Adipo-B Index as a Novel Predictor of Beta-Cell Secretory Function Without Measuring Insulin: Cross-Therapeutic Validation Against C-Peptide Index in Treatment-Naive Type 2 Diabetes

OBJECTIVE The adipo-B index (adipo-IR divided by HOMA-B) was introduced as an integrator of adipose tissue insulin resistance and pancreatic beta-cell function. Algebraic simplification reveals that insulin cancels from the formula, yielding FFA x (FBG-63)/360 - a composite of circulating free fatty acids and ambient glycemia. We investigated whether this index predicts beta-cell secretory capacity measured by HOMA-B and C-peptide index (CPR-index) across four therapeutic strategies. RESEARCH DESIGN AND METHODS A total of 253 treatment-naive subjects with T2DM received monotherapy with modified Japanese diet for diabetes (MJDD, n=61), canagliflozin (n=67), pioglitazone (n=62), or sitagliptin (n=63). Correlations between baseline adipo-B and baseline beta-cell indices, and between their longitudinal changes, were examined. This is a prospective, non-randomized observational study. RESULTS At baseline, adipo-B showed significant negative correlations with HOMA-B with all the subjects. At 3 months, adipo-B significantly decreased and HOMA-B significantly increased with all the therapeutic groups. CPR-index significantly improved with canagliflozin and sitagliptin. Pioglitazone showed a trend toward improvement while MJDD demonstrated no changes. Changes in adipo-B (delta adipo-B) significantly and negatively correlated with changes in both HOMA-B and CPR-index in MJDD, canagliflozin, and sitagliptin. With pioglitazone, no such correlations were observed - consistent with the previously reported bidirectional regulation of insulin secretion by pioglitazone depending on baseline insulin secretory status. CONCLUSIONS The adipo-B index predicted beta-cell secretory capacity - assessed independently by conventional beta-cell indices - without requiring insulin or C-peptide measurement. These findings suggest adipo-B may serve as a cost-effective surrogate for assessment of beta-cell function in routine clinical settings.