Background: Metabolic syndrome is prevalent in adults characterized by increased visceral adiposity and insulin resistance (IR). However, the link between pancreatic b-cell function and metabolic syndrome severity in adults across the glucose spectrum is unknown. We hypothesized that poor b-cell function would independently predict a higher metabolic syndrome Z-score (i.e., severity). Methods: Seventy (12 normal glucose tolerant, 37 prediabetic, 21 type 2 diabetic) obese adults [62.4 -1.1 year; 34.6 -0.6 kg/m 2 ; data are mean -standard error of the mean (SEM)] participated in this cross-sectional study. A 2-hr 75-gram oral glucose tolerance test (OGTT) was administered, and insulin and glucose area under the curve was determined for calculations of insulin action. Fasting and glucose-stimulated insulin secretion was calculated using homeostasis model assessment of insulin secretion (HOMA-B) and the insulinogenic index (i.e., I 0-30 / Glc 0-30 or I 60-120 /Glc 60-120 ), respectively. Fasting and postprandial insulin sensitivity was assessed by HOMA-IR and the Matsuda Index, respectively. b-cell function was estimated using the disposition index via HOMA-B/ HOMA-IR, I 0-30 /Glc 0-30 or I 60-120 /Glc 60-120 · Matsuda Index, which represents basal, first-, and second-phase insulin release, respectively. Body composition (via computerized tomography and dual X-ray absorptiometry) and sex-specific metabolic syndrome Z-scores were calculated from waist circumference, blood pressure, fasting glucose, triglycerides, and high-density lipoproteins. Results: Compared to those with normal glucose tolerance, visceral fat and IR were higher and b-cell function was lower in adults with glucose intolerance and type 2 diabetes mellitus. Elevated visceral fat and IR (HOMA-IR and Matsuda Index) correlated with elevated Z-scores (r = 0.51, r = 0.54, r = -0.49; all P < 0.002, respectively). Basal, first-, and second-phase b-cell function correlated with low Z-scores (r = -0.59, r = -0.51, and r = -0.43, all P < 0.001). Insulin secretion significantly predicted the Z-score independent of sex, body fat, blood lipids, blood pressure, IR, and glucose metabolism (P < 0.005). Conclusion: b-cell dysfunction is highly correlated with the severity of metabolic syndrome in adults. Future work is warranted to elucidate the mechanism by which cardiometabolic disturbances influence insulin secretion.