GLUT glucose transporter mRNA has been shown to be underexpressed in pancreatic islets of numerous animal models of non-insulin-dependent diabetes mellitus (NIDDM). It has been proposed that this molecular defect contributes to the pathogenesis of diabetes, although information concerning the expression of GLUTS in human pancreatic islet tissue is lacking, In contrast to the high abundance of GLUTS in rat islets, human islets were found to express distinctly low levels of this glucose transporter mRNA and protein, Thus, a sensitive competitive reverse transcription-polymerase chain reaction assay was developed to quantify human GLUTS mRNA. We obtained pancreases from 4 human organ donors with previously diagnosed NIDDM and 11 nondiabetic donors and found no significant differences in GLUTS mRNA between the two groups, GLUTS mRNA was 0.24 +/- 0.08 amol/mu g RNA (mean +/- SE) in pancreases from humans with diabetes and 0.27 +/- 0.06 amol/mu g RNA in those without this diagnosis. Similarly, human pancreatic islet GLUTS protein was measured by immunoblot and found to be present at similar levels in two individuals with diabetes relative to six control samples. These results thus demonstrate the existence of species differences in the abundance of islet GLUTS mRNA and protein, Furthermore, the analysis of islet GLUTS in a small sample of human organ donors with and without diabetes raises the possibility that decreased beta-cell GLUT2 may not represent a widespread feature of humans with NIDDM.