Vestibular‑visual input abnormality and sympathetic feedforward dysregulation may modulate postprandial blood glucose: a hypothesis of "perfusion‑limited impaired insulin action" in a non‑obese T2DM patient with stable β‑cell function

This is an N-of-1 self-observation case report and hypothesis-generating manuscript. The author is the sole research subject, and no other human participants are included. This work proposes a novel mechanistic hypothesis: vestibular‑visual sensory abnormality and sympathetic feedforward dysregulation lead to microcirculation perfusion‑limited insulin action impairment, which explains the extreme postprandial glycemic surge in non‑obese type 2 diabetes with normal baseline HOMA‑IR. This study only generates a testable hypothesis and does not confirm causal relationships. Ethics statement: This is self‑experiment and self‑observation by the author himself. No third‑party human subjects were recruited. Ethical committee approval is not required for this single‑person self‑observation study. All raw data are collected and verified by the author. Readers should not copy or imitate any intervention described in this article.