Research

An islet-coordination framework for the early detection of type 2 diabetes

Type 2 diabetes is conventionally defined and detected by glucose thresholds. By the time those thresholds are crossed, the pancreatic islet has already undergone years of compensatory and pathological adaptation. My program reframes T2D as progressive islet coordination failure — a structured, stageable phenomenon that can be measured before glucose itself goes out of range.

The central output is a multi-axis quantitative framework designed to detect structured metabolic dysfunction and organ-level risk prior to the onset of conventional glucose-based criteria.

Program of work

Mechanistic mouse studies

Persistent inflammatory lipotoxicity as a driver of impaired β-cell function despite glucose normalization — extending earlier postdoctoral work dissociating glucotoxicity from lipotoxicity in diet-induced obese mice.

Conceptual synthesis

A historical and conceptual synthesis of islet coordination failure, integrating decades of β-cell, α-cell, and tissue-level work into a unified staging model.

Human population validation

Full-spectrum validation in NHANES III, testing whether ICS-derived axes detect early metabolic dysfunction across demographic strata before overt hyperglycemia.

Cross-species translation

Mouse experiments designed to test ICS-relevant mechanisms — β-cell stress, dedifferentiation, glucagon signaling — and feed back into the clinical framework.

Intellectual property

Three U.S. provisional patents filed (March–April 2026) cover the ICS framework and related embodiments, including the bihormonal glucagon framework and a five-axis ICS with NHANES III validation.

For a complete record of published work, see Publications. For the full academic history, see my CV.