class I obesity without other comorbidities, or controlled type 1 diabetes (T1D) without complications or other comorbidities
The studies were performed at the University of Virginia (UVA) Clinical Research Unit (CRU) under study protocols approved by the UVA Institutional Review Board (IRB) and in accordance with the World Medical Association’s 2013 Declaration of Helsinki
Summary
Insulin increases muscle microvascular perfusion and enhances tissue insulin and nutrient delivery. INS (r = − 0.48, p ≤ 0.0001), BF (r = − 0.54, p ≤ 0.001), VO2max (r = 0.5, p ≤ 0.001), BMI (r = − 0.40, p < 0.001), WT (r = − 0.33, p = 0.001), LDL-C (r = − 0.26, p = 0.009), TG (r = − 0.25, p = 0.012) correlated with M-value While both ΔMBV (p = 0.045) and TG (p = 0.03) provided significant predictive information about M-value in the multivariate regression model, only M-value was uniquely predictive of ΔMBV (p = 0.045). Abbreviations BF Percent body fat BMI Body mass index CEU Contrast enhanced ultrasound INS Insulin LDL-C LDL cholesterol MBV Microvascular blood volume T1D Type 1 diabetes T2D Type 2 diabetes TG Triglycerides VO2max Maximum consumption of oxygen WT Total body weight. Diseases like T2D and obesity that are characterized by metabolic insulin resistance, often manifest with diminished or absent vasodilatory responses to insulin[2,15]
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