# Dysregulated autophagy at the nexus of type 2 diabetes mellitus and pancreatic cancer pathogenesis

## TL;DR

This paper explores how disrupted autophagy connects type 2 diabetes and pancreatic cancer, offering new insights into their shared mechanisms and potential treatments.

## Contribution

The paper highlights autophagy as a key link between type 2 diabetes and pancreatic cancer, proposing novel therapeutic targets.

## Key findings

- Dysregulated autophagy contributes to β-cell failure and insulin resistance in diabetes.
- Autophagy has a dual role in pancreatic cancer, suppressing tumors early but aiding progression later.
- Autophagy pathways may serve as a common pathophysiological basis for both diseases.

## Abstract

Diabetes Mellitus (DM) and Pancreatic Cancer (PC) are two major diseases that pose severe threats to global health, and their comorbidities have drawn increasing attention in recent years. Substantial epidemiological evidence indicates that type 2 diabetes mellitus (T2DM) is not only a risk factor for PC development but also an early clinical manifestation. The pathogenesis of these two conditions is interactive, wherein autophagy—a highly conserved intracellular catabolic process—plays a central role in maintaining pancreatic β-cell function, regulating insulin sensitivity, and determining the fate of PC cells. In diabetes, dysregulated autophagy contributes to β-cell failure and insulin resistance; in PC, autophagy plays a dual role, potentially suppressing tumorigenesis in early stages while supporting cancer cell survival and proliferation during progression, thereby mediating chemotherapy resistance. We review the epidemiological links, shared risk factors, and mutual influences of clinical management strategies in the comorbidity of diabetes and PC and focus on dissecting the pivotal role of autophagy at the intersection of their mechanisms. To elucidate the connection of autophagy pathways in both diseases, we aimed to provide novel perspectives on their common pathophysiological basis and identify potential targets for innovative therapeutic strategies against this comorbidity.