PubMed Health⌕ Search

PubMed · 382871

Glucose clamp technique: a method for quantifying insulin secretion and resistance.

Abstract

Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique) are described. Hyperglycemic clamp technique. The plasma glucose concentration is acutely raised to 125 mg/dl above basal levels by a priming infusion of glucose. The desired hyperglycemic plateau is subsequently maintained by adjustment of a variable glucose infusion, based on the negative feedback principle. Because the plasma glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism. Under these conditions of constant hyperglycemia, the plasma insulin response is biphasic with an early burst of insulin release during the first 6 min followed by a gradually progressive increase in plasma insulin concentration. Euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained at approximately 100 muU/ml by a prime-continuous infusion of insulin. The plasma glucose concentration is held constant at basal levels by a variable glucose infusion using the negative feedback principle. Under these steady-state conditions of euglycemia, the glucose infusion rate equals glucose uptake by all the tissues in the body and is therefore a measure of tissue sensitivity to exogenous insulin.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R A DeFronzo, J D Tobin, R Andres. 1979. Glucose clamp technique: a method for quantifying insulin secretion and resistance.. https://doi.org/10.1152/ajpendo.1979.237.3.e214

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Glucose recovery with bare and hydrogel-coated microdialysis probes: experiment and simulation of temporal effects.

In vitro microdialysis glucose sampling was used to test the transient and steady-state suitability of antifouling hydrogel coatings, composed of 2-hydroxyethyl methacrylate, vinylpyrrolidinone, and poly(ethylene glycol). The in vitro glucose diffusion coefficients of bare microdialysis membranes and hydrogel coatings were determined experimentally to be 1.1 x 10-6 and 3.2 x 10-6 cm2/s, respectively. These values were used to numerically simulate the effect of the hydrogel on glucose transport across the microdialysis membrane using a convection-diffusion transport model. The times for dialysate at the exit of the bare and hydrogel-coated microdialysis probes to reach 95% of steady state were calculated to be 20 and 66 s, respectively. However, the experimental data showed that 95% of steady-state glucose recoveries were reached after 4-5 min. Numerical simulations incorporating the Taylor dispersion in the outlet tubing showed the time difference was caused almost completely by convective transport in the outlet tubing with negligible contribution from analyte profile broadening. These data indicated that the hydrogel coatings imposed 44% reduction in glucose permeability and consequently 26% reduction in the percent recovery. The effect of hydrogel coatings on the time to reach the steady-state recovery was insignificant compared with the time required for convection of glucose in the outlet tubing.

Glucose↗

Modulation of glucose transport in skeletal muscle by reactive oxygen species.

Glucose transport is an essential physiological process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the GLUT-4 protein under conditions of increased carbohydrate utilization. The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.

Glucose↗

Glucose-specific poly(allylamine) hydrogels--a reassessment.

Polymer hydrogels synthesized by crosslinking poly(allylamine hydrochloride) with (+/-)-epichlorohydrin in the presence of d-glucose-6-phosphate monobarium salt do not show imprinting on the molecular level. A series of hydrogels was prepared using the following five templates: d-glucose-6-phosphate monobarium salt, d-glucose, l-glucose, barium hydrogen phosphate (BaHPO(4)), and d-gluconamide; a hydrogel was also prepared in the absence of a template. For all six hydrogels, batch binding studies were conducted with d-glucose, l-glucose, d-fructose, and d-gluconamide. The extent of analyte sugar binding was determined using (1)H NMR. Each hydrogel shows approximately the same relative binding affinity for the different sugar derivatives, and none displays selectivity for either glucose enantiomer. The results of the binding studies correlate with the octanol-water partition coefficients of the sugars, indicative that differential solubilities in the bulk polymer account for the binding affinities observed. Thus, in contrast to templated hydrogels prepared using methacrylate- or acrylamide-based reagents, true imprinting does not occur in this novel, crosslinked-poly(allylamine hydrochloride) system.

Glucose↗