Do We Know What Homeostasis Model Assessment Measures?
If not, does it matter?
- Edward J. Boyko, MD, MPH12 and
- Christine Chen Jensen, MD, MPH3
- 1Department of Medicine, University of Washington School of Medicine, Seattle, Washington
- 2International Diabetes Institute, Caulfield, Victoria, Australia
- 3Department of Surgery, University of Washington School of Medicine, Seattle, Washington
- Address correspondence and reprint requests to Edward J. Boyko, MD, MPH, Seattle ERIC, 1100 Olive Way, Suite 1400, Seattle, WA 98101. E-mail: eboyko{at}u.washington.edu
- HOMA, homeostasis model assessment
- HOMA-%B, HOMA of insulin secretion
- HOMA-IR, HOMA of insulin resistance
- QUICKI, quantitative insulin sensitivity check index
- WHI, Women's Health Initiative
The point-counterpoint articles in the September issue of Diabetes Care (1,2) raise several interesting issues on our understanding of insulin resistance, homeostasis model assessment (HOMA), and the future of measurement shortcuts for insulin resistance and secretion. McAuley et al. (1) provide an overview of methods to assess insulin sensitivity and secretion. The conditional nature of the title of their article implies that there is room for improvement and that something better will come along to assess insulin resistance and secretion with the convenience of HOMA but with better accuracy. For the time being, however, they support its use.
Hockaday et al. (2) bring up many points that undermine confidence in HOMA as a measure of insulin resistance. Input into HOMA consists of fasting insulin and glucose concentration and thus will reflect conditions present in the basal state, with the liver as the main target for insulin action as manifested by the suppression of gluconeogenesis. A shortcoming of HOMA is the lack of complete capture of brain glucose uptake, of which 50% is non–insulin mediated. Although HOMA has been compared against the euglycemic hyperinsulinemic clamp, the current gold standard for assessment of insulin sensitivity, the latter method assesses insulin resistance in the stimulated state, which is a function to a large extent of muscle glucose disposal. Thus, an implicit assumption of HOMA is that steady-state and stimulated insulin resistance are highly correlated. Other concerns include test variability over time and the assumption that insulin resistance, if present, is common to major sites of insulin action (liver, muscle, and adipose tissue).
Similarly, a number of concerns are raised about the use of HOMA to assess insulin secretion. Of particular concern is whether β-cell glycemic sensitivity can be assumed constant. In addition, other factors bear on insulin secretion that are not …
