Possible Giant Breakthrough in Diabetes; Recently Discovered “Inceptor” May Be a Type 2 Diabetes Therapeutic Target

Research targeting the insulin-inhibitory receptor, called “inceptor,” unveils promising avenues for beta cell protection, offering hope for causal diabetes therapy. A novel study in mice with diet-induced obesity demonstrates that the knock-out of inceptor enhances glucose regulation, prompting its further exploration as a drug target for type 2 diabetes treatment. These findings, led by Helmholtz Munich in collaboration with the German Center for Diabetes Research, the Technical University of Munich, and the Ludwig-Maximilians-University Munich, drive advancements in diabetes research.

Insulin-producing beta cells in islet of Langerhans. (Credit: Helmholtz Munich | ©Erik Bader)

Targeting “Inceptor” to Combat Insulin Resistance in Beta Cells

Insulin resistance, often linked to abdominal obesity, presents a significant healthcare dilemma in our era. More importantly, the insulin resistance of beta cells contributes to their dysfunction and the transition from obesity to overt type 2 diabetes. Currently, all pharmacotherapies, including insulin supplementation, focus on managing high blood sugar levels rather than addressing the underlying cause of diabetes: beta cell failure or loss. Therefore, research into beta cell protection and regeneration is crucial and holds promising prospects for addressing the root cause of diabetes, offering potential avenues for causal treatment. With the recent discovery of “inceptor,” the research group of beta cell expert Prof. Heiko Lickert at Technical University Munich (TUM) has uncovered an interesting molecular target. Upregulated in diabetes, the insulin-inhibitory receptor inceptor may contribute to insulin resistance by acting as a negative regulator of this signaling pathway. Conversely, inhibiting the function of inceptor could enhance insulin signaling – which in turn is required for overall beta cell function, survival, and compensation upon stress.

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