The remainder of glucose uptake by muscle ( 12– 14) and fat is both glucose and insulin dependent ( Fig.
In normal humans, 50% of the basal glucose turnover is to the nervous system, and this is a glucose-dependent process ( Fig. The basal glucose efflux of 0.8 mmol/min ( 8, 9) is assumed to enter a space of 17 l ( 9, 10). Insulin is modeled to decay with a half-life of 3.8 min with an additional slower component ( 5, 7) the insulin concentration controls glucose uptake in fat and muscle ( Fig. Hepatic glucose efflux and uptake are modeled to be dependent on plasma glucose and insulin concentrations ( Fig. 1A) was originally constructed on the basis of a basal production rate of 10 mU/min (74 pmol/min) ( 4) at a plasma glucose level of 4 mmol/l, into an insulin space of 13 l with a plasma insulin half-life of 4 min ( 5). The predictions used in the model arise from experimental data in humans and animals. The relationship between glucose and insulin in the basal state reflects the balance between hepatic glucose output and insulin secretion, which is maintained by a feedback loop between the liver and β-cells ( 3). The HOMA model is used to yield an estimate of insulin sensitivity and β-cell function from fasting plasma insulin and glucose concentrations ( 1). However, as with all models, the primary input data need to be robust, and the data need to be interpreted carefully. In conclusion, the HOMA model has become a widely used clinical and epidemiological tool and, when used appropriately, it can yield valuable data. The HOMA model compares favorably with other models and has the advantage of requiring only a single plasma sample assayed for insulin and glucose. We review the use and reporting of HOMA in the literature and give guidance on its appropriate use (e.g., cohort and epidemiological studies) and inappropriate use (e.g., measuring β-cell function in isolation). HOMA has been validated against a variety of physiological methods. The computer model is available but has not been as widely used as the approximation formulae. The original HOMA model was described in 1985 with a formula for approximate estimation.
Decreases in β-cell function were modeled by changing the β-cell response to plasma glucose concentrations. Hepatic and peripheral glucose efflux and uptake were modeled to be dependent on plasma glucose and insulin concentrations. This article summarizes the physiological basis of HOMA, a structural model of steady-state insulin and glucose domains, constructed from physiological dose responses of glucose uptake and insulin production. It has been reported in >500 publications, 20 times more frequently for the estimation of IR than β-cell function. Homeostatic model assessment (HOMA) is a method for assessing β-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin or C-peptide concentrations.