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Most Cited Journal Articles 2004-Medical Sciences

Following is a CAS database record representing a highly cited journal article.

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CAS indexed 1 chemical substance from this document. CAS subject entries for this document include: Blood plasma; Blood sugar; Process simulation, biological; and 2 additional concepts.

CAPLUS COPYRIGHT 2005 ACS on STN

TITLE:	Homeostasis model assessment: insulin resistance and .beta.-cell function from fasting plasma glucose and insulin concentrations in man
AUTHOR(S):	Matthews, D. R.; Hosker, J. P.; Rudenski, A. S.; Naylor, B. A.; Treacher, D. F.; Turner, R. C.
CORPORATE SOURCE:	Diabetes Res. Lab., Radcliffe Infirm., Oxford, OX2 6HE, UK
SOURCE:	Diabetologia (1985), 28(7), 412-19 CODEN: DBTGAJ; ISSN: 0012-186X
PUBLISHER:
LANGUAGE:	English

ABSTRACT:
The steady-state basal plasma glucose and insulin concns. are detd. by their interaction in a feedback loop. A computer-solved model was used to predict the homeostatic concns. which arise from varying degrees of .beta.-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quant. assessment of the contributions of insulin resistance and deficient .beta.-cell function to the fasting hyperglycemia (homeostasis model assessment, HOMA). The accuracy and precision of the est. were detd. by comparison with independent measures of insulin resistance and .beta.-cell function using hyperglycemic and euglycemic clamps and an i.v. glucose tolerance test. The est. of insulin resistance obtained by homeostasis model assessment correlated with ests. obtained by use of the euglycemic clamp, the fasting insulin concn., the the hyperglycemic clamp. There was no correlation with any aspect of insulin-receptor binding. The est. of deficient .beta.-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycemic clamp and with the est. from the i.v. glucose tolerance test. The low precision of the ests. from the model (coeffs. of variation: 31% for insulin resistance and 32% for .beta.-cell deficit) limits its use, but the correlation of the model's ests. with patient data accords with the hypothesis that basal glucose and insulin interactions are largely detd. by a simple feed back loop.