At the 85th Scientific Sessions of the American Diabetes Association (ADA 2025), the presentation of the Banting Medal for Scientific Achievement was undoubtedly one of the most anticipated highlights. As the highest scientific honor of the ADA, this award commemorates Dr. Frederick Banting—the medical scientist, physician, and Nobel laureate who played a pivotal role in the discovery of insulin.
This year’s award was bestowed upon Dr. Steven Kahn, Director of the Diabetes Research Center at the University of Washington, in recognition of his outstanding contributions to elucidating the central role of β‑cells in the pathogenesis and treatment of prediabetes and type 2 diabetes (T2DM).
Accumulating evidence indicates that alterations in β‑cell function and mass are central to the pathogenesis and progression of T2DM. Preclinical models and early clinical studies have identified islet amyloid deposition as one mechanism leading to β‑cell dysfunction and death, resulting in progressive deterioration of glycemic control.
Dr. Steven E. Kahn emphasized:“Studies show that islet amyloid is a mechanism of β‑cell loss in T2DM, and reducing amyloid formation can protect β‑cells by decreasing oxidative stress and inflammation. Therefore, the development of amyloid inhibitors holds promise for slowing the progression of T2DM.”
Dr. Kahn reviewed that β‑cell dysfunction in T2DM was documented as early as the 1960s, and reduced β‑cell mass was reported back in 1955.For decades, it has been recognized that the feedback interplay between insulin‑secreting cells (β‑cells) and insulin‑sensitive tissues (liver, muscle, and fat) is critical for regulating insulin secretion and maintaining glucose homeostasis.In the 1990s, Dr. Kahn’s laboratory established the hyperbolic relationship between β‑cell response and insulin sensitivity: higher insulin sensitivity correlates with greater β‑cell responsiveness. As insulin sensitivity declines, β‑cell response diminishes, leading to elevated fasting blood glucose.
A major clinical challenge in T2DM management is the decline in drug efficacy over time.Research from Dr. Kahn’s lab has shown that the effectiveness of various classes of glucose‑lowering agents, incretins, and GLP‑1 RAs gradually weakens, closely linked to progressive β‑cell dysfunction.He further noted that β‑cell function is lost more rapidly in young people compared with adults, explaining the more aggressive disease course in younger patients with T2DM.
Dr. Kahn explained that a key driver of declining β‑cell function is the progressive reduction in β‑cell mass over time.Although multiple factors contribute to β‑cell loss, islet amyloid deposition represents a major mechanism.Islet amyloid polypeptide (IAPP) is co‑secreted with insulin but abnormally aggregates into fibrils in T2DM for unknown reasons.This amyloid deposition is strongly associated with human β‑cell loss, but not in mouse models.To investigate this, Dr. Kahn’s lab developed transgenic mice expressing human islet cells, in which islet amyloid deposition induced oxidative stress—and blocking oxidative stress reduced amyloid formation and β‑cell loss.
In this mouse model, islet amyloid formation also promoted macrophage infiltration and accumulation, and enhanced the expression of inflammation‑related genes.Experiments showed that adding physiological concentrations of the pro‑inflammatory cytokine interleukin‑1β (IL‑1β) further exacerbated amyloid deposition and β‑cell death.
Dr. Kahn concluded:“We believe there is a vicious cycle: amyloid induces oxidative stress, which in turn promotes amyloid production. The data support a feed‑forward mechanism whereby amyloid formation triggers inflammation, and inflammation increases amyloid deposition via IL‑1β.”
Human cell culture studies further confirmed that reducing amyloid formation helps preserve β‑cells and their function.Dr. Kahn pointed out that amyloid inhibitors currently being developed for Alzheimer’s disease may eventually be repurposed for the treatment of T2DM.A human proof‑of‑concept study using CT/PET flutemetamol imaging has already confirmed excessive amyloid deposition in the pancreas of patients with T2DM.Dr. Kahn stated that confirmatory imaging studies are planned.